CHAPTER 5 Influenza
Influenza is a viral disease, like smallpox, but the viruses that cause influenza are far more unstable genetically than Variola major and minor, and consequently there are far more, ever-shifting varieties of the microbe that make it a much more challenging disease to combat by means of vaccination.
Like a “moving target,” influenza viruses are constantly mutating in the process of replicating copies of their RNA (ribonucleic acid) that they can only achieve by invading a host cell in order to harness its biological machinery; it is estimated that within a single cell an influenza virus can manufacture and then release up to a hundred copies of itself within five or six hours. It is because of this high rate of reproduction (without any ability to “proofread” or correct copies of its genes as in the case of deoxyribonucleic acid, or DNA) that influenza viruses remain so elusive, since the protein molecules or antigens comprising the viruses' outer coat or capsid, which are recognized and engaged by the antibodies of our immune defense system, are constantly evolving in both minor and major ways, known respectively as antigenic drift and antigenic shift. For this reason, we will probably never “conquer,” or entirely eliminate, influenza as was achieved against smallpox in the 1970s, and in this respect, influenza is more akin to the human immunodeficiency virus (HIV) that causes AIDS (acquired immune deficiency syndrome) and that will be the focus of the next chapter. Interestingly enough, it has also been recently discovered that the influenza virus can target and suppress the body's immune system, much as HIV does in AIDS, in order to give the virus time to replicate within the lungs.Due to their complexity, influenza viruses have earned an elaborate classification system whereby they are divided into three main “types,” known as A, B, and C (based on the nucleoprotein antigen), of which the type A viruses are the only ones known to cause large-scale pandemics in humans.
Within type A, influenza viruses are further classified on the basis of their outer protein coats that allow them to enter and exit a host cell: these are the hemagglutinin (H) and neuraminidase (N) glycoproteins, of which fifteen varieties are known of the former and nine of the latter. This is how various influenza viruses get their names in the news and other literature that talk about the agents responsible for particular pandemics; for example, the H1N1 virus is believed to have caused both the 1918—1919 pandemic and the recent one that made the rounds in 2009. What is not so clear is if influenza viruses only drift and shift in a cyclical manner, within the relatively limited number of antigenic combinations identified thus far, or if we are doomed to encounter ever new proteins as these constantly evolve.1Influenza is perhaps the most contagious of any infectious disease we know of; it is more transmissible than smallpox because influenza viruses, like the rhinoviruses that cause the common cold, specifically target cells in the upper and lower respiratory tract, although they can subsequently be distributed to other parts of the body, such as the brain and central nervous system, where they cause other symptoms typically associated with the disease. Influenza is therefore particularly well suited to person-to-person communication by means of sneezing, coughing, or simple breathing. And since a virus is five hundred times smaller than a bacterium, many more infectious agents are emitted by a victim of influenza with each cough or sneeze than one afflicted with a bacterial respiratory disease such as pneumonic plague or tuberculosis; this makes it far more likely not only that a person nearby will contract influenza but also that it will penetrate deeper into the lungs where it cannot easily be ejected by the cough reflex. (This is why gauze facemasks recommended by Dr. Wu Liande that protected his medical staff during the pneumonic plague outbreak in Manchuria in 1910— 1911 proved not so effective against the influenza pandemic in 1918—1919.) In addition, the influenza virus can remain infectious for up to forty-eight hours outside the host, so that one can also contract influenza by breathing in contaminated dust particles or by touching contaminated objects such as doorknobs and utensils and then ingesting the microbial agents on one's hands.
Recent experience with avian flu has likewise demonstrated that influenza can be spread, at least from animals to humans, via the gastrointestinal tract as a result of eating infected poultry products or drinking contaminated water.2As soon as one or two days from infection, the typical flu symptoms will manifest themselves, which include high fever, chills, headache and other bodily aches and pains, prostration, lethargy, and sometimes vomiting or diarrhea. In the worst-case scenario, bacterial or viral pneumonia will later emerge, due to the fact that a certain amount of synergy exists between flu and pneumonia: flu can prepare the way for pneumonic infection and vice versa.3 It is important to note that the victim is infectious even before these symptoms appear, and some people can be infected by flu without showing hardly any signs at all, becoming in effect asymptomatic carriers of the disease.4 But flu symptoms are so general that it is quite difficult to make a positive diagnosis of historical epidemics on that basis alone; usually a pattern of high morbidity accompanied by low mortality that is typical of influenza will confirm its presence in most scholars' minds.5 Influenza usually runs its course through the human body in three days, after which the patient can generally be expected to make a full recovery. Death from flu is rare, occurring on average in only one-tenth of 1 percent of all victims during most outbreaks; these unfortunates also tend to be either the very young or the very old, people already at high risk in premodern times. The exception, of course, was the 1918—1919 pandemic, when average mortality rates jumped to 2.5 to 5 percent or higher in some places, and many more victims came from among those in the prime of life, roughly between twenty and forty years of age. Morbidity rates for this pandemic were likewise unprecedented for normal influenza, comprising anywhere from 25 to 50 percent of populations, although such statistics are notoriously hard to pin down since cases of sickness were less rigorously reported than actual deaths.6
A seasonality of incidence is also associated with influenza, which strikes typically during the winter months in the northern and southern hemispheres and during the rainy or monsoon seasons in tropical zones.
