The Coming Plague (32 page)

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Authors: Laurie Garrett

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By the second week of January, David Sencer could clearly see the writing on the wall: somebody was going to have to take the blame for the entire failed Swine Flu effort, and he was the most likely fall guy. Nobody in Washington political circles cared much about the disease victories that had occurred on his watch: smallpox, Ebola, dramatic decreases in all U.S. childhood diseases.
“Somebody's head is going to be on a stake,” Sencer told his staff. As the Guillain-Barré toll mounted and members of Congress called for their sacrificial lamb, Sencer tried hard to keep a business-as-usual profile in Atlanta.
On Friday afternoon, January 14, an exhausted Sencer sat in his office sorting through a stack of messages from the likes of his nemesis, Congressman John Murphy. He was in no hurry to return the calls. Three of his key men, Walter Dowdle, Joe McDade, and Shep Shepherd poked their heads in his office, asking if the director could spare a moment.
“What's up?” Sencer asked as the men gathered around his desk.
Dowdle smiled and said, “Shep and Joe have isolated an organism that causes Legionnaires'.”
“What!” shouted Sencer as he leapt to his feet, searching the faces of Shep and Joe for corroboration.
The pair nodded, and Shep told the director, “It's a bacterium.”
Sencer grabbed his phone and called in members of the CDC's top brass, including public relations director Don Berreth.
“Now we're all here. Let's go over this very carefully,” Sencer said, looking around at the cluster of his most trusted scientists.
In painstaking detail, Shepherd and McDade explained what caused the Philadelphia deaths, and how the mysterious bug had eluded laboratory discovery for six months. The bacteria would not grow in the laboratory, for reasons the two scientists had yet to determine, but they had succeeded in obtaining evidence of its existence and pathogenicity through a series of experiments.
First, McDade removed lung samples from one of the deceased Legionnaires, mashed up the cells, and injected samples into chicken eggs. After incubating the eggs for some time, he cracked the shells and extracted the yolk sacs. The sacs were then also mashed up, and extracts were injected into the foot pads of guinea pigs; the animals developed symptoms similar to those seen in the Legionnaires'.
The scientists then took blood samples from thirty-three disease survivors—samples that presumably contained antibodies against the causative agent—and mixed them with the yolk sac isolates. Yes, they reacted, confirming that whatever was in the yolk sacs was the same agent that caused illness in those thirty-three people. Conversely, the yolk sac isolates did not prompt antibody reactions with blood samples from people who hadn't had the disease.
McDade explained that he had been stumped for months by several unusual characteristics of the bacteria. First of all, it wouldn't grow under typical laboratory conditions. They had tried putting samples from the Legionnaires' blood and tissues in petri dishes filled with standard fluid media used to grow hundreds of other bacterial varieties—nothing happened. “At that point, we figured we were dealing with a virus,” McDade explained. “So we tried to culture it in medium with antibiotics.”
Virologists always filled their culture media with antibiotics in order to eliminate any chance of bacterial contamination. By using virus-appropriate media, McDade said, they had wiped out the very organism for which they were searching. It wasn't until they injected samples into eggs not treated
with antibiotics—using the eggs as substitutes for petri dishes and growth media—that they saw clear evidence that living organisms inhabited the bodies of the deceased human beings.
Another stumbling block had been mice. Specially bred varieties of mice were the most commonly used laboratory animals, and throughout the fall of 1976, the CDC scientists had tried in vain to produce Legionnaires' Disease in the rodents. It wasn't until they switched to guinea pigs that their efforts bore fruit, and Shepherd and McDade were now certain that mice were immune to the elusive bacteria.
The men told Sencer that they still didn't know why the bugs wouldn't grow in petri dishes. And they hadn't been able to get a look at the bacteria, though they were certain it was present, swimming about on the fluid surfaces of the microscope slides. In the matrix, McDade said, they clearly had enough clues to set the algorithms in motion. It seemed to him that even lacking such matrix points as visualization of the culprit organism, the lab boys had enough dots on the matrix to point their fingers at a bacterial source for the infections.
Sencer wasn't sure what the always precise but cerebral McDade meant.
“It's just not showing up,” Shepherd explained, “but I'm sure it's there.”
“Shep, how sure are you?” Sencer asked, leaning toward the laboratory scientist.
“Better than ninety-five percent,” Shepherd said, “but I'd like to run a few more experiments before we go public on this.”
“No way!” Sencer shouted. He reminded the lab men that in the real world, far from their isolated laboratories, there was genuine fear abroad, rage directed at the CDC, congressional probes, hourly media inquiry, and a serious mandate to get reasonably reliable information to the public as quickly as possible. Berreth chimed in, describing the range of angry press queries his office was fielding.
Shepherd objected to haste, and argued that their findings should be written up and submitted to a scientific journal for publication. Yes, he said, it was potentially a six- to nine-month process, but necessary to maintain scientific credibility.
“I am not going to have Joe McDade made fun of by his peers,” Shepherd declared.
Sencer chewed the idea over for a moment, turned to Berreth, and asked, “How fast could you generate a special issue of
Morbidity and Mortality Weekly Report
?”
Berreth assured his boss that such a CDC product could be generated and posted by Tuesday. A press conference, he said, could be held Tuesday afternoon.
“That satisfy you, Joe? If we publish all your data in
MMWR
, can you abide by release next week?”
McDade agreed, and dashed off to, as was his wont, triple-confirm every possible detail before Tuesday. He called his wife and warned her that
neither she nor their two children would see much of him for the next four days, as he expected to pull all-nighters right up to Tuesday.
Sensing the CDC staff's acute need for a morale boost, Sencer arranged a most unusual press conference for Tuesday, January 18, 1977. Every CDC staffer was invited to attend, as were the Surgeon General and members of the Washington, D.C., health hierarchy.
Just hours before the expected gathering, Shepherd stormed into Sencer's office and breathlessly announced, “The same organism caused the St. Elizabeth's epidemic!”
On July 27, 1965, sixty-two mental patients living in St. Elizabeth's psychiatric hospital in Washington, D.C., had fallen ill with pneumonia. Within a month's time, nineteen more patients fell ill, fourteen had died. Overall, 1.3 percent of the hospital population had been ill, nearly all of whom had lived in the same wing of the facility. At the time, authorities scoured the hospital for clues, and tested hundreds of blood and tissue samples, but no cause was found.
49
Wisely, somebody put blood and tissue samples from St. Elizabeth's in the CDC deep freeze, and there they had remained for eleven years. Until McDade, anxious to make as strong a case as possible in the Tuesday presentation, recalled the unsolved mystery and injected the old samples into chicken eggs, afterward running antibody tests on the extracts.
“Did you get reactions?” Sencer asked.
“Yes. Definitely,” Shepherd effused.
“Well, write it up and we'll add it to today's
MMWR
.”
At three o'clock that afternoon, most Atlanta employees of the CDC, from janitors to Ph.D.s, were assembled in the agency auditorium, along with a sizable press corps. As Shepherd and an exhausted McDade presented their data and the hurriedly produced
MMWR
was distributed,
50
nobody so much as whispered. When Shepherd said, “Slide projector off, please,” and finished his closing statement, a hushed moment followed.
Then revered virologist Alex Langmuir leapt to his feet and exclaimed, “Shep, that was great!” Applause and a deluge of press questions followed, all observed by a grinning Sencer, satisfied that he had successfully fulfilled his mission—namely, shielding his staff from politicians and the public while they went about the business of doing science. Sencer now felt like gloating.
Sencer's sense of sweet revenge wouldn't last long, however.
Two weeks later David Sencer would have the dubious distinction of being the first federal official fired on national television, when President Carter's new Secretary of Health, Education, and Welfare, Joseph Califano, led him out into an HEW hallway.
“I want to say something nice about you here today,” Califano said, asking Sencer to name a few of CDC's triumphs of late that he could mention to soften the blow. But then Califano added, “I'm going in there in a few minutes and announce your resignation.”
That evening, a disheartened Sencer turned on a network TV newscast and saw film footage of Califano's whispered conversation in the HEW hall. In the voice-over to the footage, the telejournalist told viewers that they were witnessing Califano's firing of Sencer.
For years, the Swine Flu events of 1976 would be debated, analyzed, and scrutinized for lessons that might guide future public health officials, politicians, and microbe hunters faced with potential pandemics. After more than fifteen years, little controversy would be shed, and consensus on what went awry would elude the American public health community. A year after the events, Dr. Arthur Viseltear wrote:
 
