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Spanish flu
Spanish flu
from Wikipedia

Spanish flu
Soldiers from Fort Riley, Kansas, ill with Spanish flu at a hospital ward at Camp Funston
Soldiers sick with Spanish flu at a hospital ward at Camp Funston in Fort Riley, Kansas
DiseaseInfluenza
Virus strainStrains of A/H1N1
LocationWorldwide
Index caseHaskell County, Kansas
January 1918[a]
DateFebruary 1918 – April 1920[2]
Suspected cases500 million (estimated)[3]
Deaths
25–50 million (generally accepted), other estimates range from 17 to 100 million[4][5][6]
Suspected cases have not been confirmed by laboratory tests as being due to this strain, although some other strains may have been ruled out.

The 1918–1920 flu pandemic, also known as the Great Influenza epidemic or by the common misnomer Spanish flu, was an exceptionally deadly global influenza pandemic caused by the H1N1 subtype of the influenza A virus. The earliest documented case was March 1918 in Haskell County, Kansas, United States, with further cases recorded in France, Germany and the United Kingdom in April. Two years later, nearly a third of the global population, or an estimated 500 million people, had been infected. Estimates of deaths range from 17 million to 50 million,[7][8] and possibly as high as 100 million,[9] making it the deadliest pandemic in history.

The pandemic broke out near the end of World War I, when wartime censors in the belligerent countries suppressed bad news to maintain morale, but newspapers freely reported the outbreak in neutral Spain, creating a false impression of Spain as the epicenter and leading to the "Spanish flu" misnomer.[10] Limited historical epidemiological data make the pandemic's geographic origin indeterminate, with competing hypotheses on the initial spread.[3]

Most influenza outbreaks disproportionately kill the young and old, but this pandemic had unusually high mortality for young adults.[11] Scientists offer several explanations for the high mortality, including a six-year climate anomaly affecting migration of disease vectors with increased likelihood of spread through bodies of water.[12] However, the claim that young adults had a high mortality during the pandemic has been contested.[13] Malnourishment, overcrowded medical camps and hospitals, and poor hygiene, exacerbated by the war, promoted bacterial superinfection, killing most of the victims after a typically prolonged death bed.[14][15]

Etymologies

[edit]
El Sol (Madrid), 28 May 1918: "The three-day fever – In Madrid 80,000 Are Infected – H.M. the King is sick"

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.[16] 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:[b] "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?'"[18][19][20]

Descriptive names

[edit]

Outbreaks of influenza-like illness were documented in 1916–17 at British military hospitals in Étaples, France,[21] 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'.[22][23][24]

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."[25] This "purulent bronchitis" is not yet linked to the same A/H1N1 virus,[26] but it may be a precursor.[25][27][28]

In 1918, 'epidemic influenza',[29] also known at the time as 'the grip' (French: la grippe, grasp),[30] appeared in Kansas, U.S., during late spring, and early reports from Spain began appearing on 21 May.[31][32] Reports from both places called it 'three-day fever'.[33][34][35]

Associative names

[edit]

Many alternative names are exonyms in the practice of making new infectious diseases seem foreign.[36][37][38] 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'.[39][40] These epithets were re-used in the 1918 pandemic, along with new ones.[41]

'Spanish' influenza

[edit]
Advertisement in The Times, 28 June 1918 for Formamint tablets to prevent "Spanish influenza"

Outside Spain, the disease was soon misnamed 'Spanish influenza'.[42][43] 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.[44] Three weeks later The Times reported that, "Everybody thinks of it as the 'Spanish' influenza to-day."[45] Three days after that an advertisement appeared in The Times for Formamint tablets to prevent "Spanish influenza".[46][47] When it reached Moscow, Pravda announced, "Ispánka (the Spanish lady) is in town," making 'the Spanish lady' another common name.[48]

The outbreak did not originate in Spain,[49] 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,[50][51] so its newspapers freely reported epidemic effects, making Spain the apparent locus of the epidemic.[52] The censorship was so effective that Spain's health officials were unaware its neighboring countries were similarly affected.[53] 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."[54]

Front page of The Times (London), 25 June 1918: "The Spanish Influenza"

Other exonyms

[edit]

French press initially used 'American flu', but adopted 'Spanish flu' in lieu of antagonizing an ally.[55] 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.[41][38][56][57] In Senegal it was named 'Brazilian flu', and in Brazil, 'German flu'.[58] In Spain it was also known as the 'French flu' (gripe francesa),[49][10] or the 'Naples Soldier' (Soldado de Nápoles), after a popular song from a zarzuela.[c][55] Spanish flu (gripe española) is now a common name in Spain,[60] but remains controversial there.[61][62]

Othering derived from geopolitical borders and social boundaries.[63][64] In Poland it was the 'Bolshevik disease',[58][65] while in Russia it was referred to it as the 'Kirghiz disease'.[57] Some Africans called it a 'white man's sickness', but in South Africa, white men also used the ethnophaulism 'kaffersiekte' (lit.'negro disease').[41][66] Japan blamed sumo wrestlers for bringing the disease home from Taiwan, calling it 'sumo flu' (Sumo Kaze).[67][68]

World Health Organization 'best practices' first published in 2015 now aim to prevent social stigma by not associating culturally significant names with new diseases, listing "Spanish flu" under "examples to be avoided".[69][37][70] Many authors now eschew calling this the Spanish flu,[55] instead using variations of '1918–19/20 flu/influenza pandemic'.[71][72][73]

Local names

[edit]

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),[74] Yao: 'chipindupindu' (disease from seeking to make a profit in wartime), Otjiherero: 'kaapitohanga' (disease which passes through like a bullet),[75] and Persian: nakhushi-yi bad (disease of the wind).[76][77]

Other names

[edit]

This outbreak was also commonly known as the 'great influenza epidemic',[78][79] after the 'great war', a common name for World War I before World War II.[80] French military doctors originally called it 'disease 11' (maladie onze).[38] 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).[81]

A children's song from the 1889–90 flu pandemic[82] was shortened and adapted into a skipping-rope rhyme popular in 1918.[83][84] It is a metaphor for the transmissibility of 'Influenza', where that name was clipped to 'Enza':[85][86][87]

I had a little bird,
its name was Enza.
I opened the window,
and in-flu-enza.

History

[edit]

Potential origins

[edit]

Despite its name, historical and epidemiological data cannot identify the geographic origin of the Spanish flu.[3] However, several theories have been proposed.

United States

[edit]

The first confirmed cases originated in the United States. Historian Alfred W. Crosby stated in 2003 that the flu originated in Kansas,[88] and author John M. Barry described a January 1918 outbreak in Haskell County, Kansas, as the origin in his 2004 article.[80]

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.[89]

Europe

[edit]
Edvard Munch (1863–1944), Self-Portrait with the Spanish Flu (1919)

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.[1] 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.[90][1] According to Oxford, a similar outbreak occurred in March 1917 at army barracks in Aldershot,[91] and military pathologists later recognized these early outbreaks as the same disease as the Spanish flu.[92][1]

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.[91][92] 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.[93] Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza began in Austria in early 1917.[94]

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.[95]

China

[edit]

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, and the rest of the world, with Allied forces as the main disseminators.[96] Hannoun considered several alternative hypotheses of origin, such as Spain, Kansas, and Brest, as being possible, but not likely.[96]

In 2014, historian Mark Humphries of the Memorial University of Newfoundland 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 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.[97][98] No tissue samples have survived for modern comparison.[99] Nevertheless, there were some reports of respiratory illness on the path the laborers took to get to Europe, which also passed through North America.[99]

China was one of the few regions of the world seemingly less affected by the Spanish flu pandemic, where several studies have documented a comparatively mild flu season in 1918.[100][101][102] (This is disputed due to lack of data during the Warlord Period.) This has led to speculation that the Spanish flu pandemic originated in China,[102][103] as the lower mortality rates may be explained by the Chinese population's previously acquired immunity to the flu virus.[104][102] In the Guangdong Province it was reported that early outbreaks of influenza in 1918 disproportionately impacted young men. The June outbreak infected children and adolescents between 11 and 20 years of age, while the October outbreak was most common in those aged 11 to 15.[102]

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.[93] The 2016 study found that the low flu mortality rate (an estimated one in a thousand) recorded among the Chinese and Southeast Asian workers in Europe suggests that the Asian units were not different from other Allied military units in France at the end of 1918 and, thus not a likely source of a new lethal virus.[93] 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.[89]

