It generated surprisingly few headlines at the time. The pandemic’s casualties blurred together in the public mind with those who never returned from the great European bloodbath, which perhaps explains why Ernest Hemingway and F. Scott Fitzgerald, writing best-selling novels in the years immediately following the Spanish flu pandemic, never mentioned the disease even once. Moreover, the pandemic lacked a punchy name.
When it started being called the Spanish flu, the label sounded both distant and trivial. Plus, it was a misnomer, since it had nothing to do with Spain; the disease neither originated nor was particularly virulent there. The name arose because Spain’s neutrality in the Great War kept its newspapers free, and they alone reported on this new disease menace, whereas other European countries were censoring all reports of medical losses for fear of harming morale. But to those who were there, it was both horrible and strange.
We now know that the pandemic was indeed caused by influenza, a virus that we nowadays call H1N1, whose initials stand for the glycoproteins (proteins with sugarlike side chains) named haemagglutinin and neuraminidase, which are tools the virus uses to sicken humans, pigs or birds, the three species most susceptible to its attack. Haemagglutinin lets the virus attach itself to animal cells, while neuraminidase is an enzyme that helps the virus reproduce. Strains of H1N1 are widespread in swine and birds as well, and this lethal Great World War strain probably arose one day in Kansas when bird and human viral genetic material was exchanged, possible in a single fateful swine infection.
The 1918 flu outbreak infected about a third of the global human population. Yet what was particularly strange was its lethality. A normal flu epidemic kills about one in a thousand of those who contract the disease. But the 1918 Spanish flu was a hundred times deadlier, especially in vulnerable demographics, which oddly included what is normally the hardiest age group: the 20-to-40-year-olds.
The very first case may have been seen in January in Haskell County, Kansas, where a local physician was alarmed enough to report the sudden outbreak to the US government: an extraordinarily unusual thing to have done at that time. What’s indisputable is that on March 4, at a US Army base in Fort Riley, Kansas, the company’s cook came down with the flu. Exactly one week later, 100 other soldiers were in the base hospital. The casualty toll there then skyrocketed to 522 men by mid-month. At this same time, flu was breaking out in the New York City borough of Queens. At that point nothing seemed unusual, since influenza outbreaks had been familiar nuisances every few years.
Everything changed in August. Suddenly a new wave of sickness appeared in far-flung places simultaneously, and now there was a much higher mortality. The very first cases were seen in three busy port cities that were involved with war shipments and troop movements. It was quickly obvious that something very weird was happening. This was obviously a mutation of the earlier virus, since those who recovered from the milder initial infection had immunity from the second wave.
Although the symptoms were flulike, around 20 percent of the victims developed acute respiratory problems and could not be saved. At my request, the strange medical situation was analyzed by British infectious disease specialist Dr. John Froude, who lives in our area. He generously shared his professional assessment in an e-mail: “The virus has a tropism (physical attraction for) the alveolus, the little sac at the end of the bronchi where oxygen exchange takes place. It fills up with protein and you cannot oxygenate. This is called ARDS, or Adult Respiratory Distress Syndrome. When they dug up Lucy in Alaska and looked at her permafrost-preserved lungs, this is what they saw.”
By mid-November it was completely over and no new cases appeared – although, after months of inactivity, a third, less deadly wave went around the globe the following spring, of 1919. Apparently, the H1N1 virus had now mutated to a less-lethal strain. But before this cessation, the pandemic killed as many people in one year than the Black Death had claimed in a full century.
Why had the ordinary H1N1 virus become so deadly? And why the bizarre pattern of lethality among 20-to-40-year-olds? There were two main causes.
The exhumation of that Alaska woman whose body was preserved in permafrost has let medical researchers examine the responsible virus. Turned out, the young adults who died in such great numbers in 1918 had been born after 1889, so they were never exposed to the same kind of H1N1 virus, and thus they were particularly vulnerable.
But a totally different factor may have been primarily responsible for the lethality. Turned out, the 1918 H1N1 strain had the ability to cause a severe autoimmune response in humans. This so-called cytokine storm is an extreme immune response where the body overreacts to the pathogen, triggering excess white blood cells, resulting in often-fatal effects on the lungs. The patient sometimes hemorrhages from the nose, ears and lungs: symptoms that accurately describe the victims of the Spanish flu. This would also explain the odd 1918 age-specific mortality, since young adults generally have the strongest immune response. As John Froude, MD, told me, “The immune system is imperfect and has a dark side. An infection, after all, is the interaction between the pathogen and your immune system.”
But whether or not we now fully understand its odd lethality, the fact remains: The 1918 pandemic killed more people in a year than the HIV scourge has killed in the past 40. So, if you’re one of the many who are suffering from the current viral epidemic, at least you know it could be worse.
Parts of this column have been excerpted from Bob Berman’s newest book, Cataclysms: The Supernovae, Exploding Galaxies and Earthly Mayhem that Shook Our Universe, which will be published this fall by Little Brown.
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