What’s in it for me? An unflinching look at the human catastrophe wrought by the 1918 influenza pandemic.
The 1918 influenza pandemic was the worst outbreak of disease in human history.
It claimed more human lives in a year than the Black Death did in a century; it killed more people in 24 weeks than AIDS killed in 24 years.
The disease was an especially virulent strain of the flu, but it wasn’t just the illness that killed people.
Government distraction, and then inaction, was also a death sentence for people all over the world.
These statistics are alarming, but they don’t tell the true story of the pandemic.
These blinks paint the full picture of the 1918 influenza pandemic, delving into the nature of the influenza virus, the reason behind its deadliness, and why even the world’s best scientists working together were ultimately unable to prevent catastrophic loss of life.
In these blinks, you’ll learn why Harvard was actually a pretty awful medical school before the twentieth century; why the rural farm county of Haskell, Kansas, is infamous in the medical community; and how influenza might have contributed to the rise of Adolf Hitler in Germany.
“First, do no harm.
By the onset of World War I, American medical science had improved tremendously and was approaching world class status.
” You might recognize those words from the Hippocratic oath – the oath doctors take before they can start practicing.
It’s named after the ancient Greek physician Hippocrates, who lived in the fourth century BCE.
Hippocrates had ideas about medical therapy too.
He prescribed bloodletting and leeching as therapies for many ailments because they could restore harmony to a sick body’s unbalanced humors.
Until the nineteenth century, doctors still used these methods to treat various maladies.
Even in 1800, over two millennia after Hippocrates, medicine remained what one historian called “the withered arm of science.
” By contrast, nineteenth century Europe was a revolutionary place for medicine.
A wave of increasingly revolutionary discoveries culminated in 1883, when German physician Robert Koch proved that germs can cause disease.
It was the first modern breakthrough in the study of disease.
Medicine in the US, however, lagged far behind.
That was soon to change.
The key message here is: By the onset of World War I, American medical science had improved tremendously and was approaching world class status.
In 1873, business tycoon and philanthropist Johns Hopkins died, leaving $3.
5 million to found a university and hospital in Baltimore.
His trustees aimed to make the institution a beacon of American medicine.
There wasn’t much competition.
American medical schools at the time paid their faculty and earned profits from student fees, incentivizing them to admit large classes of students irrespective of academic talent.
Even the best schools operated this way: in 1870, you could get an MD from Harvard having failed four out of nine classes.
Johns Hopkins University changed all that.
By recruiting graduates from the finest German medical universities, it gained instant credibility.
One of these professors was William Welch, a charismatic young instructor who would head up Hopkins medical research arm.
Welch presided over a close-knit group of brilliant, curious researchers.
Hopkins’s new approach to medicine attracted attention.
Looking after his own legacy, business magnate John D.
Rockefeller founded the Rockefeller Institute in 1901.
As with Johns Hopkins, money bought excellence; Rockefeller’s institute quickly became influential.
Together, the Hopkins and Rockefeller institutes raised the bar for American medical schools.
In fact, by the outbreak of World War I, American doctors were becoming as good – if not better – than their European counterparts.
The feather in Welch’s cap would be a school for public health aimed at disease prevention, which he inaugurated at Hopkins on October 1, 1918.
Welch was sick that day with a cough and a violent headache.
He’d recently traveled to Boston to investigate a new epidemic engulfing the Northeast.
He suspected it was a new strain of influenza.
Influenza is a highly efficient virus, constantly mutating to evade our immune system.
When Welch started feeling under the weather on the train back to Baltimore from Boston, the virus had already been in his body for days, silently multiplying.
Welch’s every sneeze and cough carried virus molecules looking for a new host.
Presumably, his long career in public health would have made him extra careful.
But the train journey must have given the virus an opportunity to spread with chilling efficiency to other travelers.
The purpose of a virus is to replicate and find new hosts.
It’s extremely good at it.
In fact, each influenza molecule can create between 100,000 and a million new virus proteins.
The key message here is: Influenza is a highly efficient virus, constantly mutating to evade our immune system.
Influenza viruses replicate themselves by invading cells and overwriting the genetic material in those cells with their own genes.
The infected cells start doing what the virus wants: producing more viral proteins.
When the host cells die, they explode, sending hundreds of thousands more viral proteins to invade other cells.
But influenza isn’t just good at getting cells in our bodies to do its bidding.
It’s constantly getting better at it.
Influenza encodes its genes in RNA, the simpler cousin of DNA.
