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Kindle Notes & Highlights
by
Gina Kolata
Read between
January 15 - January 22, 2022
The 1918 flu epidemic puts every other epidemic of this century to shame. It was a plague so deadly that if a similar virus were to strike today, it would kill more people in a single year than heart disease, cancers, strokes, chronic pulmonary disease, AIDS, and Alzheimer’s disease combined. The epidemic affected the course of history and was a terrifying presence at the end of World War I, killing more Americans in a single year than died in battle in World War I, World War II, the Korean War, and the Vietnam War.
When the illness was first observed, doctors were reluctant even to call it the flu. It seemed to be a new disease, they said. Some called it bronchopneumonia, others called it epidemic respiratory infection. Doctors suggested it might be cholera or typhus, or perhaps it was dengue fever or botulism. Still others said it was simply an unidentified pandemic disease. Those who used the term “influenza” insisted on enclosing it in quotation marks.
What to do? If the world knew about the flu in San Sebastián, the tourist season would be finished. Who would want to go on vacation only to be laid up with the flu? Maybe the illness could be hushed up, the town’s officials reasoned. Yet the word spread—San Sebastián was a place to be avoided.
Maybe the name stuck because Spain, still unaligned, did not censor its news reports, unlike other European countries. And so Spain’s flu was no secret, unlike the flu elsewhere.
On August 28, eight men got the flu. The next day, 58 were sick. By day four, the sick toll reached 81. A week later, it was 119, and that same day the first civilian was admitted to Boston City Hospital sick with the flu.
“All the theaters and nearly all of the shops and restaurants are closed, and the streets have been full of funerals all day and ambulances all night.”
Public health departments gave out gauze masks for people to wear in public. A New York doctor and collector of historical photographs, Dr. Stanley B. Burns, has a photograph in his archive of a minor league baseball game being played during the epidemic. It is a surreal image: The pitcher, the batter, every player, and every member of the crowd are wearing gauze masks.
What was in them when no one knew what was causing the flu? He interviewed a doctor who had helped produce flu vaccines in 1918. The doctor, Crosby said, told him that the vaccines were just a soup made of blood and mucus of flu patients that had been filtered to get rid of large cells and debris. When they injected it into people’s arms their arms became horribly sore. “So they thought it really worked.”
Traditional notions of honor were abandoned, and, instead, “it was settled that present enjoyment, and all that contributed to it, was both honorable and useful.”
The plague would not have been so overwhelming if it could only spread through flea bites. It turned out that once the bacteria began infecting people, they found another way of spreading. They would infect the lungs and cause a pneumonia, whereupon sick people could infect the healthy simply by coughing or sneezing. With that mode of infection, there was no stopping the epidemic.
As the second decade of the twentieth century wound to a close, the memory of a world stalked by infectious disease had dimmed. People had become complacent, almost smug, about disease and death. It was a time when death had nearly lost its sting, an era when the miracles of medicine were portrayed as almost a new religion. And it was a time when death became separate from everyday life. The Ladies’ Home Journal proudly declared that the parlor, where the dead had been laid out for viewing, was now to be called the “living room,” a room for the living, not the dead.
Crosby examined college history textbooks, looking for the 1918 flu. He remarked that the epidemic was notable mostly by its absence.
But the flu was expunged from newspapers, magazines, textbooks, and society’s collective memory. Crosby calls the 1918 flu “America’s forgotten pandemic,” noting: “The important and almost incomprehensible fact about the Spanish flu is that it killed millions upon millions of people in a year or less. Nothing else—no infection, no war, no famine—has ever killed so many in as short a period. And yet it has never inspired awe, not in 1918 and not since, not among the citizens of any particular land and not among the citizens of the United States.”
many said that Koen was wrong and that pigs were not getting the flu. The animal industry in particular did its best to discredit Koen’s hypothesis. Hog producers were afraid that the public might become frightened by the thought that pigs could have human influenza and would refuse to eat pork.
The most reasonable interpretation, he decided, was that there was no single cause of swine influenza. Both the virus and the bacteria needed to be present, acting in synergy to cause the disease.
The 1918 epidemic came in two waves, a mild flu in the spring of 1918 followed by the killer flu in the fall. And it seemed that the two flu strains were closely related. Infection with the first strain protected against the second
It began to seem that the flu virus had gone somewhere between the first and second waves of the 1918 flu where it mutated into a killer strain. Perhaps, some thought, it had gone into animals.
Most human flu viruses are of strains they dubbed A, and these A viruses mutated rapidly, so someone who has recovered from a bout with flu can get it again the next year because the virus will have changed enough to evade the immune system’s defenses. Another type of flu, called the B strains, also could infect humans but seemed less likely to mutate from year to year.
It is those two viral proteins, the hemagglutinin and the neuraminidase, that define a flu strain, and scientists began naming strains by their hemagglutinin and neuraminidase proteins. A strain that swept the world in 1946, for example, was H1N1. The next time the flu virus underwent a major genetic change, creating a pandemic, was in 1956, with strain H2N2. The pandemic that arrived in 1968 involved a virus whose hemagglutinin had changed from the 1956 virus but whose neuraminidase had not. It was named H3N2.
It took a week for the lab at the Centers for Disease Control to discover the virus’s identity. It was a swine flu virus, one that was closely related to, if not identical to, the virus that, through the sleuthing in the 1930s by people like Richard Shope, was thought to have caused the 1918 influenza pandemic.
One reason the flu is less apparent in summer is that the virus dies quickly in high humidity. It needs dry winter air to spread and flourish, which is why flu epidemics seem to disappear when spring arrives.