Timeline

[edit]

First wave of early 1918

[edit]
Seattle policemen wearing cloth face masks handed out by the American Red Cross during the Spanish flu pandemic, December 1918
An article naming wealthy socialites for violating city law banning public gatherings, Chicago Tribune, October 19, 1918. Named violators include Joan Pinkerton Chalmers, daughter of Pinkertons private police founder Allan Pinkerton.[105]

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.[106] 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.[80] Within days of the 4 March case at Camp Funston, 522 men at the camp had reported sick.[107] By 11 March 1918, the virus had reached Queens, New York.[108] Failure to take preventive measures in March/April was later criticized.[109]

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.[106] It then quickly spread to the rest of France, Great Britain, Italy, and Spain and in May reached Wrocław and Odessa.[106] 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.[110] 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.[111] In June an outbreak was reported in China.[112] After reaching Australia in July, the wave started to recede.[111]

The first wave lasted from the first quarter of 1918 and was relatively mild.[113] 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.[3][114] In Madrid, Spain, fewer than 1,000 people died from influenza between May and June 1918.[115] 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.[116]

Deadly second wave of late 1918

[edit]
American Expeditionary Force flu patients at U.S. Army Camp Hospital no. 45 in Aix-les-Bains, France, 1918
Spanish satirical cartoon published in November 1918 depicting a "tragic game of football" between Mars, Greek god of war, and the Spanish Flu. There is a short poem as a caption which roughly translates to English as "Between flu and war, look at how they've left her, our poor Earth"
Mars, god of war, plays a "tragic game of football" with a skeleton personification of the Spanish flu, November 1918

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.[116] 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.[117] 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.[118] In July 1918, the Ottoman Empire saw its first cases, in soldiers.[119] 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.[118] From there it spread around southern Africa and beyond the Zambezi, reaching Ethiopia in November.[120] On 15 September, New York City saw its first fatality from influenza.[121] 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.[122]

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 Mashhad), and then India in September and China and Japan in October.[123] The celebrations of the Armistice of 11 November 1918 also caused outbreaks in Lima and Nairobi, but by December the wave was mostly over.[124]

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.[125] In the United States, ~292,000 deaths were reported between September–December 1918, compared to ~26,000 during the same time period in 1915.[114] The Netherlands reported over 40,000 deaths from influenza and acute respiratory disease. Bombay reported ~15,000 deaths in a population of 1.1 million.[126] The 1918 flu pandemic in India was especially deadly, as Historian David Arnold estimates at least 12 million dead, about 5% of the population.[127]

Third wave of 1919

[edit]
London weekly deaths from influenza during 1918 and 1919

Pandemic activity persisted into 1919 in many places, possibly attributable to climate, specifically in the Northern Hemisphere, where it was winter and thus the usual time for influenza activity.[128][129] The pandemic nonetheless continued into 1919 largely independent of region and climate.[128]

Cases began to rise again in some parts of the U.S. as early as late November 1918,[130] with the Public Health Service issuing its first report of a "recrudescence of the disease" in "widely scattered localities" in early December.[131] This resurgent activity varied across the country, however, possibly on account of differing restrictions.[129] Michigan, for example, experienced a swift resurgence of influenza that reached its peak in December, possibly as a result of the lifting of the ban on public gatherings.[132] Pandemic interventions, such as bans on public gatherings and the closing of schools, were reimposed in many places in an attempt to suppress the spread.[131]

There was "a very sudden and very marked rise in general death rate" in most cities in January 1919; nearly all experienced "some degree of recrudescence" of the flu in January and February.[133]: 153–154  Significant outbreaks occurred in cities including Los Angeles,[134] New York City,[2] Memphis, Nashville, San Francisco,[135] and St. Louis.[136] By 21 February, with some local variation, influenza activity was reported to have been declining since mid-January in all parts of the country.[137] Following this "first great epidemic period" that had commenced in October 1918, deaths from pneumonia and influenza were "somewhat below average" in large U.S. cities between May 1919 and January 1920.[133]: 158  Nonetheless, nearly 160,000 deaths were attributed to these causes in the first six months of 1919.[138]

It was not until later in the winter and into the spring that a clearer resurgence appeared in Europe. A significant third wave had developed in England and Wales by mid-February, peaking in early March, though it did not fully subside until May.[139] France also experienced a significant wave that peaked in February, alongside the Netherlands. Norway, Finland, and Switzerland saw recrudescences of pandemic activity in March, and Sweden in April.[95]

Much of Spain was affected by "a substantial recrudescent wave" of influenza between January and April 1919.[140] Portugal experienced a resurgence in pandemic activity that lasted from March to September 1919, with the greatest impact being felt on the west coast and in the north of the country; all districts were affected between April and May specifically.[141]

Influenza entered Australia for the first time in January 1919 after a strict maritime quarantine had shielded the country through 1918.[142] It assumed epidemic proportions first in Melbourne, peaking in mid-February.[143] The flu soon appeared in neighboring New South Wales and South Australia.[142] New South Wales experienced its first wave of infection between mid-March and late May,[144] while a second, more severe wave occurred in Victoria between April and June.[143] Land quarantine measures hindered the spread of the disease. Queensland was not infected until late April; Western Australia avoided the disease until early June, and Tasmania remained free from it until mid-August.[142] Out of the six states, Victoria and New South Wales experienced generally more extensive epidemics. Each experienced another significant wave of illness over the winter. The second epidemic in New South Wales was more severe than the first,[144] while Victoria saw a third wave that was somewhat less extensive than its second, more akin to its first.[143]

The disease also reached other parts of the world for the first time in 1919, such as Madagascar, which saw its first cases in April; the outbreak had spread to practically all sections of the island by June.[145] In other parts, influenza recurred in the form of a true "third wave". Hong Kong experienced another outbreak in June,[146] as did South Africa during its fall and winter months in the Southern Hemisphere.[147][148][149] New Zealand experienced some cases in May.[150]

Parts of South America experienced a resurgence of pandemic activity throughout 1919. A third wave hit Brazil between January and June.[128] Between July 1919 and February 1920, Chile, which had been affected for the first time in October 1918, experienced a severe second wave, with mortality peaking in August 1919.[151] Montevideo similarly experienced a second outbreak between July and September.[152]

The third wave particularly affected Spain, Serbia, Mexico and Great Britain, resulting in hundreds of thousands of deaths.[153]

Fourth wave of 1920

[edit]
Public health recommendations from the Illustrated Current News

In the Northern Hemisphere, fears of a "recurrence" of the flu grew as fall approached. Experts cited past flu epidemics, such as that of 1889–1890, to predict that such a recurrence a year later was not unlikely,[154][155] though not all agreed.[156] In September 1919, U.S. Surgeon General Rupert Blue said a return of the flu later in the year would "probably, but by no means certainly," occur.[157] France had readied a public information campaign before the end of the summer,[158] and Britain began preparations in the autumn with the manufacture of vaccine.[159]

In Japan, the flu broke out again in December and spread rapidly throughout the country, a fact attributed at the time to cold weather.[160][161] Pandemic-related measures were renewed to check the outbreak, and health authorities recommended the use of masks.[161] The epidemic intensified in the latter part of December before swiftly peaking in January.[162]

Between October 1919 and 23 January 1920, 780,000 cases were reported across the country, with at least 20,000 deaths recorded by that date. This apparently reflected "a condition of severity three times greater than for the corresponding period of" 1918–1919.[162] Nonetheless, the disease was regarded as being milder than it had been the year before, albeit more infectious.[163] Despite its rapid peak at the beginning of the year, the outbreak persisted throughout the winter, before subsiding in the spring.[164]

In the United States, there were "almost continuously isolated or solitary cases" of flu throughout the spring and summer of 1919.[165] An increase in scattered cases became apparent as early as September,[166] but Chicago experienced one of the first major outbreaks of the flu beginning in the middle of January.[167] The Public Health Service announced it would take steps to "localize the epidemic",[168] but the disease was already causing a simultaneous outbreak in Kansas City and quickly spread outward from the center of the country.[165] A few days after its first announcement, PHS issued another assuring that the disease was under the control of state health authorities and that an outbreak of epidemic proportions was not expected.[169]

