Why the Second Wave of the 1918 Flu Pandemic Was So Deadly

The horrific scale of the 1918 influenza pandemic—known as the "Spanish flu"—is hard to fathom. The virus infected and killed at least 50 million worldwide, according to the CDC. That’s more than all of the soldiers and civilians killed during World War I combined.

While the global pandemic lasted for two years, a significant number of deaths were packed into three especially cruel months in the fall of 1918. Historians now believe that the fatal severity of the Spanish flu’s “second wave” was caused by a mutated virus spread by wartime troop movements.

When the Spanish flu first appeared in early March 1918, it had all the hallmarks of a seasonal flu, albeit a highly contagious and virulent strain. One of the first registered cases was Albert Gitchell, a U.S. Army cook at Camp Funston in Kansas, who was hospitalized with a 104-degree fever. The virus spread quickly through the Army installation, home to 54,000 troops. By the end of the month, 1,100 troops had been hospitalized and 38 had died after developing pneumonia.

As U.S. troops deployed en masse for the war effort in Europe, they carried the Spanish flu with them. Throughout April and May of 1918, the virus spread like wildfire through England, France, Spain and Italy. An estimated three-quarters of the French military was infected in the spring of 1918 and as many as half of British troops. Yet the first wave of the virus didn't appear to be particularly deadly, with symptoms like high fever and malaise usually lasting only three days. According to limited public health data from the time, mortality rates were similar to seasonal flu.

Interestingly, it was during this time that the Spanish flu earned its misnomer. Spain was neutral during World War I and unlike its European neighbors, it didn’t impose wartime censorship on its press. In France, England and the United States, newspapers weren’t allowed to report on anything that could harm the war effort, including news that a crippling virus was sweeping through troops. Since Spanish journalists were some of the only ones reporting on a widespread flu outbreak in the spring of 1918, the pandemic became known as the “Spanish flu.”

Reported cases of Spanish flu dropped off over the summer of 1918, and there was hope at the beginning of August that the virus had run its course. In retrospect, it was only the calm before the storm. Somewhere in Europe, a mutated strain of the Spanish flu virus had emerged that had the power to kill a perfectly healthy young man or woman within 24 hours of showing the first signs of infection.

In late August 1918, military ships departed the English port city of Plymouth carrying troops unknowingly infected with this new, far deadlier strain of Spanish flu. As these ships arrived in cities like Brest in France, Boston in the United States and Freetown in West Africa, the second wave of the global pandemic began.

“The rapid movement of soldiers around the globe was a major spreader of the disease,” says James Harris, a historian at Ohio State University who studies both infectious disease and World War I. “The entire military-industrial complex of moving lots of men and material in crowded conditions was certainly a huge contributing factor in the ways the pandemic spread.”

From September through November of 1918, the death rate from the Spanish flu skyrocketed. In the United States alone, 195,000 Americans died from the Spanish flu in just the month of October. And unlike a normal seasonal flu, which mostly claims victims among the very young and very old, the second wave of the Spanish flu exhibited what’s called a “W curve”—high numbers of deaths among the young and old, but also a huge spike in the middle composed of otherwise healthy 25- to 35-year-olds in the prime of their life.

“That really freaked out the medical establishment, that there was this atypical spike in the middle of the W,” says Harris.

Not only was it shocking that healthy young men and women were dying by the millions worldwide, but it was also how they were dying. Struck with blistering fevers, nasal hemorrhaging and pneumonia, the patients would drown in their own fluid-filled lungs.

Only decades later were scientists able to explain the phenomenon now known as “cytokine storm.” When the human body is being attacked by a virus, the immune system sends messenger proteins called cytokines to promote helpful inflammation. But some strains of the flu, particularly the H1N1 strain responsible for the Spanish flu outbreak, can trigger a dangerous immune overreaction in healthy individuals. In those cases, the body is overloaded with cytokines leading to severe inflammation and the fatal buildup of fluid in the lungs.

British military doctors conducting autopsies on soldiers killed by this second wave of the Spanish flu described the heavy damage to the lungs as akin to the effects of chemical warfare.

Harris believes that the rapid spread of Spanish flu in the fall of 1918 was at least partially to blame on public health officials unwilling to impose quarantines during wartime. In Britain, for example, a government official named Arthur Newsholme knew full well that a strict civilian lockdown was the best way to fight the spread of the highly contagious disease. But he wouldn’t risk crippling the war effort by keeping munitions factory workers and other civilians home.

According to Harris’s research, Newsholme concluded that “the relentless needs of warfare justified incurring [the] risk of spreading infection” and encouraged Britons to simply “carry on” during the pandemic.

The public health response to the crisis in the United States was further hampered by a severe nursing shortage as thousands of nurses had been deployed to military camps and the front lines. The shortage was worsened by the American Red Cross’s refusal to use trained African American nurses until the worst of the pandemic had already passed.

But one of the chief reasons that the Spanish flu claimed so many lives in 1918 was that science simply didn’t have the tools to develop a vaccine for the virus. Microscopes couldn’t even see something as incredibly small as a virus until the 1930s. Instead, top medical professionals in 1918 were convinced that the flu was caused by a bacterium nicknamed “Pfeiffer’s bacillus.”

After a global flu outbreak in 1890, a German physician named Richard Pfeiffer found that all of his infected patients carried a particular strain of bacteria he called H. influenzae. When the Spanish flu pandemic hit, scientists were intent on finding a cure for Pfeiffer’s bacillus. Millions of dollars were invested in state-of-the-art labs to develop techniques for testing for and treating H. influenzae, all of it for naught_._

“This was a huge distraction for medical science,” says Harris.

By December 1918, the deadly second wave of the Spanish flu had finally passed, but the pandemic was far from over. A third wave erupted in Australia in January 1919 and eventually worked its way back to Europe and the United States.

Even the U.S. president wasn't spared. In April 1919, shortly after arriving at the World War I peace negotiations in Paris, Woodrow Wilson became seriously ill with influenza-like symptoms. The White House covered up the severity of his condition, claiming Wilson had merely caught a cold from the rainy weather in Paris. Despite nearly derailing the talks, Wilson eventually fully recovered and returned to the U.S. that July.

The mortality rate of the third wave was just as high as the second wave, but the end of the war removed the conditions that allowed the disease to spread so far and so quickly. Global deaths from the third wave, while still in the millions, paled in comparison to the apocalyptic losses during the second wave.