The Spanish flu, also known as
the 1918 influenza pandemic, was an unusually deadly influenza
pandemic caused by the H1N1 influenza A virus. Lasting from
February 1918 to April 1920, it infected 500 million people – about
a third of the world's population at the time – in four successive
waves. The death toll is typically estimated to have been somewhere
between 20 million and 50 million, although estimates range from a
conservative 17 million to a possible high of 100 million, making it
one of the deadliest pandemics in human history.
The first observations of illness and
mortality were documented in the United States (in Kansas) in March
1918 and then in April in France, Germany and the United Kingdom. To
maintain morale, World War I censors minimized these early reports.
Newspapers were free to report the epidemic's effects in neutral
Spain, such as the grave illness of King Alfonso XIII, and these
stories created a false impression of Spain as especially hard hit.
This gave rise to the name "Spanish" flu. Historical
and epidemiological data are inadequate to identify with certainty
the pandemic's geographic origin, with varying views as to its
location.
Most influenza outbreaks
disproportionately kill the very young and the very old, with a
higher survival rate for those in between, but the Spanish flu
pandemic resulted in a higher-than-expected mortality rate for young
adults. Scientists offer several possible explanations for the high
mortality rate of the 1918 influenza pandemic, including a severe
six-year climate anomaly that affected the migration of disease
vectors and increased the likelihood of the spread of the disease
through bodies of water. Some analyses have shown the virus to be
particularly deadly because it triggers a cytokine storm, which
ravages the stronger immune system of young adults. In contrast, a
2007 analysis of medical journals from the period of the pandemic
found that the viral infection was no more aggressive than previous
influenza strains. Instead, malnourishment, overcrowded medical camps
and hospitals, and poor hygiene, all exacerbated by the recent war,
promoted bacterial superinfection. This superinfection killed most of
the victims, typically after a somewhat prolonged death bed.
The 1918 Spanish flu was the first of
three flu pandemics caused by H1N1 influenza A virus; the most recent
one was the 2009 swine flu pandemic. The 1977 Russian flu was also
caused by H1N1 virus, but it mostly affected younger populations.
Etymology
Although its geographic origin is
unknown (see below), the disease was called Spanish flu as early as
the first wave of the pandemic. Spain was not involved in the war,
having remained neutral, and had not imposed wartime censorship.
Newspapers were therefore free to report the epidemic's effects, such
as the grave illness of King Alfonso XIII, and these widely-spread
stories created a false impression of Spain as especially hard hit.
Alternative names were also used at the
time of the pandemic. Similar to the name of Spanish flu, many of
these also alluded to the purported origins of the disease. In
Senegal it was named 'the Brazilian flu', and in Brazil 'the
German flu', while in Poland it was known as 'the Bolshevik
disease'. In Spain itself, the nickname for the flu, the "Naples
Soldier", was adopted from a 1916 operetta, The Song of
Forgetting (La canción del olvido) after one of the librettists
quipped that the play's most popular musical number, Naples Soldier,
was as catchy as the flu. Today, however, 'Spanish flu'
(Gripe Española) is the most widely used name for the pandemic in
Spain.
Other terms for this virus include the
"1918 influenza pandemic," the "1918 flu
pandemic", or variations of these.
History
Timeline
First wave of early 1918
The pandemic is conventionally marked
as having begun on 4 March 1918 with the recording of the case of
Albert Gitchell, an army cook at Camp Funston in Kansas, United
States, despite there having been cases before him. The disease had
already been observed in Haskell County as early as January 1918,
prompting local doctor Loring Miner to warn the editors of the US
Public Health Service's academic journal Public Health Reports.
Within days of the March 4 first case at Camp Funston, 522 men at the
camp had reported sick. By 11 March 1918, the virus had reached
Queens, New York. Failure to take preventive measures in March/April
was later criticized.
As the US had entered World War I, the
disease quickly spread from Camp Funston, a major training ground for
troops of the American Expeditionary Forces, to other US Army camps
and Europe, becoming an epidemic in the Midwest, East Coast, and
French ports by April 1918, and reaching the Western Front by the
middle of the month. It then quickly spread to the rest of France,
Great Britain, Italy, and Spain and in May reached Breslau and
Odessa. After the signing of the Treaty of Brest-Litovsk (March
1918), Germany started releasing Russian prisoners of war, who then
brought the disease to their country. It reached North Africa,
India, and Japan in May, and soon after had likely gone around the
world as there had been recorded cases in Southeast Asia in April. In
June an outbreak was reported in China. After reaching Australia in
July, the wave started to recede.
The first wave of the flu lasted from
the first quarter of 1918 and was relatively mild. Mortality rates
were not appreciably above normal; in the United States ~75,000
flu-related deaths were reported in the first six months of 1918,
compared to ~63,000 deaths during the same time period in 1915. In
Madrid, Spain, fewer than 1,000 people died from influenza between
May and June 1918. There were no reported quarantines during the
first quarter of 1918. However, the first wave caused a significant
disruption in the military operations of World War I, with
three-quarters of French troops, half the British forces, and over
900,000 German soldiers sick.
Deadly second wave of late 1918
The second wave began in the second
half of August 1918, probably spreading to Boston and Freetown,
Sierra Leone, by ships from Brest, where it had likely arrived with
American troops or French recruits for naval training. From the
Boston Navy Yard and Camp Devens (later renamed Fort Devens), about
30 miles west of Boston, other U.S. military sites were soon
afflicted, as were troops being transported to Europe. Helped by
troop movements, it spread over the next two months to all of North
America, and then to Central and South America, also reaching Brazil
and the Caribbean on ships. In July 1918, the Ottoman Empire saw its
first cases in some soldiers. From Freetown, the pandemic continued
to spread through West Africa along the coast, rivers, and the
colonial railways, and from railheads to more remote communities,
while South Africa received it in September on ships bringing back
members of the South African Native Labour Corps returning from
France. From there it spread around southern Africa and beyond the
Zambezi, reaching Ethiopia in November. On September 15, New York
City saw its first fatality from influenza. The Philadelphia Liberty
Loans Parade, held in Philadelphia, Pennsylvania, on 28 September
1918 to promote government bonds for World War I, resulted in 12,000
deaths after a major outbreak of the illness spread among people who
had attended the parade.