It became apparent within days of the start of Chicago's explosive growth in cases that the flu was spreading in the city at an even faster rate than in winter 1919, though fewer were dying.[170] Within a week, new cases in the city had surpassed its peak during the 1919 wave.[171] Around the same time, New York City began to see its own sudden increase in cases,[172] and other cities around the country were soon to follow.[173] Certain pandemic restrictions, such as the closing of schools and theaters and the staggering of business hours to avoid congestion, were reimposed in cities like Chicago,[174] Memphis,[175] and New York City.[176] As they had during the epidemic in fall 1918, schools in New York City remained open,[176] while those in Memphis were shuttered as part of restrictions on public gatherings.[175]

American Red Cross nurses tend to flu patients in temporary wards set up inside the Oakland Municipal Auditorium

The fourth wave in the United States subsided as swiftly as it had appeared, reaching a peak in early February.[177] "An epidemic of considerable proportions marked the early months of 1920", the U.S. Mortality Statistics would later note; according to data at this time, the epidemic resulted in one third as many deaths as the 1918–1919 experience.[178] 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.[2] Detroit, Milwaukee, Kansas City, Minneapolis, and St. Louis were hit particularly hard, with death rates higher than all of 1918.[136] Hawaii experienced its peak of the pandemic in early 1920, recording 1,489 deaths from flu-related causes, compared with 615 in 1918 and 796 in 1919.[179]

Poland experienced a devastating outbreak during the winter months, with its capital Warsaw reaching a peak of 158 deaths in a single week, compared to the peak of 92 in December 1918; however, the 1920 epidemic passed in a matter of weeks, while the 1918–1919 wave had developed over the entire second half of 1918.[180] By contrast, the outbreak in western Europe was considered "benign", with the age distribution of deaths beginning to take on that of seasonal flu.[115] Spain, Denmark, Finland, Germany and Switzerland recorded a late peak between January–April 1920.[95]

Mexico experienced a fourth wave between February and March. In South America, Peru experienced "asynchronous recrudescent waves" throughout the year. A severe third wave hit Lima, the capital city, between January and March, resulting in an all-cause excess mortality rate approximately four times greater than that of the 1918–1919 wave. Ica similarly experienced another severe pandemic wave in 1920, between July and October.[181] A fourth wave also occurred in Brazil, in February.[128]

Korea and Taiwan experienced pronounced outbreaks in late 1919 and early 1920.[182][183]

Post-pandemic

[edit]

By mid-1920, the pandemic was largely considered to be "over" by the public as well as governments.[184] Though parts of Chile experienced a third, milder wave between November 1920 and March 1921,[151] the flu seemed to be mostly absent through the winter of 1920–1921.[133]: 167  In the United States, for example, deaths from pneumonia and influenza were "very much lower than for many years".[133]: 167 

Seasonal influenza began to be reported again from many places in 1921.[133]: 168  Influenza continued to be felt in Chile, where a post-pandemic fourth wave affected 7 of its 24 provinces between June and December 1921.[151] The winter of 1921–1922 was the first major reappearance of seasonal influenza in the Northern Hemisphere, in many parts its most significant occurrence since the main pandemic in late 1918. Northwestern Europe was particularly affected. All-cause mortality in the Netherlands approximately doubled in January 1922 alone.[133]: 168  In Helsinki, a major epidemic (the fifth since 1918) prevailed between November and December 1921.[185] The flu was also widespread in the United States, its prevalence in California reportedly greater in early March 1922 than at any point since the pandemic ended in 1920.[133]: 172 

In the years after 1920, the disease came to represent the "seasonal flu". The virus, H1N1, remained endemic, occasionally causing more severe or otherwise notable outbreaks.[186] The period since its initial appearance in 1918 has been termed a "pandemic era", in which all flu pandemics have been caused by its own descendants.[187] Following the first of these post-1918 pandemics, in 1957, the virus was totally displaced by the novel H2N2, the reassortant product of the human H1N1 and an avian influenza virus, which thereafter became the active influenza A virus in humans.[186]

In 1977, an influenza virus bearing a very close resemblance to the seasonal H1N1, which had not been seen since the 1950s, appeared in Russia and subsequently initiated a "technical" pandemic that principally affected those 26 and under.[188][189] While some natural explanations, such as the virus remaining in some frozen state for 20 years,[189] have been proposed to explain this unprecedented[190] phenomenon, the nature of influenza itself has been cited in favor of human involvement of some kind, such as an accidental leak from a lab where the old virus had been preserved for research purposes.[189] Following this miniature pandemic, the reemerged H1N1 became endemic again but did not displace the other active influenza A virus, H3N2 (which itself had displaced H2N2 through a pandemic in 1968).[188][186] For the first time, two influenza A viruses were observed in cocirculation.[104] This state has persisted even after 2009, when a novel H1N1 virus emerged, sparked a pandemic, and thereafter took the place of the seasonal H1N1 to circulate alongside H3N2.[104]

Epidemiology and pathology

[edit]

Transmission and mutation

[edit]
U.S. Army flu patients at Field Hospital No. 29 near Hollerich, Luxembourg 1918. 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.[191] 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.[192][193] Modern transportation systems and increased travel was a significant factor in the worldwide occurrence.[194] Another was lies and denial by governments, leaving the population ill-prepared to handle the outbreaks.[195]

The severity of the second wave has been attributed to the First World War.[196] 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.[197]) 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.[198]

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.[80] 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.[80] 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 Finals.[199]

Signs and symptoms

[edit]
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.[200] However, during the second wave, the disease was much more serious, often complicated by bacterial pneumonia, which was often the cause of death.[200] 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.[200] Death would follow within hours or days due to the lungs being filled with fluids.[200] 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.[200] 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".[201]

The majority of deaths were from bacterial pneumonia,[202][203][204] 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.[205] The virus also killed people directly by causing massive hemorrhages and edema in the lungs.[204] 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).[80] 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.[206]

Misdiagnosis

[edit]

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.[207] 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.[207] For this reason, a vaccine that was used against that bacillus did not make infection rarer but did decrease the death rate.[208]

During the deadly second wave there were also fears that it was in fact plague, dengue fever, or cholera.[209] 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.[209] 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.[209]

Role of climate conditions

[edit]
Poster with the slogan "Coughs and sneezes spread diseases"

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.[12] 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).[210][211][212][213][214] 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.[215][216][217] 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.[218][219][220]

Responses

[edit]

Public health management

[edit]
Coromandel Hospital Board (New Zealand) advice to influenza sufferers (1918)
In September 1918, the Red Cross recommended two-layer gauze masks to halt the spread of "plague".[221]
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.[222] After October's strict containment measures showed some success, Armistice Day celebrations in November and relaxed attitudes by Thanksgiving caused a resurgence.[222]

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.[223] Nevertheless, actions were taken. Maritime quarantines were declared on islands such as Iceland, Australia, and American Samoa, saving many lives.[223] Social distancing measures were introduced, for example closing schools, theatres, and places of worship, limiting public transportation, and banning mass gatherings.[224] Wearing face masks became common in some places, such as Japan, though there were debates over their efficacy.[224][225] 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.[224] The enforcement of restrictions varied.[226] 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.[227] 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.[228]

Medical treatment

[edit]

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.[229] Traditional treatments, such as bloodletting, ayurveda, and kampo, were also applied.[230]

Information dissemination

[edit]

Due to World War I, many countries engaged in wartime censorship, and suppressed reporting of the pandemic.[231] For example, the Italian newspaper Corriere della Sera was prohibited from reporting daily death tolls.[232] The newspapers of the time were also generally paternalistic and worried about mass panic.[232] 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".[233] 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.[234]

Mortality

[edit]
Difference between the flu mortality age-distributions of the 1918 pandemic and normal epidemics – deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911–1917 (dashed line) and the pandemic year 1918 (solid line)[235]
Three pandemic waves: weekly combined flu and pneumonia mortality, United Kingdom, 1918–1919[236]

The Spanish flu infected around 500 million people, about one-third of the world's population.[3] Estimates on deaths vary greatly, but it is considered to be one of the deadliest pandemics in history.[237][238] An early estimate from 1927 put global mortality at 21.6 million.[5] An estimate from 1991 states that the virus killed between 25 and 39 million people.[113] A 2005 estimate put the death toll at 50 million, and possibly as high as 100 million.[201][239] However, a 2018 reassessment in the American Journal of Epidemiology estimated the total to be about 17 million,[5] though this has been contested.[240] Estimates done in 2021 by John M. Barry have the total death toll alone at well above 100 million.[9] With a world population of 1.8 to 1.9 billion,[241] 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.[95] The excess mortality rate in the U.K. has been estimated at 0.28%–0.4%, far below this European average.[5]

