The Coming Plague

by Laurie Garrett

  In the early 1970s members of the order had attended several days of basic medical training at the Tropical Institute in Antwerp. That was the full extent of their nursing training before venturing into the field.

  “They’re not nurses!” van der Gröen uncharacteristically shouted, realizing he was criticizing deceased nuns. Still, he pushed on. He applauded the holiness and devotion of the Sisters.

  “But no one was thinking that if you start such a medical business, and the people of the region are receiving no support from the government of Zaire, and you give out free health care, then you must be prepared to be deluged. You must be ready to safely give 300 shots a day. If you build something you call a hospital, then you must do the logistic planning, provide the resources, and train your personnel accordingly.”

  Van der Gröen’s coup de grace was an accusation: “The price for your lack of planning was high”; half the dead got Ebola in the mission hospital.

  Piot insisted that the mission hospital should either be closed or be staffed by a certified physician. And both men warned the Mother Superior that the source of Ebola was never found: it could return, and spread again inside the mission if their instructions weren’t followed.

  Though their advice was heeded for the Yambuku Mission, Piot and van der Groen left the religious order wondering just how many missionary health facilities of all denominations operated in developing countries with a similarly imbalanced mixture of hopeful devotion and tragically poor medical training and logistics. The two men, who would remain lifelong friends forever bound by their shared Zairian experience, stepped out into the icy Antwerp January morning, their minds and conversation filled with concern for the far-off tropical villages, the women in their kangas, the babies tied on their backs, and husbands earning hard livings selling wild animals they captured in the steamy rain forest—a jungle that hid Ebola.

  The following Christmas, Pierre Sureau received a letter from Sisters Marcella, Genoveva, and Mariette. He sat in his comfortable Paris apartment, trying to recall the sweltering heat and primitive mission of Yambuku as he read the Sisters’ greetings:

  Dear Doctor, we wish you a good New Year 1978. These days we talk a great deal about the events of the past year and you, who have left us with good memories. We would like to thank you again, sincerely, for coming to our aid when others dared not to come. At the moment life has returned to normal. A Zairian doctor is here: he also works with all his heart. Four Belgian volunteers and a Sister are here to rebuild the hospital. The students are back in the school, making plenty of noise. Are you well? We send you our affection. Sister Marcella, Sister Genoveva, Sister Mariette.

  Sureau affectionately refolded the letter, put the pages back inside their envelope, and put the missive into a carton marked “Yambuku.” He carefully shut the box and placed it in the back of a closet.

  Souvenirs of a plague.

  6

  The American Bicentennial

  SWINE FLU AND LEGIONNAIRES’ DISEASE

  There is evidence there will be a major flu epidemic this coming fall. The indication is that we will see a return of the 1918 flu virus that is the most virulent form of the flu. In 1918 a half million people died. The projections are that this virus will kill one million Americans in 1976.

  —F. David Mathews, Secretary of Health, Education, and Welfare

  I

  The great Ebola drama went almost unnoticed in the United States in 1976, even in the hallways of the Centers for Disease Control. The nation was preoccupied. And Africa was, in the American consciousness, far away.

  In its 200th year, the United States of America was busily celebrating patriotism with a mix of red-white-and-blue entrepreneurial souvenir sales, Hollywood extravaganzas reenacting Great Moments of History, tall-ship regattas down New York’s East River, and a good deal of boasting about the brilliance contained in the Declaration of Independence and the Constitution. Compounding the national sense of distraction was a striking new political atmosphere in which President Gerald R. Ford was struggling to defend himself in national elections against a virtually unknown southern politician named Jimmy Carter. A national soul-searching was underway, as Americans contemplated the significance of the U.S. defeat in Vietnam and the Nixon administration’s Watergate scandals.