When DNA replicates itself, it has a “proofreading” mechanism to cut down on mistakes; RNA doesn’t have this, which means more copying errors.
From the perspective of the virus, this is a good thing.
Sometimes, a particular mutation – a mistake – ends up being more effective than earlier versions.
So how can an influenza mutation be more effective?
One way is to find the maximum number of host individuals possible.
This is how influenza, which originated in wild aquatic birds, made the species jump to swine and then to humans.
But as mammals we’re not totally defenseless.
Our immune system has an arsenal of weapons.
One of the most effective is dendritic white blood cells.
These cells attack bacteria, then “teach” other white blood cells which enemies to target.
With its endless mutations, influenza is constantly testing to determine which new strain can both successfully challenge the immune system and potentially make the species jump, exponentially increasing the odds of infection.
When a new strain of influenza adapts to humans, it’s especially dangerous because human immune systems haven’t yet learned how to respond to it.
This is what leads to pandemics.
America’s effort to fight World War I created the perfect conditions for the spread of a virus.
By 1918, the world was used to death.
It was the last days of World War I, which had left much of Europe in ruins.
Over 5 million soldiers had been killed, and the horrors of trench warfare had traumatized the continent.
The US got involved in the war late, but once President Woodrow Wilson committed, he committed totally.
He forged the nation into a weapon by concentrating the efforts of every faction toward one singular goal: victory over Germany.
A draft was instated, calling all healthy men from age 18 to 45 to serve in the Army.
The key message here is: America’s effort to fight World War I created the perfect conditions for the spread of a virus.
The draft led to millions of men gathering on short notice at huge military encampments, hastily built after the US declared war.
These men came from all over the country, each with slightly different disease immunity.
Never before in American history – or perhaps all history – had so many people been brought together in such a way.
Noncombatants were also drawn to the war effort by factory work producing military matériel.
Millions of country folk descended on the cities, lured by the promise of good wages.
There was inadequate housing, so several families would crowd into one-room apartments, sharing beds in shifts.
All of this would prove disastrous when the virus hit full force.
But the war also gave the medical research community a much-needed injection.
For one thing, the Army’s budget for medical research increased massively.
World War I became the first war where medicine was used as a weapon.
The Army scooped up the Rockefeller Institute, rechristening it the Army Auxiliary Laboratory Number One.
Its medical researchers were breaking ground on a serum that would alleviate pneumonia, a dangerous lung infection that’s the most common killer in cases of influenza.
The surgeon general, monitoring the massing of troops, was concerned about the potential for a pandemic.
But as long as he had a serum for pneumonia, he wasn’t all that worried about influenza.
He should have been.
When the virus first hit, it seemed like the normal flu, but the second wave made clear that this virus was far worse.
The winter of 1917-18 was the coldest on record in Haskell County, Kansas.
Gale-force winds came off the prairie, hitting houses like a gunshot.
Folks there were used to it, though.
They were a hardy sort, sodbusters who fully expected a life of challenge and independence on the vast plains.
Haskell’s farmers probably wouldn’t have expected anything from their county to have worldwide impact.
But it was there that the 1918 strain of influenza made the jump from birds to humans.
From Haskell, someone carried it to Camp Funston in eastern Kansas, home to around 56,000 men.
In April, soldiers from Camp Funston went to war in Europe, and the virus was off to the races.
The key message here is: When the virus first hit, it seemed like the normal flu, but the second wave made clear that this virus was far worse.
The first wave of the 1918 influenza made a lot of people ill, but it wasn’t very deadly.
As it spread throughout Europe, Asia, Africa, and Australasia that summer, it picked up a catchy new name: the Spanish Flu.
The reason behind this was that Spain was neutral in the war, so its newspapers were the only in Europe uncensored by their government, and hence, free to report on the epidemic.
Then infections seemed to stop.
By August, British army command declared the epidemic over.
But the virus wasn’t finished.
A virus mutates as it passes between carriers, maximizing its ability to reproduce.
As the 1918 influenza strain became better at infecting its new host species, it became deadlier.
By April 1918, it had reached its full killing potential.
The second wave of the virus did not just have a higher mortality rate; the deaths it caused were grislier.
At Camp Devens, an Army base outside Boston, one physician described the disease as the most vicious he’d ever seen.
In addition to the usual symptoms, it turned its victims’ skin blue, then black.
And it was hitting hard.
By the end of September, the camp hospital designed for 1,200 was accommodating 6,000 patients.
Camp command was in denial.
Troop movements continued as usual, sending sick soldiers all over the world.