Some 12–17 million people died in India, about 5% of the population.[242] The death toll in India's British-ruled districts was 13.88 million.[243] Another estimate gives at least 12 million dead.[244] The decade between 1911 and 1921 was the only census period in which India's population fell, mostly due to devastation of the pandemic.[245][246] 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%).[5] 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."[247]

In Finland, 20,000 died out of 210,000 infected.[248] In Sweden, 34,000 died.[249]

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.[164]

In the Dutch East Indies (now Indonesia), 1.5 million were assumed to have died among 30 million inhabitants.[250] In Tahiti, 13% of the population died in one month. Similarly, in Western Samoa 22% of the population of 38,000 died within two months.[251]

In Istanbul, capital of the Ottoman Empire, 6,403[252] to 10,000[119] died, giving the city a mortality rate of at least 0.56%.[252]

In New Zealand, the flu killed an estimated 6,400 Pākehā (or "New Zealanders primarily of European descent") and 2,500 Māori in six weeks, with Māori dying at eight times the rate of Pākehā.[253][254]

In Australia, the flu killed around 12,000[255] to 20,000 people.[256] The country's death rate, 2.7 per 1,000 people, was one of the lowest recorded; however, as much as 40 percent of the population were infected, and a mortality rate of 50 percent was recorded by some Aboriginal communities.[257][256] New South Wales and Victoria saw the greatest relative mortality, with 3.19 and 2.40 deaths per 1,000 people respectively, while Western Australia, Queensland, Southern Australia, and Tasmania experienced rates of 1.70, 1.14, 1.13, and 1.09 per 1,000 respectively. In Queensland, at least one-third of deaths recorded were in the Aboriginal population.[143]

In the U.S., about 20 million out of a population of 105 million became infected in the 1918–1919 season, and an estimated 500,000 to 850,000 died (0.5 to 0.8 percent of the U.S. population).[258][259][260] Native Americans tribes were particularly affected. In the Four Corners area, there were 3,293 registered deaths among Native Americans.[261] Entire Inuit and Alaskan Native village communities died in Alaska.[262] In Canada, 50,000 died.[263]

In Brazil, 300,000 died, including president Rodrigues Alves.[264]

In the UK, as many as 250,000 died; in France, more than 400,000.[265]

In Ghana, the influenza epidemic killed at least 100,000 people.[266] Tafari Makonnen (the future Emperor of Ethiopia) was one of the first Ethiopians who contracted influenza but survived.[267][268] Estimates for fatalities in the capital city, Addis Ababa, range from 5,000 to 10,000, or higher.[269]

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".[113] 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.[270]

Devastated communities

[edit]
Deaths from all causes for New York, London, Paris, and Berlin with peaks in October and November 1918

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.[271]

Bristol Bay, a region of Alaska populated by Indigenous people, suffered a death rate of 40 percent, with some villages entirely disappearing.[272] 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.[273]

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).[274] 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.[274] 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.[275]

In Iran, the mortality was estimated at between 902,400 and 2,431,000, or 8% to 22% of the total population.[276] 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.[277][278]

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.[279] Almost a quarter of the working population of Kimberley, consisting of workers in the diamond mines, died.[280] In British Somaliland, one official estimated that 7% of the native population died.[281] This huge death toll resulted from an extremely high infection rate of up to 50% and the extreme severity of the symptoms.[113]

Other areas

[edit]

In the Pacific, American Samoa[282] and the French colony of New Caledonia[283] 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.[284] 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.[284] Australia also managed to avoid the first two waves with a quarantine.[223] Iceland protected a third of its population from exposure by blocking the main road of the island.[223] By the end of the pandemic, the isolated island of Marajó, in Brazil's Amazon River Delta had not reported an outbreak.[285] Saint Helena also reported no deaths.[286]

Japanese women in Tokyo during the Spanish flu pandemic, 1920

Estimates for the death toll in China have varied widely,[287][113] 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.[102][104][288] However, some reports from its interior suggest that mortality rates from influenza were perhaps higher in at least a few locations in 1918.[270] At the very least, there is little evidence that China as a whole was seriously affected by the flu compared to other countries.[289]

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.[100][290] 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.[291] 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.[287] 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.[270]

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.[292] As a whole, data from China's port cities show low mortality rates compared to other cities in Asia.[292] 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.[292] 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.[292] 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%).[292] 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.[292]

However, the influenza mortality rate in Hong Kong and Canton are under-recorded, because only the deaths that occurred in colony hospitals were counted.[292] Similarly, in Shanghai, these statistics are limited to that area of the city under the control of the health section of the Shanghai International Settlement; the actual death toll in Shanghai was much higher.[292] The medical records from China's interior indicate that, compared to cities, rural communities have substantially higher mortality rate.[293] A published influenza survey in Houlu County, Hebei Province, found that the case fatality rate was 9.77% and 0.79% of county population died from influenza in October and November 1918.[294]

Patterns of fatality

[edit]
A nurse wears a cloth face mask while treating a flu patient in Washington, DC, c. 1919

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.[295] 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.[296] 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%.[297] Of the pregnant women who survived childbirth, over one-quarter (26%) lost the child.[298] Another oddity was that the outbreak was widespread in the summer and autumn (in the Northern Hemisphere); influenza is usually worse in winter.[299]

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.[300] 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.[300] Cities were affected worse than rural areas.[300] 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.[301]

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.[302] 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.[300] These disparities reflected worse diets, crowded living conditions, and problems accessing healthcare.[300] Paradoxically, however, African Americans were relatively spared.[300]

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.[301] For the same reason men also were more likely to have pre-existing tuberculosis, which severely worsened the chances of recovery.[301] However, in India the opposite was true, potentially because Indian women were neglected with poorer nutrition, and were expected to care for the sick.[301]

A study conducted by He et al. (2011) 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.[303] 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.[304]

Effects

[edit]

World War I

[edit]

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.[94] 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%).[247]

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.[305]

Economic

[edit]
Provincial Board of Health poster from Alberta, Canada

Many businesses in the entertainment and service industries suffered losses in revenue, while the healthcare industry reported profit gains.[306] 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.[307]

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.[308][309] However, the validity of this study has been questioned because of the coincidence of WWI and other problems with data reliability.[310]

Long-term effects

[edit]

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."[311] A 2018 study found that the pandemic reduced educational attainment in populations.[312] The flu has also been linked to the outbreak of encephalitis lethargica in the 1920s.[313]

Survivors faced an elevated mortality risk. Some survivors did not fully recover from physiological conditions resulting from infection.[314]

Legacy

[edit]
Mass burial site of flu victims from 1918 in Auckland, New Zealand

The Spanish flu began to fade from public awareness over the decades until the bird flu and other pandemics in the 1990s and 2000s.[315][316] This has led some historians to label the Spanish flu a "forgotten pandemic".[88] 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.[316]

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.[317] In some areas, the flu was not reported on, the only mention being that of advertisements for medicines claiming to cure it.[318]

Additionally, the outbreak coincided with the deaths and media focus on the First World War.[319] 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.[295] 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.[295]

In literature and other media

[edit]
US comic published in 1922

Despite the toll of the pandemic, it was never a large theme in American literature.[320] Alfred Crosby suspects it was overshadowed by World War I.[321] Katherine Anne Porter's 1939 novella Pale Horse, Pale Rider is one of the most well-known fictional accounts of the pandemic.[320] 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.[322] 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.[323]

Comparison with other pandemics

[edit]

Major modern influenza pandemics[324][325]
Name Date World pop. Subtype Reproduction number[326] Infected (est.) Deaths worldwide Case fatality rate Pandemic severity
Spanish flu[327] 1918–20 1.80 billion H1N1 1.80 (IQR, 1.47–2.27) 33% (500 million)[328] or >56% (>1 billion)[329] 17[330]–100[331][332] million 2–3%,[329] or ~4%, or ~10%[333] 5
Asian flu 1957–58 2.90 billion H2N2 1.65 (IQR, 1.53–1.70) >17% (>500 million)[329] 1–4 million[329] <0.2%[329] 2
Hong Kong flu 1968–69 3.53 billion H3N2 1.80 (IQR, 1.56–1.85) >14% (>500 million)[329] 1–4 million[329] <0.2%[329][334] 2
1977 Russian flu 1977–79 4.21 billion H1N1 ? ? 0.7 million[335] ? ?
2009 swine flu pandemic[336][337] 2009–10 6.85 billion H1N1/09 1.46 (IQR, 1.30–1.70) 11–21% (0.7–1.4 billion)[338] 151,700–575,400[339] 0.01%[340][341] 1
Typical seasonal flu[t 1] Every year 7.75 billion A/H3N2, A/H1N1, B, ... 1.28 (IQR, 1.19–1.37) 5–15% (340 million – 1 billion)[342]
3–11% or 5–20%[343][344] (240 million – 1.6 billion)
290,000–650,000/year[345] <0.1%[346] 1
Notes
  1. ^ Not pandemic, but included for comparison purposes.