From Europe, the second wave swept
through Russia in a southwest–northeast diagonal front, as well as
being brought to Arkhangelsk by the North Russia intervention, and
then spread throughout Asia following the Russian Civil War and the
Trans-Siberian railway, reaching Iran (where it spread through the
holy city of Mashhad), and then later India in September, as well as
China and Japan in October. The celebrations of the Armistice of 11
November 1918 also caused outbreaks in Lima and Nairobi, but by
December the wave was mostly over.
The second wave of the 1918 pandemic
was much more deadly than the first. The first wave had resembled
typical flu epidemics; those most at risk were the sick and elderly,
while younger, healthier people recovered easily. October 1918 was
the month with the highest fatality rate of the whole pandemic. In
the United States, ~292,000 deaths were reported between
September–December 1918, compared to ~26,000 during the same time
period in 1915. The Netherlands reported 40,000+ deaths from
influenza and acute respiratory disease. Bombay reported ~15,000
deaths in a population of 1.1 million. The 1918 flu pandemic in India
was especially deadly, with an estimated 12.5–20 million deaths in
the last quarter of 1918 alone.
Third wave of 1919
In January 1919, a third wave of the
Spanish Flu hit Australia, where it killed around 12,000 people
following the lifting of a maritime quarantine, and then spread
quickly through Europe and the United States, where it lingered
through the spring and until June 1919. It primarily affected Spain,
Serbia, Mexico and Great Britain, resulting in hundreds of thousands
of deaths. It was less severe than the second wave but still much
more deadly than the initial first wave. In the United States,
isolated outbreaks occurred in some cities including Los Angeles, New
York City, Memphis, Nashville, San Francisco and St. Louis. Overall
American mortality rates were in the tens of thousands during the
first six months of 1919.
Fourth wave of 1920
In spring 1920, a fourth wave occurred
in isolated areas including New York City, Switzerland, Scandinavia,
and some South American islands. New York City alone reported 6,374
deaths between December 1919 and April 1920, almost twice the number
of the first wave in spring 1918. Other US cities including Detroit,
Milwaukee, Kansas City, Minneapolis and St. Louis were hit
particularly hard, with death rates higher than all of 1918. Peru
experienced a late wave in early 1920, and Japan had one from late
1919 to 1920, with the last cases in March. In Europe, five countries
(Spain, Denmark, Finland, Germany and Switzerland) recorded a late
peak between January–April 1920.
Potential origins
Despite its name, historical and
epidemiological data cannot identify the geographic origin of the
Spanish flu. However, several theories have been proposed.
United States
The first confirmed cases originated in
the United States. Historian Alfred W. Crosby stated in 2003 that the
flu originated in Kansas, and author John M. Barry described a
January 1918 outbreak in Haskell County, Kansas, as the point of
origin in his 2004 article.
A 2018 study of tissue slides and
medical reports led by evolutionary biology professor Michael Worobey
found evidence against the disease originating from Kansas, as those
cases were milder and had fewer deaths compared to the infections in
New York City in the same period. The study did find evidence through
phylogenetic analyses that the virus likely had a North American
origin, though it was not conclusive. In addition, the haemagglutinin
glycoproteins of the virus suggest that it originated long before
1918, and other studies suggest that the reassortment of the H1N1
virus likely occurred in or around 1915.
Europe
The major UK troop staging and hospital
camp in Étaples in France has been theorized by virologist John
Oxford as being at the center of the Spanish flu. His study found
that in late 1916 the Étaples camp was hit by the onset of a new
disease with high mortality that caused symptoms similar to the flu.
According to Oxford, a similar outbreak occurred in March 1917 at
army barracks in Aldershot, and military pathologists later
recognized these early outbreaks as the same disease as the Spanish
flu. The overcrowded camp and hospital at Etaples was an ideal
environment for the spread of a respiratory virus. The hospital
treated thousands of victims of poison gas attacks, and other
casualties of war, and 100,000 soldiers passed through the camp every
day. It also was home to a piggery, and poultry was regularly brought
in from surrounding villages to feed the camp. Oxford and his team
postulated that a precursor virus, harbored in birds, mutated and
then migrated to pigs kept near the front.
A report published in 2016 in the
Journal of the Chinese Medical Association found evidence that the
1918 virus had been circulating in the European armies for months and
possibly years before the 1918 pandemic. Political scientist Andrew
Price-Smith published data from the Austrian archives suggesting the
influenza began in Austria in early 1917.
A 2009 study in Influenza and Other
Respiratory Viruses found that Spanish flu mortality simultaneously
peaked within the two-month period of October and November 1918 in
all fourteen European countries analyzed, which is inconsistent with
the pattern that researchers would expect if the virus had originated
somewhere in Europe and then spread outwards.
China
In 1993, Claude Hannoun, the leading
expert on the Spanish flu at the Pasteur Institute, asserted the
precursor virus was likely to have come from China and then mutated
in the United States near Boston and from there spread to Brest,
France, Europe's battlefields, the rest of Europe, and the rest of
the world, with Allied soldiers and sailors as the main
disseminators. Hannoun considered several alternative hypotheses of
origin, such as Spain, Kansas, and Brest, as being possible, but not
likely. In 2014, historian Mark Humphries argued that the
mobilization of 96,000 Chinese laborers to work behind the British
and French lines might have been the source of the pandemic.