William Welch, Head of Public Health at Johns Hopkins, was urgently called up from Baltimore.
He was tasked with leading the scientific push to come up with a solution – any solution – to this terrifying new problem.
But Welch didn’t have an answer.
And he wouldn’t be much help in the horrible months to come; he himself picked up the flu while investigating the Devens outbreak.
He would be out of commission for the remainder of the pandemic, leaving the American medical community he’d helped establish to fend for itself.
In the fall of 1918, the virus hit with terrible ferocity, exacerbated by the bungled response by city and Army officials.
On September 7, 1918, 300 soldiers arrived in Philadelphia from Boston, bringing death with them.
By September 15, the virus had made 600 soldiers sick enough to require hospitalization.
More men were reporting ill every few minutes.
The disease threatened to engulf the city, heaving as it was with overcrowded slums, factories, and tenement houses.
Philadelphia public health director Wilmer Krusen was aware of the crisis in his city, as well as burgeoning deaths at camps and cities around the country.
But he took no action.
Not only did he publicly deny that influenza threatened the city, he didn’t prepare emergency stockpiles or action plans.
He thought that any action would lead to panic and interfere with the ongoing war effort.
The key message here is: In the fall of 1918, the virus hit with terrible ferocity, exacerbated by the bungled response by city and Army officials.
A massive city parade was scheduled in Philadelphia for September 28 to drum up support for the war effort.
Doctors urged Krusen to cancel it, warning of impending catastrophe, but he stayed the course.
Over 200,000 people jammed the parade route, having been assured by their government that there was no danger.
The incubation period for the flu was 24 to 72 hours.
Two days after the parade, Krusen was forced to admit the flu had hit Philadelphia.
Within 72 hours of the parade, all the hospital beds in the city were filled with dying patients.
Morgues filled up with blackened bodies, and the city ran out of coffins.
Entire families fell ill to the point that they couldn’t remove their dead family members from their beds.
Bodies began to putrefy and stink.
Terror and grief gripped the city.
After the horror at Boston’s Camp Devens, the Army surgeon general sent warnings to camps throughout the country.
Army commanders didn’t respond any better than the city officials of Philadelphia.
The commanding officer at Camp Grant in Illinois refused to limit troop training exercises and continued to send troops to other camps throughout the country, to the dismay of camp doctors.
In six days, the camp hospital went from 610 occupied beds to 4,100.
In a single day, 1,800 troops reported ill.
Finally realizing his mistake, the commanding officer shot himself.
But his death didn’t stop the carnage.
The 1918 flu was quick, grisly, and more likely to come for the young and healthy.
The 1918 strain of influenza was a particularly nasty one, but it was still just the flu.
As such, while it made hundreds of millions around the world ill, the vast majority got well again.
But for an unlucky minority, it was worse than any flu before – or since.
This meant not only more pain and horror, but also more patients who developed pneumonia, which led directly to a higher death rate.
The key message here is: The 1918 flu was quick, grisly, and more likely to come for the young and healthy.
This flu diverged from normal in an unusual way.
The victims of the typical flu are predominantly the very young and the very old, and those with weakened immune systems.
By contrast, this flu proved especially fatal for 20- and 30-somethings in the prime of life.
Pregnant women were particularly susceptible.
In these cases, it wasn’t actually the virus that was killing them.
It was the vigorous responses of their immune systems, which would fill up the lungs with fluid and dead cell debris to prevent the takeover of the virus, killing them in the process.
And death came fast – sometimes as soon as 12 hours after the first symptoms.
The surgeon Harvey Cushing, who himself would die of the flu, described these victims as “doubly dead in that they died so young.
” Victims of especially virulent cases were wracked with agonizing pain and high fevers that caused delusions.
Many developed subcutaneous emphysema, or air bubbles under the skin.
Caregivers knew the end was near once patients’ skin started turning blue.
The 1918 influenza killed more American military personnel than the entire Vietnam War.
But compared to most other parts of the world, Americans got off easy.
In 1918, most Americans had already been exposed to some kind of flu, thus developing an immunity.
In the US, cases led to pneumonia 10 to 20 percent of the time.
In more isolated areas, like jungle villages of inland Gambia or Pacific islands untouched by past influenza, the virus led to pneumonia in over 20 percent of cases.
In Western Samoa, 22 percent of the population died as a result of the flu.
America’s best scientists set about understanding what caused the virus, but their research only led to more questions.
Unlike their political contemporaries, the leading scientists of the US fully realized the catastrophic potential of the pandemic and did everything they could to move more quickly.