Research

[edit]
An electron micrograph showing recreated 1918 influenza virions

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.[347][348] More recent research has suggested the strain may have originated in a nonhuman, mammalian species,[349] in 1882–1913.[350] 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.[350]

Dr Terrence Tumpey examines a reconstructed version of the Spanish flu virus at the CDC

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.[351][352][353][348] 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.[354] These were subsequently used to experimentally infect mice, ferrets, and macaques, providing information about how to prevent and control future pandemics.[355]

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.[356] 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.[357]

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.[358]

In 2008 an investigation used the virus sequence to obtain the Hemagglutinin (HA) antigen and observe the adaptive immunity in 32 survivors of the 1918 pandemic; all of them presented seroreactivity and 7 of 8 further tested presented memory B cells able to produce antibodies that bound to the HA antigen, highlighting the ability of immunological memory.[359][348]

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.[360]

In 2013, the AIR Worldwide Research and Modeling Group "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.[361]

In 2018, Michael Worobey, a 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.[362][363][364] Worobey extracted tissue from the slides to potentially reveal more about the origin of the pathogen.[26]

See also

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Footnotes

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References

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Further reading

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The 1918–1920 influenza pandemic, known as the Spanish flu, was a worldwide outbreak caused by an H1N1 subtype of influenza A virus with avian genetic origins. It infected roughly 500 million people—about one-third of the global population—and resulted in estimates of 50–100 million deaths, marking it as the deadliest pandemic in recorded history. The name "Spanish flu" arose not from its origin but because Spain, neutral in World War I, reported the epidemic freely without wartime censorship, unlike Allied and Central Powers nations that minimized coverage to preserve public morale. The pandemic unfolded in three waves: a relatively mild first wave in spring 1918, a far deadlier second wave in fall 1918 that accounted for most fatalities, and a third wave in early 1919. Distinct from typical seasonal influenza, which primarily kills the very young and elderly, the Spanish flu exhibited an atypical W-shaped mortality curve, with disproportionate deaths among healthy young adults aged 20–40, attributed to hyperactive immune responses triggering cytokine storms and frequent secondary bacterial pneumonias in the absence of antibiotics. The virus's precise zoonotic emergence remains debated, with genetic evidence pointing to a novel reassortment shortly before 1918, possibly in the United States or Europe, though early cases appeared in military camps like Camp Funston, Kansas. Lacking vaccines or antivirals, responses relied on non-pharmaceutical interventions such as quarantines, school closures, and mask mandates, which varied in enforcement and effectiveness, highlighting early challenges in pandemic management. The event's scale overwhelmed healthcare systems, exacerbated wartime conditions, and left lasting demographic impacts, including population declines and shifts in global influenza dynamics.

Naming and Etymology

Origins of the Term "Spanish Flu"

The term "Spanish flu" arose during due to wartime in Allied nations, which suppressed reports of outbreaks to preserve and support for the , while neutral freely published accounts of the disease's impact. Belligerent countries like the , , and the minimized or delayed disclosures of cases in military camps and civilian populations, fearing it would signal weakness or disrupt mobilization. In contrast, Spanish newspapers provided detailed coverage without such restrictions, leading foreign observers to associate the prominently with despite its global emergence. A pivotal event amplifying this perception occurred in early May 1918, when King contracted severe influenza, nearly succumbing to the illness; his high-profile case received extensive uncensored reporting in the Spanish press, including headlines in outlets like El Sol on May 28, which highlighted the epidemic's toll. This royal affliction, combined with Spain's neutrality, fostered the misconception that the outbreak originated there, as Allied media increasingly referenced "Spanish" cases to deflect scrutiny from domestic or military sources. Empirical records contradict the nomenclature's implication of Spanish origins, documenting the earliest confirmed outbreak on , 1918, at in , , where over 100 U.S. soldiers reported flu-like symptoms amid crowded training conditions. By late March, the illness had spread to other American military bases, predating widespread Spanish reporting by nearly two months and underscoring how propaganda-driven labeling obscured the pandemic's North American genesis in public discourse.

Alternative and Local Names

The 1918 influenza pandemic elicited a range of alternative and local designations that mirrored regional symptom interpretations, epidemiological observations, and socio-political contexts. In the United States and parts of , early mild cases prompted the term "three-day fever," highlighting the rapid resolution in non-severe instances, as noted in contemporary reports and 's El Sol on 28 May 1918 reporting over 80,000 infections in the city. In , "Blitzkatarrh" (lightning ) captured the explosive onset and catarrhal symptoms akin to a sudden , evoking wartime imagery of swift attacks among soldiers. referred to it as "purulent " emphasizing suppurative respiratory complications, while used "sandfly fever" drawing parallels to vector-borne illnesses despite viral . Severe manifestations inspired evocative sobriquets like "purple death," alluding to the heliotrope cyanosis—bluish-purple skin discoloration from fluid accumulation and hypoxia—in terminal patients, particularly documented in military camps. Other locale-specific terms included "Flanders grippe" in Britain linking to Western Front trenches, "Naples soldier" in possibly referencing troop movements, "Bolshevik fever" in amid revolutionary unrest, and "wrestler's fever" in connoting physical . These varied monikers, often avoiding national stigma or aligning with immediate experiences, precluded a singular contemporaneous label; post hoc virological analysis identifies the as A(H1N1), favoring empirical subtype over descriptive or geographic proxies.

Virological and Pathological Characteristics

Identification and Genetic Reconstruction

The identification of the 1918 virus as an H1N1 subtype began with the extraction of viral RNA from formalin-fixed lung tissues preserved from samples of victims who died in the autumn of 1918. In 1995, a team at the Armed Forces Institute of Pathology (AFIP), led by molecular pathologist Jeffery Taubenberger, identified suitable archival materials from U.S. and civilians, initiating a multi-year effort to sequence fragmented viral genetic material using (RT-PCR) techniques. Initial progress included the full sequencing of the (HA) gene by 1997, revealing phylogenetic divergence from known human strains and closer affinity to A viruses, indicating a introduction into human populations rather than reassortment with circulating human viruses. Subsequent sequencing efforts, involving collaborators Ann and others, expanded to the neuraminidase (NA) and other internal genes between and , overcoming challenges posed by RNA degradation through multiple amplification rounds and comparison with partial sequences from permafrost-preserved Alaskan tissues. The complete was achieved in 2005 through a collaborative project at the Centers for Disease Control and Prevention (CDC), where Taubenberger's AFIP data were integrated with synthetic to reconstruct infectious virus clones under 3 conditions. This reconstruction confirmed the virus's avian genetic roots, with all eight segments deriving from a purely avian-like that underwent adaptive for host replication efficiency prior to or during 1918. Key genetic features identified included specific in the HA gene, such as substitutions at positions enabling preferential binding to human-type α-2,6-linked receptors while retaining for deeper alveolar epithelial cells, a pattern distinct from modern seasonal H1N1 strains that primarily target upper airways. These HA alterations, absent in avian progenitors, facilitated enhanced replication in mammalian lung tissue, as demonstrated and in models using the reconstructed virus. The full genomic data also enabled functional studies revealing the virus's capacity to induce hyperinflammatory responses, including elevated production in infected cells, underpinning its exceptional pathogenicity without reliance on bacterial superinfections.