Humphries, of the Memorial University of Newfoundland in St. John's,
based his conclusions on newly unearthed records. He found archival
evidence that a respiratory illness that struck northern China (where
the laborers came from) in November 1917 was identified a year later
by Chinese health officials as identical to the Spanish flu. However,
no tissue samples have survived for modern comparison. Nevertheless,
there were some reports of respiratory illness on parts of the path
the laborers took to get to Europe, which also passed through North
America.
One of the few regions of the world
seemingly less affected by the Spanish flu pandemic was China, where
several studies have documented a comparatively mild flu season in
1918. (Although this is disputed due to lack of data during the
Warlord Period, see Around the globe.) This has led to speculation
that the Spanish flu pandemic originated in China, as the lower rates
of flu mortality may be explained by the Chinese population's
previously acquired immunity to the flu virus.
A report published in 2016 in the
Journal of the Chinese Medical Association found no evidence that the
1918 virus was imported to Europe via Chinese and Southeast Asian
soldiers and workers and instead found evidence of its circulation in
Europe before the pandemic. The 2016 study suggested that the low
flu mortality rate (an estimated one in a thousand) found among the
Chinese and Southeast Asian workers in Europe meant that the deadly
1918 influenza pandemic could not have originated from those workers.
Further evidence against the disease being spread by Chinese workers
was that workers entered Europe through other routes that did not
result in a detectable spread, making them unlikely to have been the
original hosts.
Epidemiology and pathology
Transmission and mutation
As U.S. troops deployed en masse for
the war effort in Europe, they carried the Spanish flu with them.
The basic reproduction number of the
virus was between 2 and 3. The close quarters and massive troop
movements of World War I hastened the pandemic, and probably both
increased transmission and augmented mutation. The war may also have
reduced people's resistance to the virus. Some speculate the
soldiers' immune systems were weakened by malnourishment, as well as
the stresses of combat and chemical attacks, increasing their
susceptibility. A large factor in the worldwide occurrence of the flu
was increased travel. Modern transportation systems made it easier
for soldiers, sailors, and civilian travelers to spread the disease.
Another was lies and denial by governments, leaving the population
ill-prepared to handle the outbreaks.
The severity of the second wave has
been attributed to the circumstances of the First World War. In
civilian life, natural selection favors a mild strain. Those who get
very ill stay home, and those mildly ill continue with their lives,
preferentially spreading the mild strain. In the trenches, natural
selection was reversed. Soldiers with a mild strain stayed where they
were, while the severely ill were sent on crowded trains to crowded
field hospitals, spreading the deadlier virus. The second wave began,
and the flu quickly spread around the world again. Consequently,
during modern pandemics, health officials look for deadlier strains
of a virus when it reaches places with social upheaval. The fact that
most of those who recovered from first-wave infections had become
immune showed that it must have been the same strain of flu. This was
most dramatically illustrated in Copenhagen, which escaped with a
combined mortality rate of just 0.29% (0.02% in the first wave and
0.27% in the second wave) because of exposure to the less-lethal
first wave. For the rest of the population, the second wave was far
more deadly; the most vulnerable people were those like the soldiers
in the trenches – adults who were young and fit.
After the lethal second wave struck in
late 1918, new cases dropped abruptly. In Philadelphia, for example,
4,597 people died in the week ending 16 October, but by 11 November,
influenza had almost disappeared from the city. One explanation for
the rapid decline in the lethality of the disease is that doctors
became more effective in the prevention and treatment of pneumonia
that developed after the victims had contracted the virus. However,
John Barry stated in his 2004 book The Great Influenza: The Epic
Story of the Deadliest Plague In History that researchers have found
no evidence to support this position. Another theory holds that the
1918 virus mutated extremely rapidly to a less lethal strain. Such
evolution of influenza is a common occurrence: there is a tendency
for pathogenic viruses to become less lethal with time, as the hosts
of more dangerous strains tend to die out. Some fatal cases did
continue into March 1919, killing one player in the 1919 Stanley Cup
Finals.
Signs and symptoms
US Army symptomology of the flu
The majority of the infected
experienced only the typical flu symptoms of sore throat, headache,
and fever, especially during the first wave. However, during the
second wave, the disease was much more serious, often complicated by
bacterial pneumonia, which was often the cause of death. This more
serious type would cause heliotrope cyanosis to develop, whereby the
skin would first develop two mahogany spots over the cheekbones which
would then over a few hours spread to color the entire face blue,
followed by black coloration first in the extremities and then
further spreading to the limbs and the torso. After this, death
would follow within hours or days due to the lungs being filled with
fluids. Other signs and symptoms reported included spontaneous mouth
and nosebleeds, miscarriages for pregnant women, a peculiar smell,
teeth, and hair falling, delirium, dizziness, insomnia, loss of
hearing or smell, blurred vision, and impaired color vision. One
observer wrote, "One of the most striking of the
complications was hemorrhage from mucous membranes, especially from
the nose, stomach, and intestine. Bleeding from the ears and
petechial hemorrhages in the skin also occurred". The
severity of the symptoms was believed to be caused by cytokine
storms.
The majority of deaths were from
bacterial pneumonia, a common secondary infection associated with
influenza. This pneumonia was itself caused by common upper
respiratory-tract bacteria, which were able to get into the lungs via
the damaged bronchial tubes of the victims. The virus also killed
people directly by causing massive hemorrhages and edema in the
lungs. Modern analysis has shown the virus to be particularly deadly
because it triggers a cytokine storm (overreaction of the body's
immune system). One group of researchers recovered the virus from
the bodies of frozen victims and transfected animals with it. The
animals suffered rapidly progressive respiratory failure and death
through a cytokine storm. The strong immune reactions of young adults
were postulated to have ravaged the body, whereas the weaker immune
reactions of children and middle-aged adults resulted in fewer deaths
among those groups.