At times, however, influenza can come on in waves, as it did in 1918—1919. In this particular outbreak, historians have noted three successive waves of the disease, a first and mild one occurring in the spring to midsummer of 1918, the second and most severe wave starting almost immediately thereafter in the late summer and autumn, and finally a third and again mild wave during the early months of 1919.7 The flu pandemic that ran its course in the United States during the latter half of 2009 peaked in September and October, rather than during the usual bad months for flu of December and January. A combination of social and environmental factors are thought responsible for flu's seasonal behavior. Certainly, overcrowding of populations that tend to occur with the onset of bad weather will greatly facilitate spread of influenza, but the virus also does best in conditions of low humidity and sunlight such as we find in winter. Human immune systems are also more likely to be compromised as the body fights off the effects of cold or rain. Yet, a certain amount of mystery remains in this regard: laboratory experiments with mice have found flu behaving seasonally even when conditions of temperature and humidity are equal.8Such are the bare epidemiological facts about influenza that distinguish it from other infectious diseases we have discussed thus far. Compared to those of plague, smallpox, or cholera, its symptoms are not especially memorable, dramatic, or enduring. In most cases, an entire epidemic or even pandemic comes and goes quickly, in a matter of months, leaving behind relatively few to mourn and those at the life-expectant margins of society. This has made it easy for both past and present cultures to overlook influenza, seeing it, perhaps, as no worse than a severe cold. And yet the 1918—1919 pandemic overturned all these expectations about this otherwise seemingly benign disease, for in that one outbreak influenza swept across as many categories of society as the “danse macabre” of plague; in some unforgettable cases, it brought on the heliotrope or blue-black cyanosis of the face so typical of cholera, and it marked its survivors with a trauma as tangible, even if not as visible, as the pockmarks of smallpox.
Remarkably, influenza in this particular instance behaved both like the worst of infectious diseases in the minority of cases it did kill, striking with a virulence that invited comparisons with the Black Death, and like any other flu outbreak in terms of the usual pattern of low mortality and high morbidity: horrifying as the deaths from flu were, the vast majority of people still recovered from or did not get the disease. In a sense, here was influenza on the grand scale, with a much higher incidence of the disease than normal and across a broader spectrum of the population, accompanied by a higher mortality rate within that subgroup, in a particularly far-reaching pandemic that left practically no part of the world, even in its remotest spaces, untouched. In other words, influenza was still influenza, only this time morphed into a monstrous version of itself that, of necessity, impinged upon the consciousness of all. Although the historian Alfred Crosby has dubbed it the “forgotten pandemic” among its own contemporary generation, the outbreak of 1918—1919 has since cast a long shadow over almost every subsequent pandemic threat of influenza.9 It is quite simply the deadliest single outbreak of disease in history, surpassing even the Black Death in terms of sheer numbers of people directly killed by its onslaught, with the most recent estimates ranging anywhere from fifty to one hundred million dead worldwide. Why and how this happened are mysteries that are still in the process of being answered.Before we get to the infamous 1918—1919 pandemic, however, it is advisable to trace the prior history of this disease. Influenza viruses have been around for millions of years, where their natural host reservoir has been and continues to be ducks and other aquatic wildfowl, which are generally immune to the disease and instead act as carriers, continually shedding viruses in their feces. When humans began domesticating ducks around four thousand years ago, the influenza virus was then able to make this species leap, even though the current human strains of influenza had already emerged toward the start of the Neolithic age another four thousand years earlier.
As humans domesticated other animals, particularly pigs and chickens, influenza was able to make its endemic home in human populations across much of the ancient world. (In addition to the above species, influenza epidemics are also known to afflict horses, dogs, and cats.) However, the source of most new outbreaks of human influenza, both then and now, is thought to be China and Southeast Asia, due to its ancient practice of rice growing and fish farming, where live ducks living in the water were used for weeding and their feces as fertilizer and fish food. When pigs were added to this microbial stew, passage of the influenza virus from animals to humans became much easier, since pigs, having an anatomy much closer to humans than do birds, were able to be infected by both human and avian strains of influenza and thus became a kind of “mixing bowl” for emerging flu pandemics.10 Yet, the influenza virus can and does pass directly from birds to humans, and indeed this is what is now thought to have occurred during the influenza pandemic of 1918—1919, as well as in the current outbreaks of avian flu that have menaced the world for at least the past decade.The ancient Greek physician Hippocrates provides perhaps our first written description of influenza in his Epidemics composed sometime during the fourth century B.C.E., and down through to the Middle Ages flu outbreaks may have been subsumed under references to “fevers,” “rheums,” and “catarrhs.” The term “influenza” itself was apparently first introduced from the Italian in 1504 to describe any general disease epidemic that afflicted large numbers of people due to the “influence” of the stars; the modern sense of the word does not seem to emerge, however, until the eighteenth century, when the “grippe” also came into usage to refer to the disease. Some convincing descriptions of influenza epidemics in Britain and Europe can be produced for the sixteenth and seventeenth centuries, but it is quite likely that any such outbreaks were sporadic and not very widespread.11 There may be any number of reasons for this. One explanation that has not been considered thus far is that, at this time, health manuals, plague treatises, and dietary regimens all advised that people steer clear of waterfowl, such as ducks and geese, not only on the grounds that their “watery” meat would produce watery, easily corruptible blood but also because they fed on unclean, noxious things in often foul, stagnant waters.12 While of course ignorant of the fact that waterfowl were the natural hosts of the influenza virus, such medical prescience may nonetheless have limited the opportunities for the virus to become endemic in human populations, at least in Europe, where this advice was proffered. Moreover, human traffic to the Far East, presumably the ancient home of influenza, would have taken too long and would not have been of high enough volume to really sustain too many pandemics.