  Even if Americans hadn’t been in an isolationist mood in 1976, their limited attention spans would still have been unable to absorb the events of Yambuku, for they had more than enough disease news upon which to focus. After all, 1976 was the year of two of the most exhaustive and expensive investigations in the history of the U.S. Public Health Service: the Swine Flu affair and Legionnaires’ Disease.1

  Overall, Swine Flu and Legionnaires’ Disease boiled down to the same set of troubling perceptions for the American public, and, to a lesser extent, the Canadian, Mexican, Australian, New Zealand, and European publics: something new and very scary was coming; nobody was sure what it was, but the experts were certain it was dangerous; the federal government seemed quite distressed about the matters, but the experts and authorities didn’t seem to agree as to what, if anything, should be done to protect the public; and it was all costing taxpayers a pretty penny. In both cases, public apprehension would eventually yield to impatience and allegations of incompetence, even scandal. Each step of the investigations would take place under the full glare of television lights and public scrutiny.

  Ultimately, one disease would emerge, the other would not.

  While Karl Johnson’s team combed the villages of the Bumba Zone in search of Ebola cases, the American public health establishment, from low-level municipal officials all the way up the ladder to the President of the United States, anxiously monitored hospital records and physicians’ reports for hints of the emergence of the so-called Swine Flu.

  It began in January 1976 at Fort Dix, a U.S. Army training center in New Jersey. A young, highly motivated recruit, Private David Lewis, felt the dizziness, nausea, fatigue, fever, and muscle aches that are the hallmarks of influenza. Several of his fellow recruits were similarly stricken during that cold, wet week following the New Year, and some sought comfort in the base dispensary.

  Eighteen-year-old Lewis, however, was determined to excel in basic training. Though he had been assigned by a medical officer to remain in quarters for forty-eight hours, Lewis loaded his fifty-pound pack and joined his platoon for an all-night hike in the bitter New Jersey winter.2 Overcome by fever, the teenager forced himself to keep marching, though he lagged far behind his fellow soldiers. After a few hours he collapsed.

  Lewis died just hours after reaching the base hospital.3

  Nearly two decades later scientists would still be asking, “Did Private Lewis die because he was infected with a particularly lethal, virulent strain of influenza, or did the young man die because he went on an overnight winter full-pack forced march while in peak viremia with a modestly dangerous influenza strain?”

  Knowing the answer to that fundamental question would make all the difference in interpreting the events of 1976. Lewis would be the only American whose influenza death in the 1976–77 flu season seemed out of the ordinary, based on his youth and physical fitness. Typically, influenza sickened thousands of people every year, but claimed only the lives of the very old or those weakened by other ailments that stress the human immune system. It is rare, indeed, for a healthy teenager to die of influenza. A hallmark of the great 1918–19 influenza pandemic was the virus’s ability to kill young adults and children.

  By the end of January, Fort Dix medical commander Colonel Joseph Bartley had a widespread flu problem on his hands, with some 300 recruits hospitalized or confined to quarters. At his request, New Jersey State Health Department laboratory director Martin Goldfield received nineteen throat-wash specimens from ailing recruits, including a sample taken during autopsy from Private Lewis. Goldfieldâ�
�™s lab put droplets from the nineteen sample tubes onto nutrient-rich petri dishes, allowing the cultures to grow. Once the viral colonies were large enough to be studied, Goldfield’s team ran a series of antibody tests aimed at determining what strain of influenza was attacking the Fort Dix recruits.

  At the time scientists like Goldfield knew that when the human immune system successfully overcame influenza infection, antibodies were made against two proteins that protruded from the outer envelope of the spherical virus: hemagglutinin and neuraminidase. The influenza virus was otherwise well protected by a tough protein-and-fat armor made of two layers of viral enveloping: one layer was almost entirely composed of the human heart’s nemesis, cholesterol. But the virus was caught in something of a Catch-22: it could not infect and destroy cells without the use of its neuraminidase and hemagglutinin proteins, yet these very compounds were what attracted the usually successful attack of the immune system.