Misdiagnosis
Because the virus that caused the
disease was too small to be seen under a microscope at the time,
there were problems with correctly diagnosing it. The bacterium
Haemophilus influenzae was instead mistakenly thought to be the
cause, as it was big enough to be seen and was present in many,
though not all, patients. For this reason, a vaccine that was used
against that bacillus did not make an infection rarer but did
decrease the death rate.
During the deadly second wave there
were also fears that it was in fact plague, dengue fever, or cholera.
Another common misdiagnosis was typhus, which was common in
circumstances of social upheaval, and was therefore also affecting
Russia in the aftermath of the October Revolution. In Chile, the
view of the country's elite was that the nation was in severe
decline, and therefore doctors assumed that the disease was typhus
caused by poor hygiene, and not an infectious one, causing a
mismanaged response which did not ban mass gatherings.
The role of climate conditions
Studies have shown that the immune
system of Spanish flu victims was weakened by adverse climate
conditions which were particularly unseasonably cold and wet for
extended periods of time during the duration of the pandemic. This
affected especially WWI troops exposed to incessant rains and
lower-than-average temperatures for the duration of the conflict, and
especially during the second wave of the pandemic.
Ultra-high-resolution climate data combined with highly detailed
mortality records analyzed at Harvard University and the Climate
Change Institute at the University of Maine identified a severe
climate anomaly that impacted Europe from 1914 to 1919, with several
environmental indicators directly influencing the severity and spread
of the Spanish flu pandemic. Specifically, a significant increase in
precipitation affected all of Europe during the second wave of the
pandemic, from September to December 1918. Mortality figures follow
closely the concurrent increase in precipitation and decrease in
temperatures. Several explanations have been proposed for this,
including the fact that lower temperatures and increased
precipitation provided ideal conditions for virus replication and
transmission, while also negatively affecting the immune systems of
soldiers and other people exposed to the inclement weather, a factor
proven to increase likelihood of infection by both viruses and
pneumococcal co-morbid infections documented to have affected a large
percentage of pandemic victims (one fifth of them, with a 36%
mortality rate). A six-year climate anomaly (1914–1919) brought
cold, marine air to Europe, drastically changing its weather, as
documented by eyewitness accounts and instrumental records, reaching
as far as the Gallipoli campaign, in Turkey, where ANZAC troops
suffered extremely cold temperatures despite the normally
Mediterranean climate of the region. The climate anomaly likely
influenced the migration of H1N1 avian vectors which contaminate
bodies of water with their droppings, reaching 60% infection rates in
autumn. The climate anomaly has been associated with an
anthropogenic increase in atmospheric dust, due to the incessant
bombardment; increased nucleation due to dust particles (cloud
condensation nuclei) contributed to increased precipitation.
Responses
1918 Chicago newspaper headlines
reflect mitigation strategies such as increased ventilation, arrests
for not wearing face masks, sequenced inoculations, limitations on
crowd size, selective closing of businesses, curfews, and lockdowns.
After October's strict containment measures showed some success,
Armistice Day celebrations in November and relaxed attitudes by
Thanksgiving caused a resurgence.
Public health management
While systems for alerting public
health authorities of infectious spread did exist in 1918, they did
not generally include influenza, leading to a delayed response.
Nevertheless, actions were taken. Maritime quarantines were declared
on islands such as Iceland, Australia, and American Samoa, saving
many lives. Social distancing measures were introduced, for example
closing schools, theatres, and places of worship, limiting public
transportation, and banning mass gatherings. Wearing face masks
became common in some places, such as Japan, though there were
debates over their efficacy. There was also some resistance to their
use, as exemplified by the Anti-Mask League of San Francisco.
Vaccines were also developed, but as these were based on bacteria and
not the actual virus, they could only help with secondary infections.
The actual enforcement of various restrictions varied. To a large
extent, the New York City health commissioner ordered businesses to
open and close on staggered shifts to avoid overcrowding on the
subways.
A later study found that measures such
as banning mass gatherings and requiring the wearing of face masks
could cut the death rate up to 50 percent, but this was dependent on
their being imposed early in the outbreak and not being lifted
prematurely.
Medical treatment
As there were no antiviral drugs to
treat the virus, and no antibiotics to treat the secondary bacterial
infections, doctors would rely on a random assortment of medicines
with varying degrees of effectiveness, such as aspirin, quinine,
arsenics, digitalis, strychnine, epsom salts, castor oil, and iodine.
Treatments of traditional medicine, such as bloodletting, ayurveda,
and kampo were also applied.
Information dissemination
Due to World War I, many countries
engaged in wartime censorship, and suppressed reporting of the
pandemic. For example, the Italian newspaper Corriere della Sera was
prohibited from reporting daily death tolls. The newspapers of the
time were also generally paternalistic and worried about mass panic.
Misinformation also spread along with the disease. In Ireland there
was a belief that noxious gases were rising from the mass graves of
Flanders Fields and being "blown all over the world by
winds". There were also rumors that the Germans were behind
it, for example by poisoning the aspirin manufactured by Bayer, or by
releasing poison gas from U-boats.
Mortality
Around the globe
The Spanish flu infected around 500
million people, about one-third of the world's population. Estimates
as to how many infected people died vary greatly, but the flu is
regardless considered to be one of the deadliest pandemics in
history. An early estimate from 1927 put global mortality at 21.6
million. An estimate from 1991 states that the virus killed between
25 and 39 million people. A 2005 estimate put the death toll at 50
million (about 3% of the global population), and possibly as high as
100 million (more than 5%). However, a 2018 reassessment in the
American Journal of Epidemiology estimated the total to be about 17
million, though this has been contested. With a world population of
1.8 to 1.9 billion, these estimates correspond to between 1 and 6
percent of the population.
