1918–1920 flu pandemic

Etymologies

This pandemic was known by many different names depending on place, time, and context. The etymology of alternative names historicises the scourge and its effects on people who would only learn years later that viruses caused influenza. The lack of scientific answers led the Sierra Leone Weekly News (Freetown) to suggest a biblical framing in July 1918, using an interrogative from Exodus 16 in ancient Hebrew: "One thing is for certain—the doctors are at present flabbergasted; and we suggest that rather than calling the disease influenza they should for the present until they have it in hand, say Man hu—'What is it?'"

Descriptive names

Outbreaks of influenza-like illness were documented in 1916–17 at British military hospitals in Étaples, France, and just across the English Channel at Aldershot, England. Clinical indications in common with the 1918 pandemic included rapid symptom progression to a "dusky" heliotrope face. This characteristic blue-violet cyanosis in expiring patients led to the name 'purple death'.

The Aldershot physicians later wrote in The Lancet, "the influenza pneumococcal purulent bronchitis we and others described in 1916 and 1917 is fundamentally the same condition as the influenza of this present pandemic." This "purulent bronchitis" is not yet linked to the same A/H1N1 virus, but it may be a precursor.

In 1918, 'epidemic influenza', also known at the time as 'the grip' (French: la grippe, grasp), appeared in Kansas, U.S., during late spring, and early reports from Spain began appearing on 21 May. Reports from both places called it 'three-day fever'.

Associative names

Many alternative names are exonyms in the practice of making new infectious diseases seem foreign. This pattern was observed even before the 1889–1890 pandemic, also known as the 'Russian flu', when the Russians already called epidemic influenza the 'Chinese catarrh', the Germans called it the 'Russian pest', and the Italians called it the 'German disease'. These epithets were re-used in the 1918 pandemic, along with new ones.

Outside Spain, the disease was soon misnamed 'Spanish influenza'. In a 2 June 1918 The Times of London dispatch titled, "The Spanish Epidemic," a correspondent in Madrid reported over 100,000 victims of, "The unknown disease...clearly of a gripal character," without referring to "Spanish influenza" directly. Three weeks later The Times reported that, "Everybody thinks of it as the 'Spanish' influenza to-day." Three days after that an advertisement appeared in The Times for Formamint tablets to prevent "Spanish influenza". When it reached Moscow, Pravda announced, "Ispánka (the Spanish lady) is in town," making 'the Spanish lady' another common name.

The outbreak did not originate in Spain, but reporting did, due to wartime censorship in belligerent nations. Spain was a neutral country unconcerned with appearances of combat readiness, and without a wartime propaganda machine to prop up morale, so its newspapers freely reported epidemic effects, making Spain the apparent locus of the epidemic. The censorship was so effective that Spain's health officials were unaware its neighboring countries were similarly affected. In an October 1918 "Madrid Letter" to the Journal of the American Medical Association, a Spanish official protested, "we were surprised to learn that the disease was making ravages in other countries, and that people there were calling it the 'Spanish grip'. And wherefore Spanish? ...this epidemic was not born in Spain, and this should be recorded as a historic vindication."

French press initially used 'American flu', but adopted 'Spanish flu' in lieu of antagonizing an ally. In the spring of 1918, British soldiers called it 'Flanders flu', while German soldiers used 'Flandern-Fieber' (Flemish fever), both after a battlefield in Belgium where many soldiers on both sides fell ill. In Senegal it was named 'Brazilian flu', and in Brazil, 'German flu'. In Spain it was also known as the 'French flu' (gripe francesa), or the 'Naples Soldier' (Soldado de Nápoles), after a popular song from a zarzuela. Spanish flu (gripe española) is now a common name in Spain, but remains controversial there.

Local names

Some language endonyms did not name specific regions or groups of people. Examples specific to this pandemic include: Northern Ndebele: 'Malibuzwe' (let enquiries be made concerning it), Swahili: 'Ugonjo huo kichwa na kukohoa na kiuno' (the disease of head and coughing and spine), Yao: 'chipindupindu' (disease from seeking to make a profit in wartime), Otjiherero: 'kaapitohanga' (disease which passes through like a bullet), and Persian: nakhushi-yi bad (disease of the wind).

