The Pandemic Century
Page 1
THE
PANDEMIC
CENTURY
ONE HUNDRED YEARS OF
PANIC, HYSTERIA,
AND HUBRIS
MARK HONIGSBAUM
W. W. NORTON & COMPANY
Independent Publishers Since 1923
New York | London
FOR MARY-LEE
“Everybody knows that pestilences have a way of recurring in the world; yet somehow we find it hard to believe in ones that crash down on our heads from a blue sky. There have been as many plagues as wars in history; yet plagues and wars always take people by surprise.”
—ALBERT CAMUS, The Plague
CONTENTS
PROLOGUE: SHARKS AND OTHER PREDATORS
CHAPTER I: THE BLUE DEATH
CHAPTER II: PLAGUE IN THE CITY OF ANGELS
CHAPTER III: THE GREAT PARROT FEVER PANDEMIC
CHAPTER IV: THE “PHILLY KILLER”
CHAPTER V: LEGIONNAIRES’ REDUX
CHAPTER VI: AIDS IN AMERICA, AIDS IN AFRICA
CHAPTER VII: SARS: “SUPER SPREADER”
CHAPTER VIII: EBOLA AT THE BORDERS
CHAPTER IX: Z IS FOR ZIKA
EPILOGUE: THE PANDEMIC CENTURY
Acknowledgments
Abbreviations
Notes
Illustration Credits
Illustrations Insert
Index
THE
PANDEMIC
CENTURY
PROLOGUE
SHARKS AND OTHER PREDATORS
Sharks never attack bathers in the temperate waters of the North Atlantic. Nor can a shark sever a swimmer’s leg with a single bite. That’s what most shark experts thought in the blisteringly hot summer of 1916 as New Yorkers and Philadelphians flocked to the beaches of northern New Jersey in search of relief from the sweltering inland temperatures. That same summer the East Coast had been gripped by a polio epidemic, leading to the posting of warnings about the risk of catching “infantile paralysis” at municipal pools. The Jersey shore was considered a predator-free zone, however.
“The danger of being attacked by a shark,” declared Frederic Lucas, director of the American Museum of Natural History in July 1916, “is infinitely less than that of being struck by lightning and . . . there is practically no danger of an attack from a shark about our coasts.” As proof, Lucas pointed to the reward of $500 that had been offered by the millionaire banker Hermann Oerlichs “for an authenticated case of a man having being attacked by a shark in temperate waters [in the United States, north of Cape Hatteras, North Carolina]”—a sum that had gone unclaimed since Oerlichs had posted the challenge in the New York Sun in 1891.
But Oerlichs and Lucas were wrong, and so were Dr. Henry Fowler and Dr. Henry Skinner, the curators of Philadelphia’s Academy of Natural Science who had categorically stated, also in 1916, that a shark lacked the power to sever a man’s leg. The first exception to these known facts had come on the evening of July 1, 1916, when Charles Epting Vansant, a wealthy young broker holidaying in New Jersey with his wife and family, decided to go for a predinner swim near his hotel at Beach Haven. A graduate of the University of Pennsylvania’s class of 1914, Vansant, or “Van” to his chums, was a scion of one of the oldest families in the country—Dutch immigrants who had settled in the United States in 1647—and famed for his athleticism. If he had any concerns about entering the cool Atlantic waters that evening, they would have been offset by the familiar sight of the beach lifeguard, Alexander Ott, a member of the American Olympic swimming team, and a friendly Chesapeake Bay retriever that ran up to him as he slid into the surf. In the fashion of young Edwardian men of the time, Vansant swam straight out beyond the lifelines, before turning to tread water and call to the dog. By now his father, Dr. Vansant, and his sister, Louise, had arrived on the beach and were admiring his form from the lifeguard station. Much to their amusement, the hound refused to follow. Moments later, the reason became apparent—a black fin appeared in the water, bearing down on Vansant from the east. Frantically, his father waved for his son to swim to shore, but Vansant spotted the danger too late and when he was fifty yards from the beach he felt a sudden tug and an agonizing pain. As the sea around him turned the color of wine, Vansant reached down to discover that his left leg was gone, severed neatly at the thigh bone.