The short and not so very happy life history of the national swine influenza program has already become a classic health policy case study because the elements of policy and politics are so illustratively intertwined … . If one wishes to find heroes and villains in the piece, they will certainly be found; if one wishes to view the Congress as a moribund or trifling institution, there is abundant evidence to do so; if one wishes to interpret the actions of the administration and its scientists as being politically motivated and self-serving, he will find circumstantial evidence to support the theory; and if one wishes to view the President's decision as being based upon some real or imagined bicentennial or electoral bonanza, he will also find evidence to support that thesis. But he will also find, as others have found, men and institutions muddling through, making their decisions hastily and under conditions of chronic obscurity, where chance, accident, confusion, and stupidity play a larger role than certitude or calculation.
51
 
On an ominous note, Viseltear concluded: “If the events of 1976 are not to recur, then the Congress and the administration had better ensure that these issues are addressed now.”
Echoing that sentiment, Neustadt and Fineberg, while conceding that improper decisions were made in 1976, wrote:
 
We find no villains in the Federal government's officials and advisors then and think that anyone (ourselves included) might have done as they did—but we hope not twice … . These remain our sentiments. The opposite danger, of course, is that the lessons of the crash program are learned too well—too literally—producing stalemate in the face of the next out-of-routine threat from influenza. Someday there will be one.
52
 