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, a rat- and flea-based disease that could follow the movements of grain and merchandise shipments, influenza had to wait until modern technology made hu- man-to-human transmission across long distances possible. Also, cities now began to greatly increase in size and density, especially 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 still the norm in terms of treatment. However, because influenza was a relatively mild disease, at least compared to plague or smallpox, that killed 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 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 both spread the flu and pillaged agricultural lands, which then could not be replanted 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 re-creation 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 experiment 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 Yersiniapestis. We have already noted that bacterial pneumonia is an opportunistic disease of influenza, and in any 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 weaponry 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
saved many lives by denying to flu its tinder of mass numbers of men in cramped quarters. But given the enormous pressure and demand for American troops to seal an Allied victory, at a time when Britain and France were exhausted and spent, there was perhaps little choice left for the president to make. However, America did learn the hard lesson that it needed to provide better medical support services to its troops and not build hospitals at its bases last.26
Even countries in the very thick of the fighting, such as France, found it was the logistics of war, rather than the war itself, that most contributed to influenza, as troops were transported to and from the front and civilian populations were starved of supplies that were sent instead to the soldiers, thus facilitating both the spread of the disease and host susceptibility to it. And yet Spain, a neutral country in the war, apparently suffered equally from influenza, to the point that the epidemic in Europe began to be called the “Spanish Flu” or the “Spanish Lady,” an unfair designation as Spain was simply one of the few countries publishing its statistics on the disease. Counterintuitively, war could even be a benefit to a country struck suddenly and unexpectedly by influenza, as was found to be the case in New Zealand where a heightened state of preparedness during wartime helped mobilize emergency relief efforts in response to the disease. The connection between flu and other factors, such as overcrowding and socioeconomic disparities, could likewise be called into question on the basis of figures from Britain, which show flu mortalities being distributed fairly equally.27 But how else to explain the fact that India's death rate from the flu was twelve times higher than that of the United States or Europe, unless a completely different strain of the virus prevailed in Asia, which seems unlikely?28 This conundrum of flu needs to be solved if we are to draw the right lessons from 1918, to wit, if the flu's mortality was largely biological, as was the case with plague in Europe during the Middle Ages or smallpox in the New World during the sixteenth century, when human populations had little immunity to these diseases, then experts think it quite likely, indeed almost inevitable, that another such devastating pandemic will occur. If, however, flu deaths were primarily the product of the unique historical context of 1918—1919, including the First World War and its aftermath, bad weather and widespread crop failures, inadequate medical knowledge of and preparedness for the disease, and so forth, then there is hope the disaster will not be repeated.29 I think the odds are that it was a combination of both: the emergence of an unusually virulent strain of influenza in 1918 and circumstances that greatly facilitated its spread and mortality, especially from opportunistic diseases like pneumonia. If this is the case, then at the very least we can expect to mitigate (or else amplify) any future flu's impact, even one as deadly as that in 1918. Then there is also the possibility that, in our current climate, the two sides of the equation are inextricable: that some of our more destructive social behaviors, such as environmental degradation or factory farming and food production, are in fact creating the very conditions in which new biological strains of influenza, and of other exotic viral diseases, can occur.
Historians have noted that the 1918—1919 flu pandemic broke all the rules. In some ways, it acted like any other influenza outbreak, striking most places with high morbidity and relatively lower mortality, but in other respects it flagrantly bucked the trend of the way flu was expected to behave. One of the more shocking things that was happening at the time was that people in the prime of life, between twenty and forty years of age, were the ones being most struck down, which wasn't normally supposed to happen in a typical flu outbreak; as already explained, this was due to the unique cytokine response that the 1918 virus induced, which would be most expressive in robust, healthy adults. This was an anomaly noted all over the world, but it should be remembered that virtually all age groups, including the very young and the very old that were typically targeted by flu, were experiencing above-average mortality at this time. Flu was behaving like the Black Death of the Middle Ages in this respect. Life expectancies were set back by ten years or more even in advanced industrialized countries not directly invaded by the war, such as the United States, and generally women (particularly those who were pregnant) seem to have lost their longevity advantages over men.30 When influenza's effects are combined with losses from the war, which also targeted the most productive (in this case male) members of society, it is easy to see why this became the “lost generation” of its time. The spectacle of corpses stacked like “cordwood” in hospital corridors and bodies lying unburied due to lack of space or a shortage of gravediggers naturally evoked memories of plague, as did reports of panicked flight and scapegoating early in the pandemic, which quickly subsided once it was realized that no one was exempt and there was nowhere to run. Like the Black Death, the influenza pandemic of 1918—1919 was both an urban and a rural phenomenon. Doctors once again found themselves utterly impotent for all their recent advances in bacteriology. Discovery of a potential cause of the disease in “Pfeiffer's Bacillus,” a bacterium allegedly found in flu patients by the German physician Richard Pfeiffer, proved premature and discouragingly anticlimactic; the first flu virus was not to be isolated from human subjects until 1933. On the other hand, female nurses found themselves empowered due to the fact that simple bed rest and nursing care proved the most effective remedy, or at least provided some comfort to suffering victims in their last hours, especially in an age that preceded antibiotics as a “miracle cure” for pneumonic infections.31
Campaigns to improve sanitation and hygiene, such as local laws that forbade coughing and spitting, were reminiscent of what was tried during cholera epidemics in Europe in the previous century. In an even earlier throwback to the time of plague, authorities also proscribed communal spaces—now to include schools and movie theaters in addition to churches (but not bars, since alcohol and tobacco were believed to be prophylactic against the flu!). And predictions of the apocalypse, or end of the world, once again came into fashion, as they had been in the Middle Ages. Influenza even inspired its own nursery rhyme, comparable to the “ring around the rosy” ditty composed during the London plague of 1665, which was sung in 1918 by my grandmotherin-law and which proved remarkably prescient, given what we now know about the probable avian origins of the virus:
I had a little bird
And its name was Enza
I opened up the window
And in-flu-enza!