A 2009 study in Influenza and Other
Respiratory Viruses based on data from fourteen European countries
estimated a total of 2.64 million excess deaths in Europe
attributable to the Spanish flu during the major 1918–1919 phase of
the pandemic, in line with the three prior studies from 1991, 2002,
and 2006 that calculated a European death toll of between 2 million
and 2.3 million. This represents a mortality rate of about 1.1% of
the European population (c. 250 million in 1918), considerably higher
than the mortality rate in the US, which the authors hypothesize is
likely due to the severe effects of the war in Europe. The excess
mortality rate in the UK has been estimated at 0.28%–0.4%, far
below this European average.
Some 12–17 million people died in
India, about 5% of the population. The death toll in India's
British-ruled districts was 13.88 million. Another estimate gives at
least 12 million dead. The decade between 1911 and 1921 was the only
census period in which India's population fell, mostly due to
devastation of the Spanish flu pandemic. While India is generally
described as the country most severely affected by the Spanish flu,
at least one study argues that other factors may partially account
for the very high excess mortality rates observed in 1918, citing
unusually high 1917 mortality and wide regional variation (ranging
from 0.47% to 6.66%).[4] A 2006 study in The Lancet also noted that
Indian provinces had excess mortality rates ranging from 2.1% to
7.8%, stating: "Commentators at the time attributed this huge
variation to differences in nutritional status and diurnal
fluctuations in temperature."
In Finland, 20,000 died out of 210,000
infected. In Sweden, 34,000 died.
In Japan, 23 million people were
affected, with at least 390,000 reported deaths. In the Dutch East
Indies (now Indonesia), 1.5 million were assumed to have died among
30 million inhabitants. In Tahiti, 13% of the population died during
one month. Similarly, in Western Samoa 22% of the population of
38,000 died within two months.
In Istanbul, capital of the Ottoman
Empire, 6,403 to 10,000 died, giving the city a mortality rate of at
least 0.56%.
In New Zealand, the flu killed an
estimated 6,400 Pakeha and 2,500 indigenous Maori in six weeks, with
Māori dying at eight times the rate of Pakeha.
In the US, about 28% of the population
of 105 million became infected, and 500,000 to 850,000 died (0.48 to
0.81 percent of the population). Native American tribes were
particularly hard hit. In the Four Corners area, there were 3,293
registered deaths among Native Americans. Entire Inuit and Alaskan
Native village communities died in Alaska. In Canada, 50,000 died.
In Brazil, 300,000 died, including
president Rodrigues Alves.
In Britain, as many as 250,000 died; in
France, more than 400,000.
In Ghana, the influenza epidemic killed
at least 100,000 people. Tafari Makonnen (the future Haile Selassie,
Emperor of Ethiopia) was one of the first Ethiopians who contracted
influenza but survived. Many of his subjects did not; estimates for
fatalities in the capital city, Addis Ababa, range from 5,000 to
10,000, or higher.
The death toll in Russia has been
estimated at 450,000, though the epidemiologists who suggested this
number called it a "shot in the dark". If it is
correct, Russia lost roughly 0.4% of its population, meaning it
suffered the lowest influenza-related mortality in Europe. Another
study considers this number unlikely, given that the country was in
the grip of a civil war, and the infrastructure of daily life had
broken down; the study suggests that Russia's death toll was closer
to 2%, or 2.7 million people.
Devastated communities
Even in areas where mortality was low,
so many adults were incapacitated that much of everyday life was
hampered. Some communities closed all stores or required customers to
leave orders outside. There were reports that healthcare workers
could not tend the sick nor the gravediggers bury the dead because
they too were ill. Mass graves were dug by steam shovel and bodies
buried without coffins in many places.
Bristol Bay, a region of Alaska
populated by indigenous people, suffered a death rate of 40 percent
of the total population, with some villages entirely disappearing.
Several Pacific island territories were
hit particularly hard. The pandemic reached them from New Zealand,
which was too slow to implement measures to prevent ships, such as
Talune, carrying the flu from leaving its ports. From New Zealand,
the flu reached Tonga (killing 8% of the population), Nauru (16%),
and Fiji (5%, 9,000 people). Worst affected was Western Samoa,
formerly German Samoa, which had been occupied by New Zealand in
1914. 90% of the population was infected; 30% of adult men, 22% of
adult women, and 10% of children died. By contrast, Governor John
Martin Poyer prevented the flu from reaching neighboring American
Samoa by imposing a blockade. The disease spread fastest through the
higher social classes among the indigenous peoples, because of the
custom of gathering oral tradition from chiefs on their deathbeds;
many community elders were infected through this process.
In Iran, the mortality was very high:
according to an estimate, between 902,400 and 2,431,000, or 8% to 22%
of the total population died. The country was going through the
Persian famine of 1917–1919 concurrently.
In Ireland, during the worst 12 months,
the Spanish flu accounted for one-third of all deaths.
In South Africa it is estimated that
about 300,000 people amounting to 6% of the population died within
six weeks. Government actions in the early stages of the virus'
arrival in the country in September 1918 are believed to have
unintentionally accelerated its spread throughout the country.
Almost a quarter of the working population of Kimberley, consisting
of workers in the diamond mines, died. In British Somaliland, one
official estimated that 7% of the native population died. This huge
death toll resulted from an extremely high infection rate of up to
50% and the extreme severity of the symptoms, suspected to be caused
by cytokine storms.
Less-affected areas
In the Pacific, American Samoa and the
French colony of New Caledonia succeeded in preventing even a single
death from influenza through effective quarantines. Australia also
managed to avoid the first two waves with a quarantine. Iceland
protected a third of its population from exposure by blocking the
main road of the island. By the end of the pandemic, the isolated
island of Marajó, in Brazil's Amazon River Delta had not reported an
outbreak. Saint Helena also reported no deaths.