  Over 700 of these proteins protruded from the surface of each virus. The long rod-shaped hemagglutinin proteins performed the job of grabbing on to red blood cells, connecting one cell to another and causing formation of clumps of cells in the bloodstream. Neuraminidase in turn pinched off pieces of the cellular membrane that were wrapped around newly formed viruses, allowing the microbes to flood out into the bloodstream.

  In 1976 scientists believed that the relative danger and virulence of a particular influenza strain were a function of three things: the efficiency of its hemagglutination ability, the functional abilities of its particular neuraminidase proteins, and the immunity of the animal or human host it infected. The first two factors were controlled by viral genetics; the last was under host regulation.

  Unlike such relatively simple viruses as Lassa and Marburg, influenza proved to have a complex genetic organization. Long, single strands of RNA genetic material were entwined around themselves, forming a spiral structure. Five such RNA spirals were further entwined with protective proteins, forming genetic packages similar to those seen in human and animal cells, called chromosomes. When the virus reproduced itself, the chromosomes had to unwind and make duplicate sets of their proteins and RNA. In the process, parts of one chromosome might overlap with another, extraneous bits of RNA from the cell in which the virus resided might get copied as well, and the whole mess would be reassorted and reassembled to yield an intact parent virus and its packaged, somewhat different, offspring.

  At the heart of such complexity lay many opportunities for genetic change, some of which might be lethal for the viruses, others of which might prove fatal for the targeted human hosts.

  By 1976 virus specialists were beginning to appreciate that influenza was a sort of microbial chameleon that had thrived over the millennia by rigorously adhering to a single maxim: Adapt or die. If this constant process of genetic shuffling didn’t frequently yield new types of hemagglutinin and neuraminidase, all target humans could eventually be immune to influenza and the virus species might die out. While the chances of the planet’s entire human population becoming immune to a rare virus such as Ebola were nil, it was possible that an easily transmitted, ubiquitous respiratory virus like influenza would infect billions of human beings in less than five years’ time, kill off all the susceptibles, and leave the world’s survivors completely immune.

  Global pandemics were, in fact, a hallmark of influenza that spanned recorded human history. Charlemagne’s conquest of Europe was slowed by an A.D. 876 flu epidemic that spread across the continent and claimed much of his army. Many suspected influenza epidemics followed, though history can only vaguely discriminate between ancient accounts of influenza and other respiratory diseases. In 1580, however, the world was clearly hit by a major pandemic that followed trade and early colonial routes across Africa, Europe, and the Americas. So devastating was the epidemic that “some Spanish cities were said to be nearly dispopulated.”4

  By examining the more clearly recorded histories of influenza epidemics of the eighteenth and nineteenth centuries, scientists were able to recognize some patterns. First, the virus seemed to successfully change itself often enough so that at least once in every human generation a significantly new strain appeared that could elude the human immune system. Usually, after a great pandemic that killed hundreds of thousands—or millions—of people, survivors would have made antibodies that recognized and quickly neutralized the neuraminidase and hemagglutinin proteins of that strain. For several years thereafter the influenza viral population would undergo incremental changes that would result in modest alterations in its two crucial proteins, but not enough to render most immunized people vulnerable to infection.

  The hemagglutinin and neuraminidase proteins constituted antigens, or targets for the human immune system’s antibodies. As influenza made small genetic changes, the antigens would “drift” a bit from their standard form, and antibodies might not be able to lock on to the new types with quite as snug a fit over time. Nevertheless, most otherwise healthy people could successfully overcome antigen drift swiftly, making suitably adapted antibodies that would obliterate the viruses after a relatively mild bout of flu. Only people whose immune systems were weak, such as the elderly or malnourished, would die of influenza during such antigenic drift epidemics.

  But sometimes something far more serious would happen. The antigens would do more than drift incrementally from their original genetic blueprint; a serious mutation event would occur and the hemagglutinin and neuraminidase proteins would suddenly be so different as to render human antibodies utterly useless. If the new forms of the proteins were also highly efficient in their tasks of clumping up blood cells and punching holes in cell membranes, a devastating global epidemic could result.