Some aspects of the 1918—1919 pandemic also foreshadowed future concerns about disease: for example, some American cities mandated the wearing of gauze masks, but when these proved ineffectual, civil liberty suits were brought because they were uncomfortable or embarrassing for some. The millions of dollars in business losses, such as were sustained by the life insurance industry, as death rates soared in 1918 added an economic dimension on a scale that was to become a familiar one in the calculations of the impact of all subsequent pandemics.32
Above all, the influenza outbreak of 1918—1919 is unique in terms of how contemporaries chose to historicize this disease. In contrast to the plague, for example, it became the “forgotten pandemic” and not just in the United States or Europe but also in other countries around the globe, such as Senegal. Why this is so has been variously explained. For much of the Western world, the unprecedented violence and brutality of the previous four years of war perhaps inured it to the “just another millions” more deaths from influenza, which did not produce the political and diplomatic legacy of Versailles, or maybe the quiet deaths from disease were not heroic or dramatic enough even for a generation that had lost its romantic love affair with war. The nature of influenza itself also encouraged collective amnesia about it. As Crosby notes, it came and went relatively quickly, and compared to a more deadly disease per incidence like plague, it did not inspire the same degree of terror when most people who contracted it could still expect to survive, even in 1918. In the end, people may simply have wished to forget its horrors, after everything else they had been through, and remember it just like any other influenza.33 Yet, this is now no longer the case. Since 1976, the recovered memory of what happened in 1918—1919 has cast a long shadow, as dark and ominous as the Black Death, over every real and potential pandemic of the flu.
After 1919, influenza pandemics seemed to subside for the next three decades: During that time, viruses were successfully scanned by the new technology of electron microscopes, antibiotics were discovered and first tested on humans, and the World Health Organization (WHO) was formed in 1948, with a World Influenza Center established the following year, in order to coordinate worldwide responses to disease and share information from laboratories in forty-five countries around the globe. Thereafter, an influenza pandemic looked set to be occurring once a decade with the advent of airline travel and an ever-shrinking world: pandemics occurred in 1946—1949—in the aftermath of World War II; in 1957; and in 1968—the so-called Hong Kong Flu. All these pandemics were considerably milder than the one in 1918—1919, conforming once again to flu's typical pattern of targeting the very young and the very old, and WHO demonstrated that vaccination programs could be coordinated on a global scale, experience it was to use to good effect in its smallpox eradication campaign of the 1970s. But the disturbing thing about these pandemics was that they demonstrated the rapidly mutating capability of the flu virus. The one of the 1940s was a H1N1 strain to which many must have had some immunity from the 1918 pandemic; those of 1957 and 1968, however, were caused by entirely new strains (antigenic shift) of H2N2 and H3N2 respectively, which successively crowded out earlier ones. These pandemics are also believed to have come from the Far East, specifically China, and to have come on in waves, like in 1918, with the second wave seemingly more virulent (both in terms of morbidity and mortality) than the first, showcasing an evolutionary process whereby the virus was evidently adapting itself more successfully to humans. Yet, as in 1918, those who caught the flu in the first, milder wave seem to have acquired some immunity to later incidences of the disease, and it is thought that the strains of 1957 and 1968 may have circulated in the late nineteenth century, conferring some protection to the older generation who were most susceptible. This time the viruses responsible are thought to have arose through “reassortment” of human and avian strains in a third host, such as pigs, rather than making a direct leap from birds to humans as in 1918, which means that these later pandemics would act less like “virgin soil” diseases in human populations and were less likely to provoke in them uncontrolled immune responses, such as a cytokine storm. Yet, all was not smooth sailing, as Communist China under Chairman Mao Zedong maintained a closed-door policy with respect to reporting flu cases, a pattern that has continued recently with avian flu; to this day, we still do not know how many Chinese died in 1957, with some scholars believing that a good proportion of the thirty million who died during the “Great Leap Forward” collectivization program between 1958 and 1961 may be attributed to flu. Even in Western democratic developed countries, such as Britain, authorities were slow to follow WHO recommendations and close schools, which has been proven to halt epidemics, and hospital facilities and staff were at times overwhelmed.34
The postwar experience of a flu pandemic occurring once every decade looked set to continue when in January 1976 more than two hundred army recruits at Fort Dix in New Jersey came down with an H1N1 “swine flu” strain, although several dozen victims were also infected with the H3N2 virus that had last circulated in 1968. Of great concern at the time was that the swine flu virus was demonstrated to be transmissible from person to person and that it seemed to be related to the exceptionally virulent strain of 1918, since serum obtained from individuals over fifty years of age, who were likely to have been exposed to the earlier virus, contained antibodies to the present one. This also meant that much of the population, particularly the younger generation, would have no immunity to this virus since they had been born after the strain of 1918 had ceased circulating, which raised the specter of another “virgin soil”—type pandemic. As it turns out, we have already seen that recent biomolecular archaeology on autopsy samples from victims of the 1918 flu indicate that it was an avian strain, not a swine one, yet this information was simply not available in 1976; in fact, this “epidemic that wasn't” was the first to demonstrate that a major antigenic shift can occur in an influenza virus without producing a widespread outbreak. This was probably because the virus passed directly from pigs to humans without recombination or reassortment in swine with a human viral strain, which would have made it far more transmissible person to person.35
