The Coming Plague (28 page)

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Authors: Laurie Garrett

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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.
Shope's conclusion, which would remain the dominant hypothesis six decades later, was that the great pandemic was caused by a swine type of flu virus. Shope argued that the virus came originally from some other animal, went on to infect people, and then was transmitted from people to pigs. There, the virus found a safe haven, where it remained for years.
11
Nobody knew in 1976 whether the deadly strain had remained stable—and lethal—in the pig population for six decades, though it seemed unlikely that such a lethal virus could have failed for sixty years to cause disease in at least some pig farmer.
When Goldfield and his team of New Jersey scientists tested the Fort Dix samples they didn't have on hand a test tube full of the 1918 influenza virus—nobody did. But they did have a sample of Shope's swine flu, and were able to show that some of the Fort Dix recruits had antibodies that neutralized the Shope swine flu. On the basis of those two layers of hypothetical thinking, Goldfield suggested the Fort Dix strain might be the same as, or similar to, the virus that sickened over one billion people worldwide in 1918–19, killing more than 21 million.
The Centers for Disease Control quickly repeated the New Jersey studies, confirming Goldfield's findings. Hypothetically, then, it seemed they had found a relationship between Shope's 1935 pig virus, a massive human epidemic in 1918, and some of the soldiers at Fort Dix who had antibodies that could neutralize the swine strain. Furthermore, the influenzas extracted from all the infected Fort Dix soldiers were A-type flus, the one of three
influenza serotypes that was most often responsible for large-scale pandemics. When the CDC completed all their “fingerprinting” of the Fort Dix virus it turned out to be influenza A, H1 (hemagglutinin 1) N1 (neuraminidase 1). Shope's swine virus was also an influenza A, H1N1.
In contrast, the most prevalent flu strain in the world during the early spring of 1976 was influenza A/H3N2. Dubbed the A/Victoria/75 strain, it first appeared in Victoria, Australia, a year earlier, causing relatively mild flu outbreaks from Johannesburg to Minneapolis.
12
The appearance of the Fort Dix virus, dubbed A/New Jersey/H1N1, caused considerable anxiety inside the U.S. Public Health Service.
“By every available scientific measure, the Shope strain was indistinguishable from the 1918 strain, and also indistinguishable from the Fort Dix strain,” Dr. June Osborn said nearly two decades later. In 1976, she was one of seven members of a U.S. Food and Drug Administration committee responsible for reviewing all American vaccine policies. Then a professor of medicine at the University of Wisconsin, Osborn was certain, and would remain so convinced, that the dreaded 1918 swine flu recycled back through the animal population, killing Private Lewis in the winter of 1976.
But investigations underway at Fort Dix revealed that only Private Lewis had died, and most of the illnesses at the base were due to the A/Victoria/ 75 strain. Furthermore, Lewis's sergeant attempted to revive the teen soldier when he collapsed, giving him mouth-to-mouth resuscitation. A month later the sergeant remained well and showed no signs of influenza A/New Jersey/ H1N1 infection. That certainly argued for caution in ascribing great powers of virulence and transmissibility to the new virus.
However, several dozen Fort Dix recruits tested positive for A/New Jersey /H1N1 infection, and the stakes were awfully high. As health officials would later explain, the consequences of being wrong, of denying the possibility that Private Lewis's death was a harbinger of an epidemic akin to that of 1918–19, and then having such a devastating incident catch the nation unprepared, were simply too dreadful. Though some signs in February 1976 already pointed in the direction of skepticism, they were overshadowed by the fear of having hundreds of thousands of deaths ascribed to health officials who had chosen to take a wait-and-see approach.
A final element that tipped the balance at CDC in favor of acting on the assumption that a dreaded epidemic was imminent came in the form of a widely held scientific theory. One of the most prominent virologists in the world in the mid-1970s was Dr. Edwin Kilbourne of the Mount Sinai School of Medicine in New York City. Kilbourne had shown a decade earlier that influenza viruses unusually rich in neuraminidase proteins were more easily spread from person to person. As viruses were formed in mass quantities inside a human cell, their packaged chromosomes migrated to the outer membrane of the invaded cell. Scientists could visualize this with an electron microscope, which would reveal long rows of dark spheres pushing
the membrane edges, creating bulges. Eventually, the viruses would push hard enough to pull a glob of cell membrane around their inner envelope and chromosomes, creating an outer protective coating. In this process, called budding, the new viruses would protrude sharply from the cell, but remain tethered by a final strand of host membrane. Kilbourne showed that the viruses' neuraminidase proteins would snip the tethers, freeing the newly formed microbes to enter the lungs, nasal fluids or tears of an ailing human, from there going on to infect another person. The greater the number of neuraminidase molecules, Kilbourne argued, the more rapidly viruses could complete their budding process and spread.
In essence, Kilbourne had found a possible key to both high transmissibility and virulence, explaining why some epidemics produced viruses that rapidly flooded the bloodstreams of infected people and readily became global pandemics, while others caused fairly localized mild outbreaks.
13
He proved his point by quantifying the density of neuraminidase proteins on the surface of the influenza strain responsible for the 1957 flu pandemic, a fairly severe wave that swept the world and claimed an estimated 60,000 American lives. That strain had the highest neuraminidase concentration of any influenza discovered since the 1930s.