Former congressional staffer Silverstein insisted there were no human culprits in 1976, no grave errors in political or public health judgment. Rather, he said, the only correct site upon which to fix blame was the
Swine Flu virus itself, “which failed to appear and ‘justify' the program of preventive medicine.”
Among the most haunting questions reviewed repeatedly by historians and participants in the Swine Flu campaign are: Where did the Fort Dix flu go? Would the vaccine have protected Americans if a pandemic had materialized? What caused Guillain-Barré syndrome, and could it have been prevented? If a major pandemic of any kind were on the horizon, would the American people respond to the public health authorities?
The dominant theory, reached incrementally over subsequent years, explaining the disappearance of the Fort Dix flu, was one of competition. Numerous virologists put forward the view that in any given ecological setting, two very closely related viruses would be forced to compete for hosts, and the virus with the greater transmission capabilities would be victorious. As a rule, viruses could carry only a finite amount of genetic baggage, and many species of the tiny microbes sacrificed one set of genetic capabilities for another. Thus, a highly transmissible virus might carry loads of genes that conferred the ability to remain alive while suspended in the air or resting atop steel tables, but sacrificed genes that conferred the ability to outwit certain elements of the human immune system or reproduce rapidly inside human cells.
The A/Victoria strain appears to have had the advantage on the transmission side, as it rapidly spread around the planet in several cycles, each lasting roughly one year. The A/New Jersey virus may have been virulent, if it was the cause of Private Lewis's death, but it clearly was not particularly transmissible. So, the argument goes, the two viruses were both on base at Fort Dix during January 1976, seeking human hosts to infect. In such a setting, competition would favor the more transmissible A/Victoria virus.
“The failure to detect spread of influenza A/New Jersey virus to civilian populations, however, also suggested the possibility of deficient transmissibility, as did its failure to thrive in a military population,” wrote Martin Goldfield, the New Jersey State Health Department scientist who first isolated the Fort Dix virus.
53
Nobody would ever figure out which soldier or recruit was first exposed to the pig virus, or why Private Lewis, in particular, succumbed. Not knowing how and why the virus spread inside the military setting also heightened difficulties in ascertaining why, conversely, it did not spread to the civilian population. Even the relative virulence of the A/New Jersey strain continued to be a matter of debate years later, not only because the British study in the spring of 1976 failed to find the virus particularly dangerous to human volunteers but also because the U.S. Army discovered that several of the most acutely ill Swine Flu patients at Fort Dix were simultaneously infected with
Haemophilus influenzae
, a bacterial disease that can produce pneumonia.
54
CDC studies in 1977 would show that the A/New Jersey virus replicated fairly slowly under laboratory conditions.
Throughout 1976 the National Institute of Allergy and Infectious Diseases
and FDA tried in vain to come up with a vaccine combination or dose that would raise protective anti-Swine Flu responses in youthful adults—those around the same age as Private Lewis. Though it was never the subject of widespread public attention at the time, the government never succeeded in developing a vaccine for young adults that raised much confidence in FDA or CDC circles.
Eventually, the CDC figured out that the Swine Flu vaccine worked best for adults born before 1957, a year marked by a massive global influenza A epidemic. Those who survived that epidemic seemed to respond to the Swine Flu vaccine nineteen years later as if it were a booster shot. For those born after 1957, however, the vaccine was never particularly effective, and some scientists—notably Dr. Anthony Morris of the FDA's Bureau of Biologies—openly speculated that those people would have been vulnerable if the A/New Jersey strain had spread to the civilian population.
“If we go back through time to January 1976 and have a second chance at decision making, given the same information, what would we do?” Walter Dowdle asked.
55
“We know that antigenic shifts do not necessarily lead to pandemics and that the vaccine has some risks.
“Knowing this, would the vaccine have been made at all? If so, would it have been stockpiled or given to the entire population, all those who wanted it, or only to certain target groups in the population? With the benefit of hindsight, we can now make the right decision for 1976. But what about our decision next time? It is highly unlikely that the circumstances surrounding the next potential pandemic will be precisely like those surrounding any other.”
Though errors were clearly made in the handling of a possible emergence of Swine Flu in 1976, no such flaws could be seen in the Legionnaires' Disease effort. After their dramatic January 18, 1977, announcement, Shepherd, McDade, and the rest of the CDC team swiftly determined why the elusive bug was so hard to isolate and grow in the laboratory.