However, while doing nothing was simply not an option, some at the time did counsel caution: Albert Sabin, who helped develop the polio vaccine in the 1950s, recommended to the Centers for Disease Control (CDC) and in testimony before Congress that only high-risk groups be initially targeted for vaccination and that in the meantime extra doses be stockpiled, while WHO failed to report any further outbreaks of flu cases around the world. Yet, dissenting voices were deliberately excluded from the blue-ribbon panel advising U.S. president Gerald Ford. As a consequence, an ambitious, $135 million program to mass vaccinate the entire U.S. population of roughly two hundred million people was quickly signed into law by Ford in April, and implementation began with the first shots administered in October. A number of factors went into this decision to vaccinate on such an unprecedented scale. Chief among these seem to have been fears of a repeat of 1918, with its huge potential losses in lives and treasure, this time ranging in the millions of deaths and billions of dollars. Historical writing about the flu also played its part. It was said that the secretary of the Department of Health, Education, and Welfare, David Mathews, read Crosby's new book about the 1918 pandemic, Epidemic and Peace, and warned his colleague, James Lynn, director of the Office of Management and Budget, that “we will see a return of the 1918 flu virus.” In addition, the 1957 and 1968 pandemics had demonstrated the costs in thousands of lives lost when vaccine was delivered too late or in too few doses. But this was also an election year (as well as America's bicentennial), and Ford faced strong challenges first during the Republican primary from California governor Ronald Reagan and then in the general election from his Democratic opponent, Jimmy Carter. Editorials in the New York Times indeed accused the vaccination program of being primarily motivated by politics. In the event, the ensuing “fiasco” or “debacle,” as it was called, probably cost Ford more in political capital than he gained. When an epidemic failed to materialize in the fall, this only reinforced his popular image as an incompetent bungler.36 I still remember watching a satiric spoof of the U.S. presidential debates by the Saturday Night Live comedy program, in which comedian Chevy Chase appeared as Ford with a vaccine shot still stuck in his arm! (A picture of Ford receiving his flu shot was published on the wire, perhaps to increase confidence in the vaccine.)
By mid-December the vaccination program was canceled, largely due to fears of side effects when several hundred vaccinated individuals came down with a rare and sometimes fatal neurological disease called Guillain-Barre syndrome. Although subsequent studies claim that those receiving a vaccine had a five times higher (yet still pretty remote) chance of contracting Guillian-Barre than those who did not, a more than circumstantial connection has still to be proven with this particular vaccine, since such complications can occur with any foreign substance introduced into the body.37 Despite this setback, some would argue that the 1976 vaccination was a success, in that it demonstrated how a large number of vaccine doses—over forty-three million, representing 50 percent of the high-risk group (double what is normally covered in most vaccine programs) or nearly a quarter of the general population—could be mobilized in a short amount of time. Edwin Kilbourne, who served as medical adviser and advocate of the program, summed up his justification, and that of the CDC, thus: “Better a vaccine without an epidemic than an epidemic without a vaccine.”38 Two National Immunization Conferences were also held in the immediate aftermath of 1976 under the succeeding Carter administration, which resulted in proposals for a permanent flu vaccination program supervised by the federal government as well as increased awareness of the necessity for better immunization against other infectious diseases, such as polio, measles, and diphtheria.39
But aside from the monetary cost, these benefits did not come without a price. Hostility to government vaccination programs was given free rein during the presidency of Reagan in the 1980s, which helped scuttle funding for immunization against the flu as well as against other preventable diseases like measles, while the initiative for developing future vaccines was hereafter surrendered to private industry.40 The experience of 1976, however, proved this to be a mistake, for pharmaceutical companies found they could not get insurance on their own to cover their liabilities from potential lawsuits (to date over six hundred million dollars in filed claims), which instead had to be covered by a special appropriation from Congress, and difficulties ensued with the distribution and administration of the vaccine, which was left up to local state control and was therefore very uneven. A more general fallout, but no less tangible for that, was a loss of public confidence in vaccinations, which was due to not only medical complications but also faulty manufacturing, in which one set of trial lots of the vaccine was made up with the wrong virus. All these misunderstandings could probably have been avoided or at least mitigated with better sharing of information amongst the media and the public, especially in the context of the widespread disillusionment with the federal government engendered by the recent Watergate scandal.41 It is a failure that still haunts vaccination efforts against flu to this day.