Key Viral Features Contributing to Virulence

The 1918 H1N1 influenza virus demonstrated a pronounced for the lower , replicating extensively in alveolar type II pneumocytes and macrophages, which precipitated primary rather than the secondary bacterial infections typical of milder strains. This deep-lung replication pattern, confirmed through reconstruction and animal model studies, resulted in rapid viral dissemination, epithelial , and , distinguishing it from seasonal influenzas confined largely to upper airways. The (HA) played a pivotal role in this enhanced by facilitating receptor binding in alveolar cells and promoting fusion with host membranes under conditions favoring lower respiratory infection. Genetic analyses and experiments swapping the 1918 HA into modern strains induced severe lung , including marked and dysregulation, underscoring HA's contribution to tissue and immune hyperactivation. Complementing this, the neuraminidase (NA) and basic 1 (PB1) genes supported efficient viral release and replication kinetics in mammalian lungs. The PB2 subunit of the RNA polymerase further amplified lethality by optimizing cap-snatching and transcription efficiency in human cells at physiological temperatures, leading to elevated viral loads and exacerbated proinflammatory signaling. Unlike avian-adapted polymerases, the 1918 PB2 configuration enabled sustained replication without reliance on specific mammalian mutations like E627K, yet drove dysregulated host responses, including impaired lung repair via Wnt pathway interference. An introduced novel HA and NA subtypes absent in human circulation since the late , engendering near-universal susceptibility across age groups, particularly young adults lacking cross-protective immunity from prior H3-dominant epidemics. This immunological , coupled with the virus's evasion of innate defenses through polymerase-mediated nuclear trafficking, permitted unchecked proliferation before adaptive responses could mitigate damage.

Transmission Mechanisms and Mutations

The 1918 influenza A (H1N1) virus primarily transmitted through s and aerosols expelled during coughing, sneezing, talking, or breathing by infected individuals, facilitating close-range person-to-person spread in crowded settings such as military camps and urban areas. This mode was amplified by troop mobilizations, which concentrated susceptible populations and enabled rapid dissemination across continents via rail, ship, and overland routes. Experimental studies using reconstructed 1918 virus in animal models, including ferrets, confirmed efficient transmission, underscoring the dominance of airborne routes over alternatives. Fomite-mediated transmission via contaminated surfaces played a minor role, as evidenced by the virus's environmental persistence being insufficient for significant indirect spread under typical conditions, with contact-tracing data from contemporaneous outbreaks prioritizing droplet exposure. Genetic analyses of archived 1918 viral sequences reveal mutations in the (HA) that enhanced binding affinity to human α2,6-linked receptors, promoting efficient and thereby boosting transmissibility compared to avian-adapted precursors. These HA receptor-binding site variants, including substitutions like Glu190Asp, emerged early in the and were conserved across isolates, enabling sustained human-to-human propagation without requiring extensive reassortment. Subsequent evolution during serial passages in human hosts yielded second-wave strains with further polymerase (PB1) and neuraminidase adaptations that optimized replication and shedding, as reconstructed from lung tissue genomes showing increased viral fitness. Epidemiological models derived from city-level outbreak data estimate the (R0) for the 1918 virus at 1.4–2.8, exceeding that of seasonal (typically ~1.3) due to prolonged infectious periods facilitated by and pre-symptomatic shedding, particularly in young adults whose immune responses delayed overt symptoms while allowing viral dissemination. Contact-tracing from military bases and genomic phylogenies indicate local chains of transmission interspersed with long-distance seeding events, consistent with droplet-driven propagation rather than sustained fomite or vector roles. No single universally accounted for heightened transmissibility, but cumulative HA and internal changes collectively lowered the transmission threshold in naive populations.

Origins and Emergence

Evidence for North American Origin

The earliest documented outbreak of the occurred in , in January 1918, where local physician Dr. Loring Miner observed an unusually severe form of causing rapid deterioration and deaths among patients. Miner reported these cases to U.S. Public Health Service authorities, marking the first known alert of atypical severity worldwide. This rural, isolated county's preceded similar reports elsewhere, with affected individuals including recruits who soon traveled to nearby at . On March 4, 1918, the first confirmed military case emerged at Camp Funston, a major U.S. Army training base with over 26,000 troops, shortly after Haskell County residents enlisted there. The camp's crowded conditions facilitated rapid spread, sickening hundreds within days and resulting in dozens of deaths from secondary pneumonia. Infected soldiers were mobilized overseas, with troop ships carrying the virus to Europe by late March, aligning temporally with early outbreaks in Brest, France, among arriving American Expeditionary Forces. This pattern of dissemination via U.S. military movements provides epidemiological linkage absent in alternative origin claims. Virological evidence from the reconstructed 1918 H1N1 genome supports mammalian adaptation consistent with North American precursors, including concurrent respiratory outbreaks in U.S. swine populations that shared genetic markers with the human pandemic strain. Phylogenetic analyses position the 1918 hemagglutinin genes as mammalian-like, basal to modern human and classical swine H1 clades, which originated post-1918 in North America rather than aligning closely with pre-existing Asian avian or swine strains. Genomic continuity between preserved 1918 U.S. samples and early European isolates further corroborates transatlantic seeding from American sources over independent Eurasian emergence. These findings, derived from fixed tissue sequencing, underscore the Kansas region's role as the empirical epicenter, prioritizing direct outbreak records over speculative zoonotic jumps elsewhere lacking contemporaneous data.

Competing Hypotheses from and

One for a European origin centers on outbreaks at the British military camp in , , during the winter of –1917, where a respiratory illness labeled "purulent " infected thousands of soldiers amid overcrowding, animal proximity (including ducks and pigs), and potential irritants from wartime chemical agents. Pathologists from Étaples and barracks retrospectively linked these events to the 1918 , proposing the camp's conditions facilitated viral from avian or swine sources to humans. However, no genomic sequencing from Etaples samples exists to confirm identity with the reconstructed 1918 H1N1 virus, and diagnoses likely conflated influenza-like illnesses with concurrent wartime pathogens such as Bartonella quintana () or secondary bacterial infections, given diagnostic limitations and incomplete records. Wartime reporting biases, including suppression of health data to maintain morale, further undermine retrospective attributions. An Asian origin theory invokes northern , where respiratory outbreaks reportedly struck laborer recruitment areas in November 1917, potentially spreading via over 140,000 Chinese workers shipped and other European sites by mid-1918 for support roles. Advocates point to shipment timings aligning with early European cases and archival mentions of flu-like illnesses in and northern provinces. Contradictorily, serological antibody surveys from the era reveal no elevated pre-1918 immunity clusters in those regions, inconsistent with an epicenter of emergence, while China's comparatively low pandemic mortality—estimated at under 1% versus global averages—suggests either effective containment, , or absence of the virulent strain's initial adaptation there. Direct tracing fails to connect laborer movements to the specific H1N1 genomic signature, with analyses concluding insufficient evidence for this vector. These theories share vulnerabilities from World War I-era underreporting and , which delayed or obscured notifications across military fronts, complicating precedence claims; no hypothesis yields a uniquely verifiable pre-1918 viral isolate, highlighting reliance on symptomatic correlations over molecular proof.

Factors Influencing Initial Emergence

The 1918 H1N1 influenza virus likely emerged via zoonotic spillover from avian reservoirs, with genetic evidence indicating an avian-like that adapted to mammals through minimal genetic changes. Reconstruction and sequencing of the virus from preserved human tissues reveal that its eight genome segments exhibit characteristics, distinct from contemporary human strains, supporting a direct or indirect jump from birds without requiring extensive reassortment. served as a probable intermediate host, as concurrent respiratory outbreaks in U.S. pigs mirrored early human cases, facilitating viral adaptation via a "mixing vessel" mechanism where avian and mammalian viruses co-circulate. Agricultural practices in the early 20th-century , characterized by of , swine, and humans, heightened interspecies contact and thus opportunities for spillover. Proximity of to human populations, including on bases and rural farms, created environmental preconditions for , though direct causation remains inferred from phylogenetic patterns rather than contemporaneous records. Animal model experiments confirm the virus's efficient mammalian adaptation, with only 11 key coding —such as PB2 E627K—enabling high replication in human cells and in ferrets and mice without further . World War I-era conditions further lowered barriers to viral establishment by inducing and immune suppression across populations, reducing innate defenses against novel pathogens. Studies in malnourished animal models demonstrate enhanced replication and severity, mirroring how wartime food shortages and stress could have facilitated initial human infections by impairing responses and epithelial barriers. No empirical or genetic evidence supports laboratory origins or intentional release; all reconstructed sequences align with natural evolutionary trajectories from avian sources, predating modern .