Estimates for the death toll in China
have varied widely, a range which reflects the lack of centralized
collection of health data at the time due to the Warlord period.
China may have experienced a relatively mild flu season in 1918
compared to other areas of the world. However, some reports from its
interior suggest that mortality rates from influenza were perhaps
higher in at least a few locations in China in 1918. At the very
least, there is little evidence that China as a whole was seriously
affected by the flu compared to other countries in the world.
The first estimate of the Chinese death
toll was made in 1991 by Patterson and Pyle, which estimated a toll
of between 5 and 9 million. However, this 1991 study was criticized
by later studies due to flawed methodology, and newer studies have
published estimates of a far lower mortality rate in China. For
instance, Iijima in 1998 estimates the death toll in China to be
between 1 and 1.28 million based on data available from Chinese port
cities. The lower estimates of the Chinese death toll are based on
the low mortality rates that were found in Chinese port cities (for
example, Hong Kong) and on the assumption that poor communications
prevented the flu from penetrating the interior of China.
However, some contemporary newspaper
and post office reports, as well as reports from missionary doctors,
suggest that the flu did penetrate the Chinese interior and that
influenza was severe in at least some locations in the countryside of
China.[
Although medical records from China's
interior are lacking, extensive medical data were recorded in Chinese
port cities, such as then British-controlled Hong Kong, Canton,
Peking, Harbin and Shanghai. These data were collected by the Chinese
Maritime Customs Service, which was largely staffed by non-Chinese
foreigners, such as the British, French, and other European colonial
officials in China. As a whole, accurate data from China's port
cities show astonishingly low mortality rates compared to other
cities in Asia. For example, the British authorities at Hong Kong and
Canton reported a mortality rate from influenza at a rate of 0.25%
and 0.32%, much lower than the reported mortality rate of other
cities in Asia, such as Calcutta or Bombay, where influenza was much
more devastating. Similarly, in the city of Shanghai – which had a
population of over 2 million in 1918 – there were only 266 recorded
deaths from influenza among the Chinese population in 1918. If
extrapolated from the extensive data recorded from Chinese cities,
the suggested mortality rate from influenza in China as a whole in
1918 was likely lower than 1% – much lower than the world average
(which was around 3–5%). In contrast, Japan and Taiwan had
reported a mortality rate from influenza around 0.45% and 0.69%
respectively, higher than the mortality rate collected from data in
Chinese port cities, such as Hong Kong (0.25%), Canton (0.32%), and
Shanghai.
Patterns of fatality
The pandemic mostly killed young
adults. In 1918–1919, 99% of pandemic influenza deaths in the U.S.
occurred in people under 65, and nearly half of deaths were in young
adults 20 to 40 years old. In 1920, the mortality rate among people
under 65 had decreased sixfold to half the mortality rate of people
over 65, but 92% of deaths still occurred in people under 65. This
is unusual since influenza is typically most deadly to weak
individuals, such as infants under age two, adults over age 70, and
the immunocompromised. In 1918, older adults may have had partial
protection caused by exposure to the 1889–1890 flu pandemic, known
as the "Russian flu". According to historian John
M. Barry, the most vulnerable of all – "those most likely,
of the most likely", to die – were pregnant women. He
reported that in thirteen studies of hospitalized women in the
pandemic, the death rate ranged from 23% to 71%. Of the pregnant
women who survived childbirth, over one-quarter (26%) lost the child.
Another oddity was that the outbreak was widespread in the summer
and autumn (in the Northern Hemisphere); influenza is usually worse
in winter.
There were also geographic patterns to
the disease's fatality. Some parts of Asia had 30 times higher death
rates than some parts of Europe, and generally, Africa and Asia had
higher rates, while Europe and North America had lower ones. There
was also great variation within continents, with three times higher
mortality in Hungary and Spain compared to Denmark, two to three
times higher chance of death in Sub-Saharan Africa compared to North
Africa, and possibly up to ten times higher rates between the
extremes of Asia. Cities were affected worse than rural areas.
There were also differences between cities, which might have
reflected exposure to the milder first wave giving immunity, as well
as the introduction of social distancing measures.
Another major pattern was the
differences between social classes. In Oslo, death rates were
inversely correlated with apartment size, as the poorer people living
in smaller apartments died at a higher rate. Social status was also
reflected in the higher mortality among immigrant communities, with
Italian Americans, a recently arrived group at the time, were nearly
twice as likely to die compared to the average Americans. These
disparities reflected worse diets, crowded living conditions, and
problems accessing healthcare. Paradoxically, however, African
Americans were relatively spared by the pandemic.
More men than women were killed by the
flu, as they were more likely to go out and be exposed, while women
would tend to stay at home. For the same reason men also were more
likely to have pre-existing tuberculosis, which severely worsened the
chances of recovery. However, in India the opposite was true,
potentially because Indian women were neglected with poorer
nutrition, and were expected to care for the sick.
A study conducted by He et al. (2011)
used a mechanistic modeling approach to study the three waves of the
1918 influenza pandemic. They examined the factors that underlie
variability in temporal patterns and their correlation to patterns of
mortality and morbidity. Their analysis suggests that temporal
variations in transmission rate provide the best explanation, and the
variation in transmission required to generate these three waves is
within biologically plausible values. Another study by He et al.
(2013) used a simple epidemic model incorporating three factors to
infer the cause of the three waves of the 1918 influenza pandemic.
These factors were school opening and closing, temperature changes
throughout the outbreak, and human behavioral changes in response to
the outbreak. Their modeling results showed that all three factors
are important, but human behavioral responses showed the most
significant effects.