In recent years, fears have been raised about a possible pandemic of avian flu, caused by the H5N1 virus. The virus first came to the world's attention in 1997 with an outbreak in Hong Kong, where an epidemic was averted by the culling of about one and a half million market poultry, a policy that Hong Kong has adopted ever since in response to any reported outbreak of avian flu. As of the end of 2009, WHO reported a total of 467 human cases of avian flu around the world, resulting in 282 deaths, representing a mortality rate of just over 60 percent.42 Some would argue, however, that this vastly overstates the virulence of avian flu, since many more cases where flu symptoms are quite mild simply go unreported. Over half of the known cases occurred in Indonesia and Vietnam, with the next most numerous cases occurring in Egypt, China, Thailand, Turkey, Cambodia, and Azerbaijan, in that order. Again, this may reflect honesty of reporting just as much as actual cases. Typically, those who have come down with avian flu contracted it directly from domestic birds, who are likewise highly susceptible to the virus (to date millions upon millions have died); in most cases, the virus was transmitted either by eating infected poultry products (such as raw duck blood, considered a delicacy in Vietnam) or by breathing in dust particles contaminated with bird feces, within which the virus is shed in huge numbers. However, clusters of cases of human-to-human transmission have also occurred, although these are usually confined to family members where close contact with infection sources likewise seems to be a prerequisite and where the virus seems to have weakened in virulence with each subsequent transmission. Some flu victims exhibited symptoms of a cytokine storm, or immune overreaction to the virus, much like what happened during the 1918 pandemic, but in other cases symptoms were delayed or much less severe; such variations seem to be due to different genetic responses to the virus in respective hosts.43
There is much debate about whether an avian flu pandemic is likely to occur outside what so far have been very localized outbreaks. Some say it is inevitable that the H5N1 virus will undergo a genetic shift and thereby evolve an ability to pass directly from human to human in a far more efficient manner than hitherto, since this has always been the past history of influenza. Others counter that the “not if but when” fears of an avian flu pandemic is all a hoax perpetrated largely by the media establishment and the pharmaceutical industry, who stand to benefit substantially from manufacturing an avian flu vaccine or antiviral drugs.44 In this scenario, avian flu will simply be a dead-end disease in its animal hosts, never breaking out widely in humans because its unique genetic and protein makeup is incompatible with that of human cells, as seems to have been the case with the overblown “swine flu” of 1976. In the case of avian flu, it is thought that the surface proteins of the virus are unable to bind to the sugar molecules in the cells of our nose and throat but can do so once the virus is deep in the lungs in the alveoli; this is why it is hard to contract yet is deadly once it happens. A sanguine view of avian flu also depends on the notion that a genetic hybrid or mixing (reassortment) of bird and human strains in a third host, such as a pig, is naturally impossible, which hasn't stopped recent efforts to artificially create one in the lab in the hopes of heading off its occurrence in nature, another Frankenstein's monster experiment that, as with the resurrection of the 1918 virus, is controversial.45
A further focus of debate concerns the source pools of infection for avian flu. In most literature this has been identified as the poor, rural areas of southern China, such as the Guangdong province, where human populations mingle with huge flocks of domestic ducks, geese, chickens, and turkeys that roam freely or are transported across vast areas of land with ample opportunities for contact with wild birds harboring the H5N1 virus; from there, the virus is then alleged to spread out to Hong Kong, Korea, Japan, and Southeast Asia. However, as was noted toward the start of this chapter, China's poultry farming practices go back to time immemorial, and so far, it does not seem that the virus has migrated with wild bird flocks outside its endemic areas, perhaps because most carriers die before they can get very far, as happened to wild geese and other waterfowl in some of China's nature reserves in 2005. Although other H5 and some H7 bird flu strains have appeared in the West, including the United States, Canada, Italy, Ireland, and, most recently in 2003, the Netherlands, these have been confined to animals or have not been very deadly to humans.46
An alternative hypothesis places the blame squarely on the industrialized production of food and factory farms, or Concentrated Animal Feeding Operations (CAFOs), the so-called bird jails where enormous numbers of poultry are kept confined at close quarters in cages and often in contact with other animal populations, such as pigs. This “livestock revolution” has been a relatively recent phenomenon, cresting, it has been noted, in the 1990s at the same time that avian flu first made its appearance. It is associated with Asian conglomerates such as Charoen Pokphand (CP) based in Bangkok, Thailand, and with American versions such as Tyson Foods and Perdue. These food monopolies produce mass quantities of chicken manure, which are sometimes used as fertilizer or otherwise present run-off hazards for the environment; appropriate or drive out smaller, free-range family farms; use antibiotics or genetically engineered embryos to maintain product quality (while increasing the risk of drug-resistant viral strains); adopt risky feeding practices such as the chopped-up remains of other animals (which is how bovine spongiform encephalopathy, or “mad cow disease,” emerged); and can best absorb the costs of governmental oversight aimed at preventing or halting disease migration from animals to humans, such as the culling of at-risk herds or monitoring programs such as the National Animal Identification System (NAIS) proposed by the U.S. Department of Agriculture. Although claims are made that such confinement operations are healthier because they keep their animals separate from wild reservoirs of disease, it is just as likely it is the other way around, that wild birds have picked up exotic viruses from chance encounters with artificial environments that receive little ventilation or sunlight and whose denizens are forced to defecate on each other and otherwise live in incredibly unhygienic, not to say inhumane, conditions.47
What is the solution, or rather denouement, to the avian flu dilemma? Even if we don't have to worry about a pandemic of avian flu, we probably would be wise to keep searching for better ways to medically prevent and treat the disease. Some antiviral drugs, like oseltamivir and zanamavir that inhibit the N protein responsible for new viral copies budding out from the host cell, may have some effect against avian flu, but the most they do is alleviate symptoms—they are not a cure. The drugs' main use, if stockpiled and administered shortly after flu symptoms appear, is to buy some time for vaccine development and distribution. Current vaccines for H5N1 are only 50 percent effective and must be administered in doses twelve times higher than that for regular vaccines, which increases the likelihood of side effects and makes them almost impractical for inoculating large numbers of people quickly in response to an emerging pandemic. Avian flu vaccines are notoriously hard to produce because they naturally kill off the fertilized chicken egg cultures in which the formulas are usually grown; genetically engineered vaccines may get around this problem and would also be far easier to manufacture at short notice. Another possibility is to use the antibodies of those who have survived or who happen to be immune to avian flu; this possibility parallels similar work being done with AIDS. Still a third alternative in the vaccine arsenal uses the harmless adenovirus to carry the H surface protein of avian flu, which seems to be effective against multiple strains caused by antigenic drift since it stimulates both antibodies and immune cell activity in the host. This would make for a vaccine that could be effective year to year, until a major genetic shift occurs. The holy grail of this kind of vaccine would be one that focuses on a protein common to all flu strains, meaning that one shot would confer immunity to flu for all time.48 This would then set up an eradication campaign for flu equivalent to what was done for smallpox in the 1970s.