The
Legionella
bacterium, as it was dubbed, had peculiar dietary needs. Standard laboratory culture media wouldn't support growth of the persnickety microbe: it needed supplements of the amino acid cysteine, vitamins, and minerals, particularly iron. Accustomed to living in what is politely referred to as pond scum,
Legionella
preferred dark, nutrient-rich, almost anoxic environments. It also enjoyed living inside the cytoplasms of larger one-celled organisms.
56
These conditions rendered the organism impossible to see through microscopes with standard techniques. When treated with silver, however, the organism clearly revealed itself, and Shepherd and McDade saw the long, round rods of
Legionella
squirming on their slides.
The epidemiology team in Philadelphia meanwhile noticed that most of the Legionnaires' Disease sufferers had spent time schmoozing in the five cocktail suites run by the candidates for leadership of the veterans' group. Further analysis revealed that the bacteria thrived in the Bellevue-Stratford
Hotel's cooling tower. From that water supply, the hotel derived its air conditioning. The
Legionella
organisms were hidden in biofilm “scums” along the edges of the cooling tower, and were actively pumped into the hotel's hospitality suites during the hot month of July.
It wasn't long before similar cases of Legionnaires' Disease surfaced all over the world. First, the CDC spotted isolated cases in eleven different states.
57
By September 1977, the federal agency was busily tracking three hospital outbreaks in Ohio,
58
one in Vermont,
59
and one in Tennessee.
60
The combined fatalities in the Ohio, Vermont, and Tennessee outbreaks and sporadic isolated cases in 1977 reached thirty-two by December, about 25 percent of all reported Legionnaires' cases.
61
In the fall of 1977 a small epidemic of Legionnaires' broke out in a hospital in Nottingham, England, leaving three patients dead.
62
In the summer of 1977 Legionnaires' struck a brand-new hospital located in one of the wealthiest parts of Los Angeles. The Wadsworth Medical Center, a veterans hospital, situated between the posh communities of Bel Air and Brentwood, was the site of a yearlong outbreak of the disease that infected about 3 percent of all patients who passed through the facility, caused disease in both staff and patients, and claimed sixteen lives.
63
By late 1978 scientists had discovered the
Legionella
bacterium in soil samples, ponds, cooling towers, water-driven condensers, slow-flowing creeks, mud, polluted and silty water, at construction sites, and in steam turbines. In coming years, they would find the dangerous organism in shower heads, grocery store vegetable counter misters, hot tubs, fountains, and a wide variety of humidifiers and other devices that aerosolized water.
Clinically, it was soon apparent that the organism was most dangerous to cigarette smokers, people recovering from surgery, and individuals who were suffering some type of immunosuppression. It seemed the bacteria were inhaled from the environment; never were they transmitted from person to person. Once somebody was infected, the
Legionella
were tough to defeat because they were resistant to a wide spectrum of antibiotics.
Air-conditioning standards changed after 1976, with federal agencies all over the world requiring far more stringent cleaning and hygiene provisions for cooling towers and large-scale air-conditioning systems.
In the case of
Legionella
, a new human disease had emerged in 1976, brought from ancient obscurity by the modern invention of air conditioning.
At the CDC's International Legionnaires' Disease meeting in 1978, several particularly ominous facets of the bug were scrutinized. CDC scientists revealed that the organism could be found in tap water, shower nozzles, and other allegedly clean water sources. One tap water study showed
Legionella
could survive over a year inside pipe biofilms, emerging in wholly infectious form once the faucet was turned on full force. It thrived in temperatures from ice cold to steamy hot. Even distilled water samples occasionally contained small numbers of
Legionella
organisms.
A team of scientists from the Denver Veterans Administration Medical
Center was particularly prescient, predicting the bacteria might survive chlorine purification efforts. “The residual amount of chlorine recommended (0.2 ppm) for standard water purification may not be sufficient for killing the LD bacterium when it is present in high concentrations,” the group wrote.
64
Bacteriologist Mortimer Stall, of the University of California, Davis, warned that the soils and waters of the earth were replete with organisms not yet identified, many of which might, like
Legionella
, one day be provided the proper circumstances for their emergence as human pathogens. Plant bacteria such as
Serratia
and
Pseudomonas
were known to cause human disease, he noted, and it would be arrogant for humanity to assume it had identified all of its flora, marine, and soil microbial enemies.

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