But with the arrival of the Hong Kong A flu in 1968, public health experts worldwide were taken by surprise. Though most had predicted the winter of 1968–69 would have only mild flu, the Hong Kong strain caused a huge global epidemic that proved less deadly than the 1957 pandemic, but caused far more widespread illness. Whereas the Hong Kong strain had undergone sharp antigen shift in its hemagglutinin proteins, its neuraminidase component was unchanged from the previous year's mild influenza. Epidemiologists, most of whom were dumbstruck by the Hong Kong pandemic, were sobered by the virus's ability to outsmart their collective human intelligence.
“The epidemiologist must recognize that prediction of future epidemics remains a hazardous business,” warned noted Harvard epidemiologist Alexander Langmuir following the Hong Kong pandemic. “There does seem to be a periodicity that must relate to the balance of immunes and susceptibles and to the mutations of the virus. In a way, influenza predictions are like weather forecasts. As with hurricanes, pandemics can be identified and their probable course projected so that warnings can be issued. Epidemics, however, are more variable and the best that can be done is to estimate probabilities.”
14
Still, most influenza experts believed in the early 1970s that flu epidemics appeared in predictable cycles, with B-type and A-type viruses undergoing antigenic shifts in separate but fairly regular time periods. This was argued most persuasively by Kilbourne, who noted that major antigenic shifts had recently occurred in roughly ten-year cycles: 1947 (H1N1), 1957 (H2N2), and 1968 (H3N2).
15
In February 1976, Kilbourne wrote an opinion piece for
The New York
Times
in which he predicted that a major pandemic was coming soon, based on the theory of ten-to-eleven-year influenza cycles. He warned that “those concerned with public health had best plan without further delay for an imminent natural disaster.”
16
Although Kilbourne spoke for the dominant tendency in influenza scientific thinking of the day, there were dissidents who felt that influenza cycles were longer, shorter, varied in length by subtype, or were entirely random and unpredictable. Several scientists argued that swine strains, in particular, appeared in 90–100-year cycles and forecast a repeat of the 1918–19 disaster for sometime in the 1990s.
17
Blood tests of Americans during the 1968 Hong Kong flu pandemic showed that elderly people who had lived through the 1889 flu epidemic were immune to the 1968 strain. That seemed to indicate a cycle, at least for that A strain, of about eighty years.
18
Finally, Australia's leading influenza expert, W. I. B. Beveridge, argued that influenza was a “capricious virus that is not possible to predict,” noting that a long-term view of the historical record showed pandemics of one kind or another had surfaced after intervals of ten to forty-nine years, a range too great to represent a basis for forecasting future outbreaks.
19
While influenza was spreading around Fort Dix, most of the world's flu experts were gathered in Rougemont, Switzerland, for an international influenza meeting.
20
Completely unaware of events then unfolding in New Jersey, the scientists devoted their collective energy from January 26 to 28 to the task of deciding how humanity should best respond to a 1918-like flu pandemic.
In 1947 the World Health Organization, shortly after its inception, had created a network of laboratories throughout the world that agreed to collaborate in efforts to monitor changes in influenza patterns. By the time scientists gathered in Rougemont twenty-nine years later, there were nearly a hundred laboratories in the WHO influenza network, crossing most Cold War and economic boundaries of the day. These laboratories regularly collected samples of influenza from human flu patients, and sporadically from ailing birds and livestock, hoping to be able to detect dangerous perturbations in global influenza before millions of people were infected.
Based on the work of the CDC's Dr. Walter Dowdle and Robert G. Webster of St. Jude's Children's Hospital, Memphis, the gathered scientists knew that ducks and other wild birds carried influenza around the world along their migratory routes, passing it on to other animals via fecal droppings. The bird droppings were an ideal ecological environment for the viruses. Influenza could survive over three days outdoors or in the milieu of fecal-contaminated water.
“It appears that influenza viruses are constantly circulating among many avian species without causing panzootics [cross-species epidemics]. This suggests that influenza is a natural avian infection and may have been so for thousands of years,” Webster told the Rougemont gathering.
21
“The conclusion can be stated simply. All the genes of the influenza viruses of
the world are being maintained in the aquatic bird population, in gulls and ducks, and periodically they are transmitted to other species, including humans, usually after reassorting.”
Perhaps more important, in light of subsequent immediate events, was the Rougemont discussion of vaccination policies. Clearly, it was difficult to motivate voluntary compliance with vaccination campaigns. For example, between 1968 and 1974 the best turnout for flu immunization in the United States occurred during the 1968 Hong Kong epidemic, when a mere 10.7 percent of the population got their shots, despite the epidemic's severity. By 1974 U.S. flu vaccination rates had plummeted to 8 percent of the general population and a poor 17.4 percent showing among the elderly, who were considered at special risk for flu. Even in states such as California, where flu shots were offered gratis to citizens over sixty-five, much of the vaccine supplies rotted in warehouses in 1975 for lack of physician and public interest in immunization. And in the U.K., fewer than 12 percent of National Health Service physicians promoted the use of flu vaccine to their elderly or hospitalized patients. Most striking, less than 6 percent of London nurses agreed to have themselves vaccinated against flu in any given year from 1968 to 1975.
Were a major epidemic on the horizon, the Rougemont gathering concluded, special efforts would have to be made to find the virus soon enough to allow large-scale manufacture of vaccine. And extraordinary steps would have to be taken to mobilize massive public compliance—on the order of 80 percent of the elderly and at-risk populations—in vaccination.

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