Other names

This outbreak was also commonly known as the 'great influenza epidemic', after the 'great war', a common name for World War I before World War II. French military doctors originally called it 'disease 11' (maladie onze). German doctors downplayed the severity by calling it 'pseudo influenza' (Greek: pseudo, false), while in Africa, doctors tried to get patients to take it more seriously by calling it 'influenza vera' (Latin: vera, true).

A children's song from the 1889–90 flu pandemic was shortened and adapted into a skipping-rope rhyme popular in 1918. It is a metaphor for the transmissibility of 'Influenza', where that name was clipped to 'Enza':

History

Potential origins

Despite its name, historical and epidemiological data cannot identify the geographic origin of the Spanish flu. However, several theories have been proposed.

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 origin in his 2004 article.

A 2018 study of tissue slides and medical reports led by 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.

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 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 Étaples 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. It also was home to a piggery, and poultry was regularly brought in 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.

Timeline

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 despite there having been cases before him. The disease had already been observed 200 miles (320 km) away in Haskell County as early as January 1918, prompting local doctor Loring Miner to warn the editors of the U.S. Public Health Service's journal Public Health Reports. Within days of the 4 March 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 U.S. 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 U.S. Army camps and Europe, becoming an epidemic in the Midwest, East Coast, and French ports by April 1918, and reaching the Western Front by mid-April. It then quickly spread to the rest of France, Great Britain, Italy, and Spain and in May reached Wrocław and Odessa. After the signing of the Treaty of Brest-Litovsk (March 1918), Germany started releasing Russian prisoners of war, who 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 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; 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.

The second wave began in the second half of August 1918, probably spreading to Boston, Massachusetts 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, about 30 miles (48 km) 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 soldiers. From Freetown, the pandemic spread through West Africa along the coast, rivers, and 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 from France. From there it spread around southern Africa and beyond the Zambezi, reaching Ethiopia in November. On 15 September, 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 an outbreak causing 12,000 deaths.

Epidemiology and pathology

Transmission and mutation

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 and the stresses of combat and chemical attacks, increasing their susceptibility. Modern transportation systems and increased travel was a significant factor in the worldwide occurrence. 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 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. (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 0.29% (0.02% in the first wave and 0.27% in the second wave) because of exposure to the less-lethal first wave.

After the lethal second wave, 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 lethality 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. Fatal cases did continue into 1919, however. One notable example was that of ice hockey player Joe Hall, who died of the flu in April after an outbreak that resulted in the cancellation of the 1919 Stanley Cup Final.

Signs and symptoms

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 color the entire face blue, followed by black coloration first in the extremities and then the limbs and the torso. 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 out, delirium, dizziness, insomnia, loss of hearing or smell, and impaired 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 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. 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 in animal trials it triggers an overreaction of the body's immune system (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.

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 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 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, causing a mismanaged response which did not ban mass gatherings.

Role of climate conditions

Studies have shown that the immune system of Spanish flu victims could have been weakened by unseasonably cold and wet weather for extended periods during the pandemic. This affected especially troops exposed to incessant rains and lower-than-average temperatures during World War I, and especially during the second wave of the pandemic. Climate data and 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 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 that lower temperatures and increased precipitation provided ideal conditions for virus replication and transmission, while also negatively affecting peoples' immune systems, 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). 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

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 developed, but as these were based on bacteria and not the actual virus, they could only help with secondary infections. The enforcement of 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 an assortment of medicines with varying degrees of effectiveness, such as aspirin, quinine, arsenics, digitalis, strychnine, epsom salts, castor oil, and iodine. Traditional treatments, 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

The Spanish flu infected around 500 million people, about one-third of the world's population. Estimates on deaths vary greatly, but it is 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, and possibly as high as 100 million. However, a 2018 reassessment in the American Journal of Epidemiology estimated the total to be about 17 million, though this has been contested. Estimates done in 2021 by John M. Barry have the total death toll alone at well above 100 million. 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 1918–1919 phase of the pandemic. 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 U.S., which the authors hypothesize is likely due to the severe effects of the war in Europe. The excess mortality rate in the U.K. 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 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%). 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, the flu killed nearly 500,000 people over two waves between 1918 and 1920, with nearly 300,000 excess deaths between October 1918 and May 1919 and 182,000 between December 1919 and May 1920.