Pandemic Timeline

Antecedent Waves and Early Detection

Epidemiological analysis of mortality data from reveals an antecedent wave during the 1917/1918 season, marked by a pronounced shift in the age distribution of excess deaths. Prior to 1918, excess mortality primarily affected the elderly, but from to April 1918, it shifted toward younger adults aged 25-29, indicating possible circulation of the pandemic strain at sub-pandemic intensity levels. This pattern, while not reaching the lethality of later waves, provided early signals of viral adaptation distinct from seasonal norms. Global serological evidence further supports limited pre-1918 circulation of H1N1-related viruses, as studies detected neutralizing antibodies in individuals born before 1918 against swine H1N1 subtypes, suggesting prior human exposure without widespread pandemics. However, the precursor virus likely achieved broader human transmission only shortly before the recognized outbreak, evading detection amid seasonal flu variability. Early detection faced significant barriers due to contemporary diagnostic limitations; influenza's viral etiology was unknown until the 1930s, with cases routinely misdiagnosed as bacterial pneumonias based on postmortem findings of secondary infections like . The 1918 H1N1 strain's identity was confirmed decades later through genetic reconstruction from preserved lung tissues in 2005, highlighting how reliance on bacterial culturing obscured the primary viral driver. U.S. military training camps functioned as effective sentinels owing to mandated health surveillance, reporting outbreaks in 14 major facilities from to May 1918. The earliest documented cluster emerged at , , , on March 4, 1918, among recruits exhibiting acute respiratory symptoms that later analysis linked to the H1N1 subtype. These confined, monitored populations accelerated recognition of the pathogen's spread, though initial interpretations framed it as routine "three-day fever" rather than a novel threat.

First Wave: Spring and Summer 1918

The first documented outbreak of the 1918 occurred on March 4, 1918, at in , , where U.S. Army cook Albert Gitchell reported symptoms shortly before breakfast, followed by over 100 soldiers falling ill by noon. Cases rapidly increased, with more than 100 soldiers affected within days at this housing over 50,000 troops. The illness presented as typical symptoms, resembling a severe , and spread quickly through overcrowded military environments. From Kansas, the virus disseminated to other U.S. military installations, including Camps Hancock, Lewis, Sherman, and Fremont, as well as civilian sites like San Quentin prison in . Troop movements facilitated transatlantic transmission; approximately 84,000 U.S. soldiers shipped to in and 118,000 in carried the pathogen across the Atlantic, with early cases noted among the 15th U.S. en route, recording 36 illnesses and 6 deaths. By , outbreaks appeared among in ports like , marking the virus's arrival in . Sporadic spread continued unevenly through the , , and possibly during spring and summer. This initial wave was characterized by high illness rates but mortality comparable to seasonal , with death rates not exceeding normal levels in most areas. Case fatality remained low, estimated below 1% in affected populations, contrasting sharply with subsequent waves. Wartime and prioritization of military efforts led to underreporting, as Allied and governments minimized public disclosure of non-combat illnesses to preserve morale and operational secrecy. By , Britain reported 31,000 cases, affecting a small fraction of the population—around 1% in some regions—yet the mild nature and suppressed information allowed undetected viral circulation, potentially enabling antigenic shifts.

Second Wave: Autumn 1918 Peak Mortality

The second wave of the 1918 influenza pandemic escalated rapidly from late August through December, with peak mortality concentrated in to across multiple hemispheres, exhibiting unusual global synchronicity facilitated by intensified troop movements and maritime shipping during . In the United States, this phase accounted for the majority of the pandemic's estimated 500,000 to 675,000 excess deaths, far exceeding prior years' baselines by factors of 10 or more. Mortality patterns deviated markedly from typical seasonal flu, with disproportionate fatalities among healthy young adults aged 20 to 40—comprising nearly half of influenza-related deaths—due to the virus's capacity to trigger storms and subsequent damage in previously unexposed or partially immune individuals. Urban crowding exacerbated transmission independent of seasonal weather variations, as evidenced by synchronized outbreaks in temperate, tropical, and southern regions linked to military camps and ports rather than cold temperatures. A stark example occurred in on October 5, 1918, when city officials proceeded with a Liberty Loan attended by over 200,000 people despite early cases and medical warnings, resulting in an explosive local surge: approximately 45,000 infections and 12,000 deaths within weeks, overwhelming hospitals and morgues. Similar dynamics played out in military bases and troop ships, where confined quarters accelerated spread; for instance, U.S. Army camps reported infection rates exceeding 30% in days, with secondary waves hitting "seasoned" personnel despite prior mild exposures from the spring phase. Pathologically, the wave's lethality stemmed from the H1N1 virus predisposing hosts to rampant bacterial superinfections, particularly pneumococcal and streptococcal pneumonias, which infiltrated damaged lungs in crowded, unsanitary environments. Autopsies from the period revealed that while primary viral caused rapid deterioration in some cases, most fatalities involved bacterial coinvasion exploiting flu-induced , with influx failing to clear pathogens effectively. This interplay, amplified by wartime and delayed medical access, drove case-fatality rates above 2.5%—orders of magnitude higher than non-pandemic influenzas—and underscored crowding's role over climatic factors in the wave's ferocity.

Third and Fourth Waves: 1919–1920

The third wave of the 1918 influenza pandemic began in early 1919, manifesting with reduced lethality relative to the preceding autumn surge, though it persisted in causing elevated mortality across multiple regions. In the United States, this wave intensified during the winter months, extending the death toll from the prior outbreak and affecting urban centers with renewed hospital burdens. Globally, the wave's spread highlighted incomplete population-level immunity from earlier exposures, allowing residual transmission despite prior infections. Australia, isolated by stringent maritime quarantines until late 1918, encountered the virus primarily during this third wave starting in 1919, following the arrival of infected passengers on ships from overseas; the outbreak resulted in an estimated 12,000 to 15,000 deaths, disproportionately impacting young adults and indigenous communities. This delayed introduction underscores how geographic barriers temporarily mitigated but ultimately deferred the epidemic's impact, with the wave's milder case-fatality rate still yielding significant excess deaths in a previously unexposed population. A fragmented fourth wave emerged from December 1919 into spring 1920, blending with endemic circulation and exhibiting variable intensity by locality, such as severe localized mortality spikes in parts of the and . Across the pandemic's waves, cumulative global fatalities ranged from 50 to 100 million, reflecting the virus's sustained transmissibility amid demographic vulnerabilities. The waning of these later waves aligned with the buildup of from extensive prior infections, as epidemiological and econometric analyses indicate that achieved immunity thresholds, rather than non-pharmaceutical interventions in isolation, primarily constrained resurgence and facilitated by mid-1920.

Clinical and Epidemiological Features

Primary Symptoms and Disease Progression


The 1918 influenza presented with abrupt onset, often striking individuals with dizziness, weakness, and pain during daily activities. Initial symptoms included high fever ranging from 100°F to 104°F, chills, severe headache, myalgia affecting the back, legs, and arms, and profound prostration leading to immobilization. Respiratory manifestations followed, featuring an unproductive cough, harsh breathing, reddened mucous membranes, sneezing, and occasionally bloody nasal discharge.
In mild cases, symptoms resolved within a few days, with fever subsiding and recovery ensuing without complications. Severe cases progressed rapidly to within 2–3 days, marked by dyspnea, irregular pyrexia, toxemia, vasomotor depression, and indicating poor prognosis. The average interval from onset to death in fatal instances was approximately 9 days, with ongoing evident at . This swift deterioration to primary contrasted with the typically milder, self-limited course of seasonal . Autopsy examinations of fatal cases revealed histopathological hallmarks of primary , including (DAD) in 62% of reviewed , characterized by hyaline membranes and desquamated epithelial cells. affected 60% of cases, filling alveolar spaces with fluid, fibrin, and inflammatory cells, while acute alveolar hemorrhage occurred in 40%. These findings underscored the virus's direct cytopathic effects on and vasculature, distinguishing the from predominant bacterial pneumonias through the primacy of viral-induced damage.