By now Ott was at his side and dragging him through the water to the safety of the Engelside Hotel where his father desperately tried to stem the bleeding. But it was no use—the wound was too deep—and to his father and young wife’s horror Vansant died then and there, the first known victim of a shark attack in the North Atlantic. From that moment on, neither would be able to look at Jersey’s Atlantic seaboard without imagining the jaws lurking beneath the surface.
They were not alone. Within fourteen days, four more bathers would also be attacked on the Jersey shore and three would be killed, sparking an obsessive fear of “man-eating” sharks that persists to this day.* It makes little difference that sightings of great whites and other large sharks in the North Atlantic are rare and attacks on swimmers rarer still. Beachgoers now know better than to swim too far from shore, and should they become blasé about the risks and dismissive of the menace, there is always a rerun of Jaws or an episode of Discovery Channel’s Shark Week to set them straight. The result is that many children and a fair number of adults are now terrified of playing in the surf, and even those brave enough to venture beyond the breakers know to keep a wary eye on the horizon for the telltale sight of a dorsal fin.
AT FIRST GLANCE, the New Jersey shark attacks would seem to have little to do with the Ebola epidemic that engulfed West Africa in 2014 or the Zika epidemic that broke out in Brazil the following year, but they do, for just as in the summer of 1916 most naturalists could not conceive of a shark attack in the cool waters of the North Atlantic, so in the summer of 2014 most infectious disease experts could not imagine that Ebola, a virus previously confined to remote forested regions of Central Africa, might spark an epidemic in a major city in Sierra Leone or Liberia, much less cross the Atlantic to threaten citizens of Europe or the United States. But that is precisely what happened when, shortly before January 2014, Ebola emerged from an unknown animal reservoir and infected a two-year-old boy in the village of Meliandou, in southeastern Guinea, from whence the virus traveled by road to Conakry, Freetown, and Monrovia, and onward by air to Brussels, London, Madrid, New York, and Dallas.
And something very similar happened in 1997 when a hitherto obscure strain of avian influenza, known as H5N1, which had previously circulated in ducks and other wild waterfowl, suddenly began killing large numbers of poultry in Hong Kong, triggering a worldwide panic about bird flu. The great bird flu scare, of course, was followed by the panic about Severe Acute Respiratory Syndrome (SARS) in 2003, which was followed, in turn, by the 2009 swine flu—an outbreak that began in Mexico and set off an alarm about the threat of a global influenza pandemic that saw the drawdown of stockpiles of antiviral drugs and the production of billions of dollars’ worth of vaccines.
Swine flu did not turn into a man-eater—the pandemic killed fewer people globally than common or garden strains of flu have in the United States and the United Kingdom most years—but in the spring of 2009 no one knew that would be the case. Indeed, with disease experts focused on the reemergence of bird flu in Southeast Asia, no one had anticipated the emergence of a novel swine flu virus in Mexico, let alone one with a genetic profile similar to that of the virus of the 1918 “Spanish flu”—a pandemic that is estimated to have killed at least 50 million people worldwide and is considered a byword for viral Armageddon.�
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IN THE NINETEENTH CENTURY, medical experts thought that better knowledge of the social and environmental conditions that bred infectious disease would enable them to predict epidemics and, as the Victorian epidemiologist and sanitarian William Farr put it in 1847, “banish panic.” But as advances in bacteriology led to the development of vaccines against typhoid, cholera, and plague, and fear of the great epidemic scourges of the past gradually receded, so other diseases became more visible and new fears took their place. A good example is polio. The month before sharks began attacking bathers on the Jersey shore, a polio epidemic had broken out near the waterfront in South Brooklyn. Investigators from New York’s Board of Health immediately blamed the outbreak on recent Italian immigrants from Naples living in crowded, unsanitary tenements in a district known as “Pigtown.” As cases of polio multiplied and the papers filled with heartbreaking accounts of dead or paralyzed infants, the publicity prompted hysteria and the flight of wealthy residents (many New Yorkers headed for the Jersey shore). Within weeks, the panic had spread to neighboring states along the eastern seaboard, leading to quarantines, travel bans, and enforced hospitalizations. These hysterical responses partly reflected the then-prevalent medical conviction that polio was a respiratory disease spread by coughs and sneezes and by flies breeding in garbage.‡
In his history of poliomyelitis, the epidemiologist John R. Paul describes the epidemic of 1916 as “the high-water mark in attempts at enforcement of isolation and quarantine measures.” By the time the epidemic petered out with the cooler weather in December 1916, 27,000 cases and 6,000 deaths had been recorded in twenty-six states, making it the world’s then-largest polio outbreak. In New York alone there had been 8,900 cases and 2,400 deaths, a mortality rate of around one child in four.