Devastated communities

Even in areas where mortality was low, so many adults were incapacitated that daily 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, with some villages entirely disappearing. Nenana, Alaska, avoided the extent of the pandemic between 1918 and 1919, but the flu at last reached the town in spring 1920. Reports suggested that during the first two weeks of May, the majority of the town's population became infected; 10% of the population were estimated to have died, most of whom were Alaska Natives.

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 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, 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. 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 estimated at between 902,400 and 2,431,000, or 8% to 22% of the total population. 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. 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.

Other 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. However, the outbreak was delayed into 1926 for American Samoa and 1921 for New Caledonia as the quarantine period ended. On American Samoa, at least 25% of the island residents were clinically attacked and 0.1% died, and on New Caledonia, there was widespread illness and 0.1% population died. 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, reflecting 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 1918. At the very least, there is little evidence that China as a whole was seriously affected by the flu compared to other countries.

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 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 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. As a whole, data from China's port cities show 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 – 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. According to historian John M. Barry, the most vulnerable of all 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, 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.

More men than women were killed by the flu, as they were more likely to go out and be exposed, while women tended 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.

Effects

World War I

Academic Andrew Price-Smith has argued 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 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 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 nursing. This was due in part to the failure of medical doctors, who were predominantly men, to contain 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 U.S. cities that implemented early and extensive non-medical measures (quarantine, etc.) suffered no additional adverse economic effects due to implementing those measures. However, the validity of this study has been questioned because of the coincidence of WWI and other problems with data reliability.

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 conditions resulting from infection.

Legacy

The Spanish flu began to fade from public awareness over the decades until the bird flu and other pandemics in the 1990s and 2000s. This has led some historians to label the Spanish flu a "forgotten pandemic". However, this label has been challenged by the historian Guy Beiner, who demonstrated how the pandemic was overshadowed by the commemoration of the First World War and mostly neglected in mainstream historiography, yet was remembered in private and local traditions across the globe.

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. 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. 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 last known person to have survived the Spanish flu, José Ameal Peña, was alive as of 2020.

In literature and other media

Despite the toll of the pandemic, it was never a large theme in American literature. Alfred Crosby suspects it was overshadowed by World War I. Katherine Anne Porter's 1939 novella Pale Horse, Pale Rider is one of the most well-known fictional accounts of the pandemic. The 2006 novel The Last Town on Earth focuses on a town which attempts to limit the spread of the flu by preventing people from entering or leaving. The Pull of the Stars is a 2020 novel by Emma Donoghue set in Dublin during the Spanish flu. Publishers fast-tracked publication because of the then ongoing COVID-19 pandemic.

Research

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. More recent research has suggested the strain may have originated in a nonhuman, mammalian species, in 1882–1913. This ancestor virus diverged about 1913–1915 into 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 strain of influenza A subtype 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 in 2005 that the group had successfully determined the virus' 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. This enabled researchers at the Centers for Disease Control and Prevention (CDC) and the Mount Sinai School of Medicine, led by Dr Terrence Tumpey, to synthesize RNA segments from the H1N1 virus and reconstruct infective virus particles. These were subsequently used to experimentally infect mice, ferrets, and macaques, providing information about how to prevent and control future pandemics.

In 2007, Kobasa et al. reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from 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.

In December 2008, research by Yoshihiro Kawaoka of the University of Wisconsin linked three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from Spanish flu samples to the ability of the 1918 flu virus to invade the lungs and cause pneumonia. These genes were inserted into a modern H1N1 strain and triggered similar symptoms in animal testing.