The Coming Plague (29 page)

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Authors: Laurie Garrett

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“The most important outcome of the next epidemic may well be the lessons it will provide that can help in controlling both pandemic and epidemic influenza,” Walter Dowdle told the Rougemont gathering. He had no idea his words would prove immediately prophetic. Two weeks later the health establishment would seriously entertain the possibility that the Fort Dix virus was the same as, or a close cousin of, the 1918–19 killer microbe, and events would snowball down an icy policy slope. The perceived threat would grow larger every week as scientists were forced to yield decision making to politicians, and the highly hypothetical basis of all Swine Flu conjectures would recede further into the background. While early scientific and policy reports carefully alluded to the tentative basis of such dire forecasts, official government prognostications presented only certainties and absolutes. This contrast between a very tentative hypothetical outlook in the immediate wake of Private Lewis's death, and the federal mobilization weeks later was so striking that Dr. Joseph Califano, upon taking office a year later as Secretary of Health, Education, and Welfare in the new Carter administration, would commission an outside investigation. Two Harvard University policy analysts would be given a simple question to answer in the winter of 1977: “What went wrong?” Richard E. Neustadt had served in government during the Democratic administrations of Truman, Kennedy, and Johnson, and was on the faculty of the John F. Kennedy School of
Government at Harvard during the Swine Flu affair. Dr. Harvey Fineberg wore two hats, holding degrees in both medicine and public policy. Together in 1977 they would review the events of the previous year, trying to pin down exactly when, and why, the federal health establishment started to suspend disbelief and began its journey down the Swine Flu slippery slope.
“From one case—Private Lewis—you learn nothing,” Fineberg, seventeen years later as dean of the Harvard School of Public Health, would say. “It was in the great quiet afterwards that more genuine information was to be found,” he said, noting that the entire health establishment held its breath during the winter of 1976, waiting for signs of Swine Flu spread. Signs that never appeared.
“The issue was not the overinterpretation of early cases [at Fort Dix], but the subsequent foreclosure of doubt” about the possibility of fulfillment of a worst-case scenario, Fineberg said. “My personal view is that often in such cases it's hard to separate likelihoods from consequences. In this case the consequence of being wrong about an epidemic were so devastating in people's minds that it wasn't possible to focus properly on the issue of likelihood. Nobody could really estimate likelihood then, or now. The challenge in such circumstances is to be able to distinguish things so you can rationally talk about it. In 1976, some policy makers were simply overwhelmed by the consequences of being wrong. And at a higher level [in the Ford administration] the two—likelihood and consequence—got meshed.”
Osborn, known for her blunt and often eloquent expressions, shared no such perspective in 1976, or nearly twenty years later. She told fellow FDA advisers that there had been a long spring-to-summer silence following the first flu outbreaks of 1918—a silence that was followed in September by the greatest pandemic of the early twentieth century.
“To decide not to do something, to decide to go on pause because the virus went on pause,” Osborn argued in long conference calls to fellow scientists, “would be utterly irresponsible.”
From his perspective as director of the CDC, David Sencer also saw a very different picture in 1976—which would remain at odds with the Neustadt-Fineberg report two decades later. Jovial, self-effacing, and well liked by most CDC staffers during his reign (1966–77), Sencer was most persuaded to action by what he believed were clear cases of soldier-to-soldier spread of the apparent swine virus at Fort Dix.
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“The fact of transmission is the key,” he told his staff.
Dr. Walter Dowdle, a soft-spoken influenza virologist who viewed the world in a serious and cautious fashion, telephoned Sencer late the first Tuesday night of February to tell the director that the New Jersey state labs claimed to have found five cases of Swine Flu. Dowdle rarely raised red flags of alarm around the CDC. Forty-eight hours later, however, Dowdle told Sencer that CDC scientists had confirmed the Swine Flu findings. Sencer immediately called a meeting of top government scientists from all
over the country, and Saturday morning in Atlanta, Dowdle presented the Fort Dix case report.