Scientists could agree on precious little – but they had a starting point.
First, they knew that the flu was spread by an airborne pathogen and that it spread easily in crowds.
Second, they knew it could be caught not just through inhaling, but by hand-to-face contact.
Not that this knowledge made any difference.
No one listened to them.
Even the surgeon general was routinely ignored by city and Army officials.
The key message here is: America’s best scientists set about understanding what caused the virus, but their research only led to more questions.
One question loomed large: What caused the virus?
Armed with this knowledge, they could begin working toward a cure – or at least a treatment.
At the vanguard of the movement were Oswald Avery at the Rockefeller Institute, William Park and Anna Williams at the New York City Department of Public Health, and Paul Lewis at the University of Pennsylvania.
During a previous influenza pandemic in the late nineteenth century, highly influential microbiologist Richard Pfeiffer had found what he thought was the pathogen that causes influenza, a bacterium he confidently named Bacillus influenzae.
Williams and Park also believed it was the cause of the new virus, and their testing seemed to confirm it.
While people were literally dying on the streets outside Lewis’s Philadelphia lab, the three began to develop a vaccine.
But Oswald Avery wasn’t so sure.
He became suspicious of the assumption that B.
influenzae was the cause of the disease.
His results, based on intensive sampling of patients at Camp Devens, didn’t consistently show evidence of the bacterium.
To tell for sure, he would need to run further studies.
Meanwhile, the bodies continued to pile up.
The US government’s inaction contributed to catastrophic loss of life all over the world.
The 1918 strain of influenza was perhaps the most virulent of all time.
Once it made the jump from animal to human, there was no way to stop the virus from spreading.
The US government had several chances to slow the progress of the virus and save lives.
By slowing the virus, better healthcare would have been possible for those who did catch it.
If hospitals weren’t packed with the sick and dying, patients wouldn’t be forced to convalesce at home and risk spreading the flu to their loved ones.
But American leaders didn’t take these opportunities.
President Wilson never once acknowledged the virus that was sweeping through his country, leaving corpses in its wake.
Neither did he redirect resources to alleviate the suffering.
The key message here is: The US government’s inaction contributed to catastrophic loss of life all over the world.
As early as September 30, 1918, Army Surgeon General William Gorgas urged Army generals to stop moving troops around the country to prevent the spread of the disease.
For weeks, his warnings were dismissed.
The Allies in Europe needed fresh American men.
In October, about 100,000 troops traveled across the Atlantic.
The ships became death traps.
When the ships arrived in Europe, the ill drained the resources of the Allied armies and spread the disease further via cargo ships embarking for ports all over the world.
Troop movements were a burden, not a help.
Wilson did little to shield his troops from the disease, but he did even less for civilians.
His surgeon, General Rupert Blue, actually blocked research into a cure.
In July 1918, Blue rejected a funding request for pneumonia research designed to complement the efforts of the Rockefeller Institute.
His reasoning was that the research was not “immediately necessary.
” What’s more, the Army’s monopoly on doctors and nurses meant that civilian hospitals were either closed or understaffed.
Medical workers were dying at the same, or higher, rates than the general public.
Philadelphia staggered under the weight of the assault.
An estimated half a million people fell ill.
On one single day, October 10, 1918, nearly 800 people died.
That week, over 4,500 Philadelphians perished.
Prior to the outbreak, deaths from all causes averaged around 400 per week.
Wagons circulated in the city, calling for people to bring out their dead.
As suddenly as the virus came, it faded away.
The pandemic slowly abated, but the true scope of its consequences is hard to fathom.
By October 26, a mere two weeks after the peak of the outbreak in Philadelphia, city officials lifted the order closing public places.
Once a virus becomes efficient in its ability to infect, two processes begin.
One is immunity – once influenza passes through a population, people begin to develop some resistance to it.
For the 1918 influenza, this cycle took 6 to 8 weeks, after which reports of new cases declined dramatically.
The second process is mutation within the virus.
As with all flu viruses, the 1918 strain mutated.
It would have been difficult for the mutation to top the original in terms of virulence; the next mutation was marginally less deadly.
The one after that was even less deadly, and so on.
As a result, cities struck later in the epidemic weren’t hit as hard.
The key message here is: The pandemic slowly abated, but the true scope of its consequences is hard to fathom.
As you’ve learned, most people hit with the flu recovered.
But some developed a final, devastating complication.
The virus also impacted the brain and nervous system, sometimes leading to lasting mental instability.