  Though historians disagreed about details, there was an emerging consensus about when and where great flu pandemics had occurred in the previous 276 years, with what levels of human devastation.5 Maps were drawn, illustrating the directions of influenza’s spread around the world during the great pandemics of 1729, 1732, 1781, 1830, 1833, and 1889.

  But it was the devastating pandemic of 1918–19 that most concerned President Gerald Ford and his advisers in 1976: the specter of another 500,000 dead Americans, 21 million dead worldwide, and over 10 percent of the U.S. workforce bedridden during the upcoming winter. That was the scale of what remains the twentieth century’s worst pandemic.6 It occurred when the world’s population was far smaller, and human mobility limited to slow forms of transport, such as steamships and locomotives. Nevertheless, the epidemic moved completely around the globe in less than five months. The Ford administration knew that such an epidemic could be far worse in the age of jet travel and overpopulation.

  The world was at war in 1918, fighting a largely ground struggle with millions of troops holed up in muddy trenches from the English Channel to the Crimea. The virus appears to have swept the world in three waves over less than two years’ time, gaining virulence with each new assault. By October 1918 its strength was so great that people died with spectacular speed. There were reports of women boarding a New York subway in Coney Island feeling little else than mild fatigue, and being found dead when the train pulled into Columbus Circle, some forty-five minutes later.

  In New York City alone, over 20,000 people died during the fall of 1918. The virus spread so extensively that travelers later discovered that entire Inuit villages in remote parts of Alaska were obliterated by influenza. Autopsies performed by London coroners revealed huge hemorrhages in the lungs, unlike anything the physicians had seen in the influenza epidemics of 1873 and 1889.7

  The epidemic was by no means restricted to the war-torn Northern Hemisphere; influenza found its way from Europe to every nation on the planet. One out of every twenty citizens of Ghana died of the flu between September 1 and November 1, 1918.8 The population of Western Samoa was overwhelmed by the virus. During the months of November and December 1918, nearly all of the 38,000
residents of Western Samoa contracted the flu, and 7,500—nearly 20 percent of the population—died.9

  Medical science was then at a loss to explain the epidemic or provide sound advice to the terrorized population of any country. A Virginia State Department of Health pamphlet told the public that the disease was caused by “a tiny living plant called the germ of influenza.” The less erudite New York Post told its readers that “epidemics are the punishment which nature inflicts for the violation of her laws and ordinances.” Well-known Chicago physician Albert J. Croft said influenza was not a contagious microbe, but “small amounts of a depressing, highly irritating, high-density gas, present in the atmosphere, especially at night.”10

  Among the factors said by prominent American physicians to be responsible for influenza in 1918 were nakedness, fish contaminated by Germans, dirt, dust, unclean pajamas, Chinese people, open windows, closed windows, old books (“stay out of libraries”), and “some cosmic influence.”

  Sadly, nobody saved blood or tissue samples from victims of the disease. Such scientific forward thinking simply wasn’t commonplace in those days. In 1976, more than a few U.S. health officials would curse the oversight, regretting there was no historic sample with which Private Lewis’s influenza killer could be compared.

  The 1918–19 epidemic did, however, spark a wave of aggressive research, and in 1932 Richard Shope (father of the Yale University researcher Robert Shope, who three decades later worked with Jordi Casals) did the experiment that would result in the moniker “swine flu”: he removed nasal secretions from influenza-ailing domestic pigs and successfully infected other animals by rubbing the swine secretions on their noses or mouths. The following year, the British team of Wilson Smith, Christopher Howard Andrewes, and Sir Patrick Playfair Laidlaw isolated the influenza virus, for the first time giving the world an identity for its constant enemy. Two years later, Shope showed that people who were alive during the 1918–19 epidemic had antibodies against his pig virus, but children born after 1920 lacked such antibodies.