Dowdle carefully laid out what had transpired, leaving for last evidence that Private Lewis died of a virus which cross-reacted with the Shope swine strain. When Dowdle concluded his remarks with the words “The isolates were swine,” General Phillip Russell's jaw dropped, and the tall, muscular Army physician abruptly sat forward. As head of all military medical research in the U.S. armed forces, Russell had complete responsibility for decisions concerning vaccination of armed forces personnel. Well versed in the history of the 1918–19 epidemic and its rampant spread among World War I military personnel, Russell saw no choice in the matter: the United States should immediately develop a Swine Flu vaccine.
Sencer agreed wholeheartedly. It wasn't a question of probabilities, he argued, but of disease prevention. Even if the likelihood of a 1918–19 type of virus reappearing in the fall of 1976 was immeasurably small, he said, it would be wrong to avoid taking steps to prevent it.
“We have the technology, we have the evidence of transmission,” he told the group. “It would be irresponsible to do anything else except develop a vaccine.”
In its first official pronouncement the CDC's words were crafted with careful attention to the ambiguities and tentativeness inherent in interpretation of the Fort Dix cases. After hours of meetings with top CDC and Washington Public Health Service officials, the agency published its first Swine Flu notice on February 14, in its regular weekly publication.
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It explained that a small influenza outbreak had occurred at Fort Dix during the previous month, involving one death. Eleven blood samples had been tested, seven proving to be the relatively harmless A/Victoria strain; four resulted from an A/H1N1 strain “similar to swine influenza.”
The report also noted, “There is some evidence from antibody prevalence studies that occasional infections with swine influenza virus might have occurred in more recent [since 1970] years among persons in frequent contact with swine.”
In 1974, a sixteen-year-old Minnesota boy suffering from Hodgkin's disease (a type of blood cancer that produces severe immunodeficiency) died of what appeared to be Swine Flu. A year later, an otherwise healthy eight-year-old Wisconsin boy contracted the disease, surviving thanks to his body's production of antibodies that cross-reacted with Shope's 1930s Swine Flu virus. Both boys lived on farms and handled pigs. More important, in both cases the infection never spread to other schoolmates, and though most of the Wisconsin boy's immediate family tested antibody-positive for exposure, none had developed the flu.
In February, then, the agency readily acknowledged that there might be some low-level background rate of Swine Flu infections among people who lived around domestic pigs, and the presence of antibodies to swine antigens
did not, in and of itself, indicate that a particularly lethal or highly transmissible form of influenza was afoot in America.
Many years later CDC influenza expert Nancy Cox, who was not directly involved in the events of 1976, would summarize a large body of evidence indicating that people who lived and worked around domestic livestock were routinely exposed to the viruses those animals harbor, including swine strains of influenza. The great 1889 pandemic, for example, began as an epidemic of “the cough” among European horses (probably Russian) sometime in the early 1880s. Nearly ninety years later the 1968 Hong Kong flu also proved capable experimentally of producing “the cough” in horses.
Swine influenzas, Cox would later explain, were particularly worrisome because pigs were highly permissive hosts, capable of harboring influenzas from a wide range of animals, birds, and humans. Inside the swine, various influenza strains shared genes, and recombined, resulting in major antigen shifts.
“We do see in hindsight that the farm Swine Flu cases in 1976 were separate and isolated events from what occurred at Fort Dix,” Cox explained.
A week after the CDC's first 1976 publication, the agency noted discovery of six more Fort Dix soldiers with Swine Flu, bringing the total to ten (including the deceased Lewis). The remainder of the base's epidemic appeared to result from A/Victoria flu. An additional agricultural Swine Flu case was reported, involving a young man from Mississippi, who also suffered from Hodgkin's disease and worked in a pig slaughterhouse.