Evidence of this can be found in the very highest tiers of society.
President Woodrow Wilson caught influenza on April 3, 1919, when he was in France negotiating the end of World War I.
The illness had a tragic effect, for him as well as the world at large.
After his bout with the flu, Wilson was never the same.
Future President Herbert Hoover remarked that after his illness, Wilson’s mind lost “resiliency”; others noticed that he wasn’t as quick and easily became mentally exhausted.
Wilson also suffered from spells of paranoia: he was utterly convinced that his home was filled with French spies.
Newly weakened, he suddenly reversed his long-held position on the peace negotiation, and agreed wholesale to the terms proposed by France, which included harsh economic sanctions on Germany.
These terms would be ruinous for Germany.
The Treaty of Versailles would directly lead to economic hardship, political chaos, and the rise of Adolf Hitler.
The flu was just as bad, if not worse, for ordinary civilians.
In New York City, the flu made 21,000 children orphans.
A 1927 study found that 20 million people died worldwide.
Every revision since then has pushed the figure upward.
The latest estimate is that around 100 million people died – more than 5 percent of the world’s population at the time.
Long after the pandemic, scientists remained obsessed with finding a cure. For most, this quest ended in disappointment.
The 1918 pandemic shattered the illusion that science could solve any problem.
Every lab in the world was focused on finding a solution, but by 1920 the pandemic burned itself out with no help from science.
As one physician at the time put it, “Doctors know no more about this flu than fourteenth century Florentine doctors knew about the Black Death.
” The scientists who had worked through the pandemic had seen enough horror to haunt them for life.
But none would be able to rest until they had an answer.
It was a quest that would lead, in some cases, to tragedy.
The key message here is: Long after the pandemic, scientists remained obsessed with finding a cure.
For most, this quest ended in disappointment.
The greatest question remained: What caused the influenza?
Was it really the Bacillus influenzae?
With the carnage of 1918 on everyone’s minds, finding the answer truly seemed like a life-or-death mission.
William Park and Anna Williams, at the New York City Department of Public Health, reversed their previous claim that B.
influenzae was the cause of the virus.
Then, suddenly, funding for their research ran out, and they moved on.
Paul Lewis, of the University of Pennsylvania, and Oswald Avery, of the Rockefeller Institute, continued the quest.
Avery was never able to answer the question, although he continued working on it until 1943.
When he retired, he shocked the world of science with a new discovery.
He showed that when pneumonia bacteria enter the body, they mutate to find ways to attack our lungs more efficiently.
When they reproduce, they pass down the most effective mutations by reacting with our DNA.
DNA, therefore, is the vehicle for the transfer of genetic information.
Avery’s accomplishment is now canon; it’s the basis of molecular biology.
Lewis held firm to the idea that B.
influenzae caused the virus, in the face of mounting evidence to the contrary.
His stubbornness blinded him, ensuring that whatever science he produced subsequently failed to meet his previous standard of brilliance.
Lewis drifted from job to job, like a foundering ship.
Desperate for a win, he volunteered to go to Brazil to investigate a particularly deadly outbreak of yellow fever.
He died there, in 1929.
Two years later, Lewis’s lab made an important discovery.
Using methodology developed with Lewis, they proved that antibodies from human survivors of the 1918 flu could protect pigs against the swine flu.
In 1933, this research led to the ultimate breakthrough: the discovery of the virus that caused influenza in humans.
Final summary
The key message in these blinks: Science wasn’t ready for the 1918 strain of influenza.
Even with the best and the brightest working feverishly for a cure, the resulting pandemic caused mass carnage all over the world.
Millions of flu vaccines are now administered worldwide, but the repercussions of the 1918 pandemic are almost too wide-reaching to fathom.
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What to read next: Deadliest Enemy, by Michael T.
Osterholm PhD, MPH, and Mark Olshaker You’ve just learned the scientific and social history behind the 1918 influenza pandemic, which killed 5 percent of the world’s population at the time.
These blinks lay bare the terrifying truth: a new mutation of an old illness, one we’ve faced for millennia, can still lay bare the weaknesses in our social and political structures.
But what happens when humans are hit with a totally new illness?
How much worse could it get than 1918?
In the blinks to Deadliest Enemy, by Michael T.
Osterholm PhD, MPH, and Mark Olshaker, you’ll learn exactly how vulnerable modern humans are to pandemics.
Studying the examples of Ebola, Zika, and SARS, these blinks also put forward a practical plan for protecting humanity from its deadliest enemy.