The scale of the outbreak made polio appear a peculiarly American problem. But what most Americans did not realize is that a similarly devastating outbreak had visited Sweden five years earlier. During that outbreak, Swedish scientists had repeatedly recovered polio virus from the small intestine of victims—an important step in explicating the true etiology and pathology of the disease. The Swedes also succeeded in culturing the virus in monkeys who had been exposed to secretions from asymptomatic human cases, fueling suspicion about the role of “healthy carriers” in the preservation of the virus between epidemics. However, these insights were ignored by leading American polio experts. The result is that it was not until 1938 that researchers at Yale University would take up the Swedish studies and confirm that asymptomatic carriers frequently excreted the polio virus in their stools and that the virus could survive for up to ten weeks in untreated sewage.
Today, it is recognized that in an era before polio vaccines, the best hope of avoiding the crippling effects of the virus was to contract an immunizing infection in early childhood when polio is less likely to cause severe complications. In this respect, dirt was a mother’s friend and exposing babies to water and food contaminated with polio could be considered a rational strategy. By the turn of the nineteenth century, most children from poor immigrant neighborhoods had become immunized in exactly this way. It was children from pristine, middle-class homes and tony areas that were at the greatest risk of developing the paralytic form of the disease—people like Franklin Delano Roosevelt, the thirty-second president of the United States, who escaped polio as a teen, only to contract the disease in 1921 at the age of thirty-nine while holidaying at Campobello island, New Brunswick.
THIS IS A BOOK ABOUT the way that advances in the scientific knowledge of viruses and other infectious pathogens can blind medical researchers to these ecological and immunological insights and the epidemic lurking just around the corner. Ever since the German bacteriologist Robert Koch and his French counterpart, Louis Pasteur, inaugurated the “germ theory” of disease in the 1880s by showing that tuberculosis was a bacterial infection and manufacturing vaccines against anthrax, cholera, and rabies, scientists—and the public health officials who depend on their technologies—have dreamed of defeating the microbes of infectious disease. However, while medical microbiology and the allied sciences of epidemiology, parasitology, zoology, and, more recently, molecular biology, provide new ways of understanding the transmission and spread of novel pathogens and making them visible to clinicians, all too often these sciences and technologies have been found wanting. This is not simply because, as is sometimes argued, microbes are constantly mutating and evolving, outstripping our ability to keep pace with their shifting genetics and transmission patterns. It is also because of the tendency of medical researchers to become prisoners of particular paradigms and theories of disease causation, blinding them to the threats posed by pathogens both known and unknown.
Take influenza, the subject of the first chapter. When the so-called “Spanish flu” emerged in the summer of 1918, during the closing stages of World War I, most physicians assumed it would behave in a similar way to previous flu epidemics and dismissed it as a nuisance. Few thought the pathogen might pose a mortal threat to young adults, much less to soldiers en route to the Allied lines in northern France. This was partly because they had been informed by no less an authority than Koch’s protégé, Richard Pfeiffer, that flu was transmitted by a tiny Gram-negative bacterium, and that it would only be a matter of time before American scientists trained in German laboratory methods had manufactured a vaccine against the influenza bacillus, just as they had against cholera, diphtheria, and typhoid. But Pfeiffer and those who put their faith in his experimental methods were wrong: influenza is not a bacterium but a virus that is too small to be seen through the lens of an ordinary optical microscope. Moreover, the virus passed straight through the porcelain filters then used to isolate bacteria commonly found in the nose and throat of influenza sufferers. Although some researchers had begun to suspect that flu might be a “filter-passer,” it would be many years before Pfeiffer’s misconception would be corrected and influenza’s viral etiology divined. In the meantime, many research hours were wasted and millions of young people perished.