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Large-scale blood testing at Fort Dix soon revealed a total of 273 individuals who may have had swine antibodies, thirteen of whom had actually contracted influenza. Unclear, and never clarified in any subsequent CDC publications, was how many of the influenza-ailing soldiers were co-infected with A/New Jersey/76 and A/Victoria/75. Even thirty years later no technology could tell which strain was responsible for disease in an individual who was co-infected, although it is generally assumed that whichever strain is present in largest numbers is the pathogenic culprit.
The CDC interviewed the Fort Dix recruits to see which might have had direct contact with swine, and found twenty-two men who had been around pigs and had antibodies to the Shope swine influenza. Investigators then tested the families of those twenty-two soldiers: one family tested antibody-positive. Four out of eleven members of that family tested positive; none were sick. They were not farmers, and the flu-exposed members were all under twenty-five years old. When 200 classmates of the children were tested, no further spread of the apparent infection could be found.
Policy decisions and actions moved forward rapidly, though investigations at Fort Dix were far from complete. Army and CDC investigators would spend several more weeks combing the base for clues to the origin and spread of the apparent Swine Flu, eventually concluding that no more
than 155 recruits were definitely infected with the virus. Another 300 Fort Dix soldiers were infected with the A/Victoria/75 strain.
More important, the investigators concluded that the only time or place shared by all soldiers infected with Swine Flu prior to their illnesses was the Fort Dix reception area. The mini-epidemic began, they concluded, sometime in the first or second week of January, when hundreds of fresh recruits were processed onto the base following the Christmas holidays, and assigned to basic training. In the reception center the new recruits were given physical examinations, vaccinations, and basic military instructions.
The first of the new recruits subsequently shown to have Swine Flu arrived at the reception center on January 5. Designated only as V4, he complained of illness on January 28.
Private Lewis came through the reception center the following day. All Fort Dix Swine Flu illnesses occurred between January 12 and February 8, the time span of high reception center activity. The infections probably incubated between the initial transmissions in the reception center in early January, and the flu illnesses appeared two to three weeks later.
The only other possible shared source of infection for the thirteen soldiers struck with Swine Flu was the base medical system. All the men made visits to the base dispensary for a variety of health problems prior to developing the flu. Under General Russell's personal command, Army investigators searched for a source of viral contamination at both the reception area and the dispensary: none was found. It is not likely, however, that weeks after the events any evidence of viral contamination of equipment or medical instruments would persist, available for discovery. Thus, the possibility remained that America's Swine Flu outbreak of 1976 was iatrogenic.
By mid-March influenza of all types was on a sharp decline worldwide, even at Fort Dix, and the agency's virus branch director, Dr. Walter Dowdle, said, “Influenza in the United States has decreased markedly, and there is no longer evidence of nationwide epidemic activity.”
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“By the beginning of March,” Dowdle would write six years later, “the only signs of the Swine Flu epidemic
in the world
[his emphasis] were at Fort Dix. But the possibility of a Swine Flu outbreak in the future could not be disproved. What could not be disproved must be allowed for. Most of the scientists were well aware of the professional risks they incurred if they mounted a national immunization program and the virus did not appear. Most were equally aware of their responsibility for the public's safety in the event of an epidemic. Something had to be done.”
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On March 13, the CDC director, David Sencer, completed a special memorandum for his superiors in Washington, detailing the evidence for a Swine Flu outbreak and requesting a $134 million congressional allocation for development and distribution of vaccines. Within less than a week, word of Swine Flu was all over Capitol Hill. By March 18, Sencer's memo
had been signed by Assistant Secretary for Health Dr. Theodore Cooper, and lay upon the desk of HEW Secretary F. David Mathews awaiting his urgent attention.
Stated as certainties, rather than hypothetical conjectures, were the following points listed under the memo's heading “
Facts
”: The virus found at Fort Dix is “antigenically related to the influenza virus which has been implicated as the cause of the 1918–19 pandemic which killed 450,000 [American] people; every American under the age of fifty”is probably susceptible to this new strain”; severe flu epidemics”occur at approximately ten-year intervals.”

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