Effects
World War I
Academic Andrew Price-Smith has made
the argument that the virus helped tip the balance of power in the
latter days of the war towards the Allied cause. He provides data
that the viral waves hit the Central Powers before the Allied powers
and that both morbidity and mortality in Germany and Austria were
considerably higher than in Britain and France. A 2006 Lancet study
corroborates higher excess mortality rates in Germany (0.76%) and
Austria (1.61%) compared to Britain (0.34%) and France (0.75%).
Kenneth Kahn at Oxford University
Computing Services writes that "Many researchers have
suggested that the conditions of the war significantly aided the
spread of the disease. And others have argued that the course of the
war (and subsequent peace treaty) was influenced by the pandemic."
Kahn has developed a model that can be used on home computers to test
these theories.
Economic
Many businesses in the entertainment
and service industries suffered losses in revenue, while the
healthcare industry reported profit gains. Historian Nancy Bristow
has argued that the pandemic, when combined with the increasing
number of women attending college, contributed to the success of
women in the field of nursing. This was due in part to the failure of
medical doctors, who were predominantly men, to contain and prevent
the illness. Nursing staff, who were mainly women, celebrated the
success of their patient care and did not associate the spread of the
disease with their work.
A 2020 study found that US cities that
implemented early and extensive non-medical measures (quarantine,
etc.) suffered no additional adverse economic effects due to
implementing those measures, when compared with cities that
implemented measures late or not at all.
Long-term effects
A 2006 study in the Journal of
Political Economy found that "cohorts in utero during the
pandemic displayed reduced educational attainment, increased rates of
physical disability, lower income, lower socioeconomic status, and
higher transfer payments received compared with other birth cohorts."
A 2018 study found that the pandemic reduced educational attainment
in populations. The flu has also been linked to the outbreak of
encephalitis lethargica in the 1920s.
Survivors faced an elevated mortality
risk. Some survivors did not fully recover from physiological
condition(s).
Legacy
Despite the high morbidity and
mortality rates that resulted from the epidemic, the Spanish flu
began to fade from public awareness over the decades until the
arrival of news about bird flu and other pandemics in the 1990s and
2000s. This has led some historians to label the Spanish flu a
"forgotten pandemic".
There are various theories of why the
Spanish flu was "forgotten". The rapid pace of the
pandemic, which killed most of its victims in the United States
within less than nine months, resulted in limited media coverage. The
general population was familiar with patterns of pandemic disease in
the late 19th and early 20th centuries: typhoid, yellow fever,
diphtheria, and cholera all occurred near the same time. These
outbreaks probably lessened the significance of the influenza
pandemic for the public. In some areas, the flu was not reported on,
the only mention being that of advertisements for medicines claiming
to cure it.
Additionally, the outbreak coincided
with the deaths and media focus on the First World War. Another
explanation involves the age group affected by the disease. The
majority of fatalities, from both the war and the epidemic, were
among young adults. The high number of war-related deaths of young
adults may have overshadowed the deaths caused by flu.
When people read the obituaries, they
saw the war or postwar deaths and the deaths from the influenza side
by side. Particularly in Europe, where the war's toll was high, the
flu may not have had a tremendous psychological impact or may have
seemed an extension of the war's tragedies. The duration of the
pandemic and the war could have also played a role. The disease would
usually only affect a particular area for a month before
leaving.[citation needed] The war, however, had initially been
expected to end quickly but lasted for four years by the time the
pandemic struck.
In fiction and other literature
The Spanish flu has been represented in
numerous works of fiction:
Katherine Anne Porter's novella
Pale Horse, Pale Rider, published under the same title in a 1930
collection of three works
1918, a 1985 American drama film.
The Last Town on Earth, a 2006
novel.
Spanish Flu: The Forgotten Fallen,
a 2009 British television series.
Downton Abbey, a 2010 British
historical drama television series.
Vampyr, a 2018 video game.
Resident Evil Village, a 2021 video
game.
In addition, Mary McCarthy referred to
it in her memoir Memories of a Catholic Girlhood (1957), as she and
her three brothers were orphaned by their parents' deaths from the
flu.
Comparison with other pandemics
The Spanish flu killed a much lower
percentage of the world's population than the Black Death, which
lasted for many more years.
In the ongoing COVID-19 pandemic, as of
7 July 2021, more than 184 million cases have been identified and
more than 3.99 million deaths recorded worldwide.
Research
The origin of the Spanish flu pandemic,
and the relationship between the near-simultaneous outbreaks in
humans and swine, have been controversial. One hypothesis is that the
virus strain originated at Fort Riley, Kansas, in viruses in poultry
and swine which the fort bred for food; the soldiers were then sent
from Fort Riley around the world, where they spread the disease.
Similarities between a reconstruction of the virus and avian viruses,
combined with the human pandemic preceding the first reports of
influenza in swine, led researchers to conclude the influenza virus
jumped directly from birds to humans, and swine caught the disease
from humans.
Others have disagreed, and more recent
research has suggested the strain may have originated in a nonhuman,
mammalian species. An estimated date for its appearance in mammalian
hosts has been put at the period 1882–1913. This ancestor virus
diverged about 1913–1915 into two clades (or biological groups),
which gave rise to the classical swine and human H1N1 influenza
lineages. The last common ancestor of human strains dates between
February 1917 and April 1918. Because pigs are more readily infected
with avian influenza viruses than are humans, they were suggested as
the original recipients of the virus, passing the virus to humans
sometime between 1913 and 1918.
An effort to recreate the Spanish flu
strain (a subtype of avian strain H1N1) was a collaboration among the
Armed Forces Institute of Pathology, the USDA ARS Southeast Poultry
Research Laboratory, and Mount Sinai School of Medicine in New York
City. The effort resulted in the announcement (on 5 October 2005)
that the group had successfully determined the virus's genetic
sequence, using historic tissue samples recovered by pathologist
Johan Hultin from an Inuit female flu victim buried in the Alaskan
permafrost and samples preserved from American soldiers Roscoe
Vaughan and James Downs.