However, it would be a mistake to think that simply knowing the identity of a pathogen and the etiology of a disease is sufficient to bring an epidemic under control, for though the presence of an infectious microbe may be a necessary condition for ill health, it is rarely sufficient. Microbes interact with our immune systems in various ways, and a pathogen that causes disease in one person, may leave another unaffected or only mildly inconvenienced. Indeed, many bacterial and viral infections can lie dormant in tissue and cells for decades before being reactivated by some extrinsic event or process, whether it be coinfection with another microbe, a sudden shock to the system due to an external stress, or the waning of immunity with old age. More importantly, by taking specific microbial predators as our focus we risk missing the bigger picture. For instance, the Ebola virus may be one of the deadliest pathogens known to humankind, but it is only when tropical rain forests are degraded by clear-cutting, dislodging from their roosts the bats in which the virus is presumed to reside between epidemics, or when people hunt chimpanzees infected with the virus and butcher them for the table, that Ebola risks spilling over into humans. And it is only when the blood-borne infection is amplified by poor hospital hygiene practices that it is likely to spread to the wider community and have a chance of reaching urban areas. In such circumstances, it is worth keeping in mind the view expressed by George Bernard Shaw in The Doctor’s Dilemma, namely that “The characteristic microbe of a disease might be a symptom instead of a cause.” Indeed, updating Shaw’s axiom for the present day, we might say that infectious diseases nearly always have wider environmental and social causes. Unless and until we take account of the ecological, immunological, and behavioral factors that govern the emergence and spread of novel pathogens, our knowledge of such microbes and their connection to disease is bound to be partial and incomplete.
In fairness, there have always been medical researchers prepared to take a more nuanced view of our compl
ex interactions with microbes. For instance, writing at the height of the antibiotics revolution fifty years ago, the Rockefeller researcher René Dubos railed against short-term technological fixes for medical problems. At a time when most of his colleagues took the conquest of infectious disease for granted and assumed that the eradication of the common bacterial causes of infection was just around the corner, Dubos, who had isolated the first commercial antibiotic in 1939 and knew what he was talking about, sounded a note of caution against the prevailing medical hubris. Comparing man to the “sorcerer’s apprentice,” he argued that medical science had set in motion “potentially destructive forces” that might one day usurp the dreams of a medical utopia. “Modern man believes that he has achieved almost completely mastery over the natural forces which molded his evolution in the past and that he can now control his own biological and cultural destiny,” wrote Dubos. “But this may be an illusion. Like all other living things, he is part of an immensely complex ecological system and is bound to all its components by innumerable links.” Instead, Dubos argued that complete freedom from disease was a “mirage” and that “at some unpredictable time and in some unforeseeable manner nature will strike back.”
Yet for all that Dubos’s writings were hugely popular with the American public in the 1960s, his warnings of a coming disease Armageddon were largely ignored by his scientific colleagues. The result was that when, shortly after Dubos’s death in February 1982, the Centers for Disease Control and Prevention (CDC) coined the acronym, AIDS, to describe an unusual autoimmune condition that had suddenly appeared in the homosexual community in Los Angeles and was now spreading to other segments of the population, it took the medical world by surprise. But really the CDC shouldn’t have been surprised because something very similar had happened just eight years earlier when an outbreak of atypical pneumonia among a group of war veterans who had attended an American Legion convention at a luxury hotel in Philadelphia sparked widespread hysteria as epidemiologists scrambled to identify the “Philly Killer” (the outbreak initially flummoxed the CDC’s disease detectives and it took a microbiologist to identify the pathogen, Legionella pneumophila, a tiny bacterium that thrives in aquatic environments, including the cooling towers of hotels). That year, 1976, saw not only a panic over Legionnaires’ disease, but a panic over the sudden emergence of a new strain of swine flu at a US Army base in New Jersey—an emergence event for which the CDC and public health officials were likewise unprepared and that would eventually result in the needless vaccination of millions of Americans. And something very similar happened again in 2003 when an elderly Chinese professor of nephrology checked into the Metropole Hotel in Hong Kong, igniting cross-border outbreaks of a severe respiratory illness that was initially blamed on the H5N1 avian influenza virus but which we now know to have been due to a novel coronavirus§ associated with SARS. In that case, a pandemic was averted by some nifty microbiological detective work and unprecedented cooperation between networks of scientists sharing information, but it was a close call, and since then we have seen several more unanticipated—and initially misdiagnosed—emergence events.