Until and if that happens, however, the socioeconomic and cultural dimension of avian flu cannot be ignored. This means that, for the time being, perhaps flu can best be fought with lifestyle and behavioral changes that limit the opportunities for flu to make the leap from animals to humans. Within the endemic foci of avian flu in Asia, this would entail changing farming practices in order to better respect the boundaries between wild and domestic fowl, increasing hygiene at live poultry markets and farms, scrupulously reporting cases of sick birds or humans, and changing the ways in which poultry products are handled, cooked, or consumed. These policies have already been proven to be successful in Thailand, for example, after avian flu returned to Southeast Asia in 2004. But we must also recognize that currently there are major disincentives for doing almost all these things, such as the loss of families' livelihood and food source should their flocks be culled, or the potential damage to developing countries' economies in terms of tourism and exports should flu outbreaks be made public. Probably the only way to counter these negatives is with financial compensation forthcoming from the richer nations of the world, and perhaps the only way to persuade others to render such aid is by casting avian flu as a health problem that affects us all as part of a global network of disease, in the same way that attempts have been made to mobilize a global response to the environmental disaster of global warming. This also means that the inhabitants of the wealthier West will not be exempt from making similar social, economic, and cultural choices, such as shifting consumer patterns away from mass-produced foods and toward locally sustainable sources.49 (This is indeed the subject of the 2009 documentary Food, Inc.)
The many issues surrounding flu were recently brought back into focus with the occurrence of an H1N1 pandemic in 2009, the first flu pandemic to occur in over forty years, if one does not count the 1976 scare. The first wave in the spring was first reported in Mexico, where flu may have been present as early as January, with a second wave occurring in the autumn. (A third wave expected for the winter-spring of 2010 never materialized.) By June of 2009, the flu was officially declared a pandemic by WHO and the CDC. In the United States alone, it is estimated that to date forty-seven million people have come down with “swine flu,” representing about 15 percent of the total population, and that over two hundred thousand victims have been hospitalized and almost ten thousand people have died.50 While this is by far the largest number of flu mortalities reported in any country in the world, anecdotal evidence suggests that the flu was a lot more severe and deadly in developing countries, where access to vaccines and quality health care is quite a bit lower than in the United States.51 Moreover, the designation of “swine flu” by the media to this pandemic is an unfortunate misnomer, since the genetic makeup of the virus has been revealed to contain elements from swine, avian, and human influenza strains. Although the virus has been found in pigs in some countries, it is only transmitted person to person and has not been communicated from pigs to humans, nor by eating pork products. Nonetheless, this has not stopped some countries, such as Azerbaijan and Indonesia, from banning imports of pork, and Egypt decided to slaughter all pigs in the country (numbering over three hundred thousand) in April, despite reporting no flu cases.