“Better to store the vaccine in people than in warehouses,”
Those who had been unable to get the flu shots in time would be angry because they would be vulnerable. Those who were immunized but who caught another virus that they thought was the flu would be annoyed because they would assume that the vaccine did not work. All in all, millions of people would be upset.
Alexander posed a question to the group that Neustadt and May thought so apt that, they say, if policymakers routinely asked an “Alexander’s question,” historic blunders, as well as commonplace blunders, might be avoided. Alexander’s question was brilliantly simple. He asked what information might make the group change its mind about the need to prepare to immunize the nation against swine flu? Would it be evidence that every swine flu case was mild? Or that no one but the Fort Dix soldiers got the swine flu? Would it make a difference what the timing of the outbreaks was or where they
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‘Look, I know that the chance of a pandemic may be as little as 1 to 50 or even less, but if you were the President of the United States and were told that the country faced a 1 to 50 or maybe even a 1 to 100 chance of a national disaster—which on the basis of all available evidence could largely be averted by a vaccine program—what would you say?’
vaccine makers were told to stop making a vaccine to protect against what everyone had thought would be the predominant flu strain in the fall, A/Victoria, and shift over to making only swine flu vaccine.
if Americans have flu shots in the numbers predicted, as many as 2,300 will have strokes and 7,000 will have heart attacks within two days of being immunized. “Why? Because that is the number statistically expected, flu shots or no flu shots,” he wrote. “Yet can one expect a person who received a flu shot at noon and who that same night had a stroke not to associate somehow the two in his mind? Post hoc, ergo propter hoc,”
It’s part of the global flu surveillance network that allows virologists to discern the first signs of the next year’s predominant flu strain—in time to start making vaccines—and that lets them keep an ever-vigilant watch for new strains of flu.
Webster proposed that the worst flu pandemics, the one in 1918 being at the far end of bad, start with a bird flu. But before it can infect a person, it has to be humanized—that is, to change in a way that would allow it to keep the birdlike features that make it so infectious and yet acquire human flu-like properties that would allow it to grow in the lung cells of a human being. That crucial step, Webster said, typically takes place in pigs. Pigs bridge the gap between birds and humans—both bird flu strains and human flu strains can grow in pigs’ bodies. An unfortunate pig that happens to be
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Shortridge notes that influenza epidemics always seem to start in Asia—in southern China in particular, exactly the place where the rice-duck-pig system is in place. “Historical records always refer to this part of the world,” he said.
For all the advances in molecular biology and genetics in the years since 1918, humanity still seemed at the mercy of a genetic twist that could create a killer virus out of an ordinary flu.
“One person dies and there are repercussions through the next generation. Multiply that by 100 million and then you begin to see the effects of the flu,”
the 1918 flu resembled a bird flu but it could not have come directly from a bird—it had to have been adapted and modified first by growing in humans or pigs.
Shortridge suggests that the 1918 virus gradually changed over perhaps a fifty-year period from a bird flu to one that could infect humans. Eventually, it became a strain that would be deadly to virtually everyone in the world—everyone, that is, except people of southern China, who had been living with the strain for so long. In fact, he said, when he went back and looked at records from southern China in 1918, he discovered that the 1918 flu was not particularly deadly there, in direct contrast to its effects elsewhere.
Taubenberger and his group concluded that the 1918 virus might actually have emerged and started infecting humans sometime between 1900 and 1915. Moreover, he said, it is intriguing that the influenza death rates in the United States began rising in 1915 and continued to rise until 1917, when they dropped slightly, followed by a huge spike in influenza mortality rates in 1918. The question he cannot answer, however, is whether the gradual rise in flu deaths before 1918 was the beginning of the 1918 influenza pandemic or whether it was simply a reflection of modest changes in another, much less
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Virtually every viral disease is more deadly in teenagers than children, and more deadly in young adults than teenagers.
The question is why did the death rate drop off precipitously in people over age forty? The most likely explanation, Palese said, is that a similar virus, not as deadly, had come by earlier, providing some immunity to the 1918 flu virus to those who had been exposed to it.
When you couple the virus’s unprecedented virulence with the fact that anyone who survived it will then be immune to it—meaning that the virus will be forced to mutate or die out—it is not so surprising that the 1918 flu virus seems to have disappeared from the world, Taubenberger observed.
What if babies and children who were exposed to the 1890 flu responded by making abundant quantities of antibodies? Taubenberger asked. And what if the 1918 flu virus had a similar protein on its surface so that the antibodies to the 1890 flu also vigorously attacked the 1918 flu virus? If that happened, the immune system itself, instead of the flu virus, could be causing the flu deaths. In a gross overresponse to the 1918 virus, armies of white blood cells and fluids could rush to the lungs of flu patients. The healthier people were, and the better their immune systems, the more likely they
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If this story was fiction, the clues would yield a suspect and the suspect would reveal the weapon. But it is science, and science is not always neat and clean. In science, each new finding can open the door to a flurry of new questions.
Would a new killer flu look just like the 1918 flu? Or was that virus more of an example of what could happen if a flu virus was perfectly made to be a deadly foe? Will the next terrible influenza virus be a new strain that is, in its own way, ideally made to kill?
Perhaps, in some innocent encounter in China between a child and a bird, a new killer flu is on its way. Or perhaps, even now, a young man or a young woman has become infected with two different strains of flu viruses. They are mixing together in the person’s lungs, their genes reassorting. Emerging from that witches’ brew is a new virus, a chimera, that, like the 1918 flu virus, is perfectly suited for destruction. Perhaps, as we grow almost smug about influenza, that most quotidian of infections, a new plague is now gathering deadly force. Except this time we stand armed with a better
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