On 18 January 2007, Kobasa et al.
(2007) reported that monkeys (Macaca fascicularis) infected with the
recreated flu strain exhibited classic symptoms of the 1918 pandemic,
and died from cytokine storms – an overreaction of the immune
system. This may explain why the Spanish flu had its surprising
effect on younger, healthier people, as a person with a stronger
immune system would potentially have a stronger overreaction.
On 16 September 2008, the body of
British politician and diplomat Sir Mark Sykes was exhumed to study
the RNA of the flu virus in efforts to understand the genetic
structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a
lead coffin which scientists hoped had helped preserve the virus.
The coffin was found to be split and the cadaver badly decomposed;
nonetheless, samples of lung and brain tissue were taken.
In December 2008, research by Yoshihiro
Kawaoka of the University of Wisconsin linked the presence of three
specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived
from Spanish flu samples to the ability of the flu virus to invade
the lungs and cause pneumonia. The combination triggered similar
symptoms in animal testing.
In June 2010, a team at the Mount Sinai
School of Medicine reported the 2009 flu pandemic vaccine provided
some cross-protection against the Spanish flu pandemic strain.
One of the few things known for certain
about influenza in 1918 and for some years after was that it was,
except in the laboratory, exclusively a disease of human beings.
In 2013, the AIR Worldwide Research and
Modeling Group "characterized the historic 1918 pandemic and
estimated the effects of a similar pandemic occurring today using the
AIR Pandemic Flu Model". In the model, "a modern-day
'Spanish flu' event would result in additional life insurance losses
of between US$15.3–27.8 billion in the United States alone",
with 188,000–337,000 deaths in the United States.
In 2018, Michael Worobey, an
evolutionary biology professor at the University of Arizona who is
examining the history of the 1918 pandemic, revealed that he obtained
tissue slides created by William Rolland, a physician who reported on
a respiratory illness likely to be the virus while a pathologist in
the British military during World War One. Rolland had authored an
article in the Lancet during 1917 about a respiratory illness
outbreak beginning in 1916 in Étaples, France. Worobey traced recent
references to that article to family members who had retained slides
that Rolland had prepared during that time. Worobey extracted tissue
from the slides to potentially reveal more about the origin of the
pathogen.
Gender mortality gap
The high mortality rate of the
influenza pandemic is one aspect that sets the pandemic apart from
other disease outbreaks. Another factor is the higher mortality rate
of men compared with women. Men with an underlying condition were at
significantly more risk. Tuberculosis was one of the deadliest
diseases in the 1900s, and killed more men than women. But with the
spread of influenza disease, the cases of tuberculosis cases in men
decreased. Many scholars have noted that tuberculosis increased the
mortality rate of influenza in males, decreasing their life
expectancy. During the 1900s tuberculosis was more common in males
than females, but studies show that when influenza spread the
tuberculosis mortality rate among females changed. The death rate of
tuberculosis in females increased significantly and would continue to
decline until post-pandemic.
Death rates were particularly high in
those aged 20–35. The only comparable disease to this was the black
death, bubonic plague in the 1300s. As other studies have shown,
tuberculosis and influenza had comorbidities and one affected the
other. The ages of males dying of the flu show that tuberculosis was
a factor, and as males primarily had this disease at the time of the
pandemic, they had a higher mortality rate. Life expectancy dropped
in males during the pandemic but then increased two years after the
pandemic
Island of Newfoundland
One major cause of the spread of
influenza was social behavior. Men had more social variation and were
mobile more than women due to their work. Even though there was a
higher mortality rate in males, each region showed different results,
due to such factors as nutritional deficiency. In Newfoundland the
pandemic spread was highly variable. Influenza did not discriminate
who was infected, indeed it attacked the socioeconomic status of
people. Although social variability allowed the disease to move
quickly geographically, it tended to spread faster and affect men
more than women due to labor and social contact. Newfoundland's
leading cause of death before the pandemic was tuberculosis and this
is known to be a severe underlying condition for people and increases
the |mortality rate when infected by the influenza disease. There was
diverse labor in Newfoundland, men and women had various occupations
that involved day-to-day interaction. But, fishing had a major role
in the economy and so males were more mobile than females and had
more contact with other parts of the world. The spread of the
pandemic is known to have begun in the spring of 1918, but
Newfoundland didn't see the deadly wave until June or July, which
aligns with the high demand for employment in the fishery. The
majority of men were working along the coast during the summer and it
was typical for entire families to move to Newfoundland and work.
Studies show a much higher mortality rate in males compared with
females. But, during the first, second, and third waves of the
pandemic, the mortality shifted. During the first wave, men had a
higher mortality rate, but the mortality rate of females increased
and was higher during the second and third waves. The female
population was larger in certain regions of Newfoundland and
therefore had a bigger impact on the death rate.
Influenza pandemic among Canadian
soldiers
Records indicate the most deaths during
the first wave of the pandemic were among young men in their 20s,
which reflects the age of enlistment in the war. The mobility of
young men during 1918 was linked to the spread of influenza and the
biggest wave of the epidemic. In late 1917 and throughout 1918,
thousands of male troops gathered at the Halifax port before heading
to Europe. Any soldier that was ill and could not depart was added to
the population of Halifax, which increased the case rate of influenza
among men during the war. To determine the cause of the death during
the pandemic, war scientists used the Commonwealth War Graves
Commission (CWGC), which reported under 2 million men and women died
during the wars, with a record of those who died from 1917 to 1918.
The movement of soldiers during this time and the transportation from
United States between Canada likely had a significant effect on the
spread of the pandemic.