In terms of socioeconomic and cultural responses, the flu of 2009 produced an interesting mix of reactions, some familiar and some new. The fact that most flu deaths have occurred among healthy, vigorous adults aged between eighteen and sixty-four and among pregnant women raised fears of another pandemic like the one of 1918, even though mortalities, at least in the United States, have actually been below what is to be expected in an average flu year. In some cases, victims indeed succumbed rapidly to a cytokine storm as their robust immune systems overreacted to the new strain. Yet, the superior, modern health care now available—at least in developed countries mostly in the West that have better diagnostic techniques and treatment therapies, such as antiviral drugs like Tamiflu and antibiotics to ward off bacterial pneumonia—and the fact that this time most people's nutritional health and immune systems are not being compromised by a world war, seems to have kept such deaths to a minimum compared to 1918. Some countries, such as China, Japan, Australia, Egypt, Russia, and Taiwan, have adopted or announced quarantine measures against travelers suspected of harboring the virus, isolating them in their hotels or on cruise ships, and new technologies, such as thermal imaging systems that can detect feverish conditions in the body, have been employed at airports to keep pace with worldwide airline travel. Wearing of masks once again came into fashion, particularly in countries like Japan, where they are culturally accepted and often used to ward off pollution. Some countries have also felt a severe economic fallout from the pandemic. In Mexico, for example, the local tourism industry, such as to Cancun and other popular destination resorts, simply collapsed during the summer in the wake of its spring scare, and the country has received millions of dollars in loans from the World Bank to cope with the crisis, partly it seems as a reward for its brave, early reporting of the outbreak. In spite of fears to the contrary, the pandemic did not dim proceedings at the 2010 Winter Olympic games in Vancouver, Canada, which is currently ranked ninth in the world in terms of flu incidences and deaths. And yet, this flu has also defied expectations and posed some continuing challenges: it is still not known whether the flu will come back as a cyclical, seasonal virus or if it was just a one-off occurrence; in a high proportion of cases there were no telltale symptoms of fever and cough even though the victims were still highly infectious and remained so for up to three weeks after recovery; and, as already noted, there was a great discrepancy around the world in severity of the pandemic based on the availability of vaccines and medical care.52
Here in the United States, responses have been mostly organized at the local school and state level, some of whom had already in years past been making similar preparations in expectation of a pandemic of avian flu. At the college where I teach in Vermont, for example, regular e-mail updates on the pandemic and information fact sheets were posted campuswide, and student health services geared up for a 30 percent infection rate. Advisories included commonsense precautions, such as the washing of hands and face, coughing or sneezing away from others, self-isolation at home—if infected—for at least twenty-four hours after symptoms fade (even though this particular outbreak of flu can be contagious for far longer than that), seeking medical help if symptoms persist beyond three days or are extreme, and so on. This also meant I had to suspend my normal absentee and assignment deadline policies, which I’m sure my students appreciated! A massive vaccination program, one not seen since the polio vaccine of the 1950s, was geared up by WHO and the U.S. government in response to the pandemic, although here in the States delivery of the vaccines came late, in November, when the second wave of the flu had already struck in early autumn. This was attributed to difficulties in culturing the vaccine in fertilized chicken embryos; the virus was claimed to be exceptionally slow to replicate. It is also possible that delays came from elaborate testing protocols and safeguards for the vaccine, given the experience of 1976. An underground drumbeat against vaccination surfaced on September 26, 2009, when political commentator and cable TV talk show host Bill Maher published a brief broadside on Twitter: “If u get a swine flu shot ur an idiot.” In the second week of January 2010, U.S. president Barack Obama declared it by proclamation to be “National Influenza Vaccination Week,” and the U.S. Department of Health and Human Services editorialized in local newspapers to encourage people to get vaccinated for swine flu, indicating that we are still haunted by the ghosts of 1976. But just like back then, the state delivery system of the vaccines has also been very uneven. In my home state of Vermont, H1N1 flu clinics were mobbed, and the state ran out of vaccine early due to higher than normal demand. I remember standing outside in the cold for two and a half hours to get my own shot. But in New York City, the New York Times reported that flu clinics were deserted, which again echoes 1976, when New York had only a 10 percent vaccination rate. There has also been some debate about who should get the vaccines and who should administer them. In Vermont, vaccines were, at least initially, restricted to certain “priority” or high-risk groups, which included pregnant women, health care workers, those aged between six months and twenty- four years, and those with preexisting health conditions that made them more susceptible to flu (of which I was one). But if fulminant cases of flu are also striking down healthy, prime-age adults in other categories due to their vigorous immune systems, shouldn't vaccines also be made available to them (perhaps on a first-come, first-served basis), especially since they would be the ones, through their active lifestyles in the workplace, who would be most likely to spread the flu? At the Vermont college where I teach, for example, I attempted to get an H1N1 vaccine offered at health services, but I was told that shots were restricted to students. This makes sense if students are spreading flu in their dorms, but professors are also at the “flashpoint” of this pandemic and their sick leaves, it could be argued, will have a greater impact on the continued viability of campus life, particularly in terms of instruction. In the event, hundreds of elementary and secondary schools throughout the country did temporarily close in response to the pandemic, in spite of CDC recommendations against this. I also question the delivery method of special public clinics for the vaccines, since the holding area where my wife and I along with dozens of other families were milling around filling out paperwork seemed a perfect environment for spreading the flu. Instead, perhaps flu shots and live vaccine nasal sprays would have been better administered at general practices, where staggered appointments could be made. Despite these difficulties, however, my overall impression as of 2010 is that the pandemic was successfully contained. The disaster that some of us anticipated did not happen, and 1918 was not repeated. Indeed, the fact that a pandemic has taken so long to reemerge, whereas previously a pandemic was to be expected every decade, is a very hopeful sign. We can all congratulate ourselves for that. But there are still some lessons to be learned with regard to the next flu pandemic, when and if this should occur.
More on the topic CHAPTER 5 Influenza:
- CHAPTER 2 INFLUENZA VIRUS INFECTIONS
- INFLUENZA
- Anti-Influenza Agents
- AVIAN INFLUENZA
- INFLUENZA IN AQUATIC MAMMALS
- INFLUENZA IN OTHER SPECIES
- Chapter 2 Refraining from Seeking Clarification: A Chapter from al-Wafl fl sharh al-Wafiya of al-Acraji (d. 1227/1812)
- Chapter 8 Why Early Muslims Divided into Sects? A Chapter from the Mukhtasar al-usul of cAli b. Muhammad b. al-Walid (d. 612/1215)1
- Chapter 7 The Role of Consensus in Legal Hermeneutics: A Chapter from the
- Chapter 1 Are Rulings of the Prophet Due to Ijtihad and Are all Mujtahids Always Correct? A Chapter from the Sharh. Zubdat al-usul of al-Mazandarani (d. 1081/1670)