Atypical Fatality Patterns Among Young Adults

The 1918 influenza pandemic deviated markedly from the typical age distribution of mortality, which usually follows a U-shaped curve with peaks among infants and the elderly due to vulnerabilities in immature or waning immune systems. Instead, excess death rates formed a distinctive W-shaped pattern, featuring an additional peak among young adults aged approximately 20–40 years, where mortality was disproportionately high relative to other age groups. , this translated to death rates in the 20–40 age bracket exceeding pre-pandemic levels by over 20 times, accounting for roughly half of the total 675,000 influenza-associated fatalities despite comprising a smaller proportion of the population. This anomaly contrasted sharply with subsequent pandemics, such as the 1957 H2N2 and 1968 H3N2 events, where aligned more closely with seasonal patterns, disproportionately affecting those over 65 years and showing lower representation of deaths under age 65 (36% in 1957 and 48% in 1968). The 1918 pattern's emphasis on young adults—peaking around ages 25–34—challenged assumptions of inherent frailty in extremes of age, as working-age individuals, often previously healthy, succumbed at rates far exceeding expectations for respiratory pathogens. Causally, the elevated young adult mortality has been linked to an overexuberant , termed a , in which vigorous T-cell and production by fit, unexposed immune systems damaged pulmonary tissues more severely than the virus itself. Reconstruction of the 1918 H1N1 virus and its testing in animal models, including ferrets and nonhuman primates, replicated this : young animals exhibited hypercytokinemia, , and high lethality mirroring human autopsy findings, whereas older models showed milder responses, supporting the role of age-related immune vigor in driving fatalities. This mechanism explains the inversion of standard vulnerability without invoking confounding factors like bacterial superinfections, though direct viral remained essential.

Role of Secondary Bacterial Infections

Historical analyses of autopsy records from the 1918–1919 indicate that secondary bacterial pneumonias accounted for the majority of fatalities, with over 90% of deaths involving superinfections by pathogens such as , , and . These exploited damage to the caused by the virus, leading to rapid progression from viral to and . Contemporary clinicians and pathologists frequently isolated these organisms from lung tissues, blood, and pleural fluids of deceased patients, underscoring their direct causal role in mortality absent effective antibacterial therapies. The virus's cytopathic effects, including of ciliated epithelial cells and impaired , created an environment conducive to bacterial colonization and invasion, amplifying lethality beyond primary viral . Pre-antibiotic era diagnostics often conflated viral and bacterial components, with bronchial lavage and cultures revealing mixed infections in nearly half of severe cases examined. This predisposition was evident in camps, where and poor facilitated bacterial dissemination among virus-compromised hosts. Reconstruction of the 1918 H1N1 and subsequent animal modeling confirm its independent virulence—inducing severe and death in ferrets and mice without bacterial involvement—but highlight synergistic enhancement in scenarios mirroring human outcomes. In murine models, sequential with the reconstructed followed by S. pneumoniae shortened survival times and increased bacterial loads compared to either alone, demonstrating how viral suppression of innate immunity facilitates bacterial proliferation. These findings align with historical data, indicating that while the initiated tissue destruction, unchecked secondary infections drove the pandemic's exceptional mortality, particularly among young adults with robust but dysregulated immune responses.

Public Health Interventions and Medical Treatments

Non-Pharmaceutical Measures and Their Implementation

In response to the escalating outbreak in 1918, authorities in the United States implemented a range of non-pharmaceutical interventions, including closures of schools, churches, theaters, and other public venues, as well as prohibitions on mass gatherings such as parades, fairs, and sporting events. These measures varied significantly by locality; for instance, cities like enacted early and comprehensive bans on public assemblies starting in late September 1918, while others, such as , delayed restrictions despite rising cases, allowing events like the Liberty Loan parade on September 28 that drew over 200,000 participants. Bans often extended to funerals, limiting attendance to immediate family and requiring closed caskets to minimize exposure risks. Mask-wearing mandates emerged as a prominent intervention in densely populated areas, particularly on public transportation and in indoor spaces. In , the passed an ordinance on October 18, 1918, requiring gauze masks in streetcars, theaters, and crowded areas, which was enforced through fines up to $100 or jail time; this was lifted after the armistice on but reinstated on January 17, 1919, amid a resurgence. Similar requirements appeared in cities like , where police officers patrolled in masks to model compliance, and Oakland, where violations led to arrests. Isolation of the ill and quarantine of contacts were standard protocols, often involving home confinement or designated facilities, though enforcement relied on voluntary reporting in many jurisdictions. Within U.S. military camps, which housed hundreds of thousands of troops amid wartime mobilization, commanders imposed to contain outbreaks, such as segregating barracks and restricting inter-camp travel following initial detections at , , in March 1918. These efforts included halting troop movements and screening arrivals, temporarily limiting spread within isolated bases, though lapses occurred due to overcrowding and rapid personnel turnover. Internationally, some nations enacted travel restrictions; , for example, closed ports to infected ships and imposed a maritime that postponed the pandemic's arrival until January 1919. In and the U.S., wartime and troop transports complicated full closures, resulting in partial curbs like ship inspections that delayed but did not avert transoceanic dissemination. Compliance with these measures proved uneven, marked by public defiance and organized resistance. In , the second mask ordinance sparked the formation of the Anti-Mask League in January 1919, which petitioned for repeal citing discomfort and inefficacy, leading to widespread non-adherence and arrests of "slackers." Store owners in openly violated closure orders by remaining open, while clergy in multiple cities protested bans on religious services, arguing hypocrisy when saloons stayed operational amid debates. Political opposition framed restrictions as overreach, with critics decrying them as tyrannical impositions , particularly during armistice celebrations that prompted unauthorized gatherings in defiance of lingering prohibitions. Black markets for exemptions and informal networks evading quarantines further undermined enforcement in urban centers.

Empirical Evidence on Intervention Effectiveness

Analyses of excess mortality data from 43 U.S. cities during the 1918-1919 influenza pandemic indicate that early and layered implementation of nonpharmaceutical interventions, such as school closures, bans on public gatherings, and isolation measures, was associated with reductions in peak death rates by 48% in cities like St. Louis compared to later or less comprehensive efforts. These findings, derived from contemporaneous death certificate records and newspaper reports on intervention timing, suggest that interventions implemented two weeks before a city's epidemic peak lowered transmission rates by up to 30-50% in responsive locales like San Francisco and Milwaukee. However, overall mortality reductions were more modest, averaging 10-30%, as interventions were often temporary and did not eliminate subsequent waves. Timing of interventions proved more critical than their duration or stringency, with cities acting preemptively—before local case surges—achieving disproportionate benefits, while prolonged measures in non-compliant areas yielded . Confounders in these assessments include variable enforcement, seasonal weather patterns favoring viral decline, and differences in baseline population immunity or bacterial co-infections, which could independently suppress or exacerbate mortality independent of interventions. Retrospective modeling corroborates moderate transmission reductions but highlights data limitations from inconsistent vital statistics reporting amid wartime disruptions. Critiques of intervention efficacy note widespread evasion and non-compliance, such as anti-mask campaigns in and illegal gatherings, which eroded public adherence and potentially amplified spread in overreaching jurisdictions. Wartime in Allied nations suppressed reporting of intervention failures or high mortality in camps, potentially inflating perceptions of uniform success by obscuring regional disparities and undercounting deaths. Econometric reviews of city-level data further indicate that while pandemics themselves depressed short-term activity, interventions did not cause sustained economic harm, with recoveries offsetting initial disruptions, though such analyses control for mortality as a primary driver rather than policy alone.

Treatment Approaches and Limitations

Supportive care formed the cornerstone of treatment for influenza patients during the 1918–1919 pandemic, emphasizing , hydration, nutrition, and interventions such as sponge baths and clean bedding to manage symptoms like fever and weakness. Physicians prioritized these measures because the viral of influenza remained unknown, with many attributing the disease to like Haemophilus influenzae (then called Pfeiffer's bacillus). Without or intensive care units, outcomes depended heavily on addressing and secondary complications through fluids and rest, though overwhelmed medical systems limited their consistent application. Pharmacological interventions were largely empirical and ineffective against the itself. Aspirin, newly available since , was widely prescribed in high doses—often 975–1,300 mg per administration, totaling up to 8 grams daily—to combat fever and pain, exceeding modern safe limits of about 4 grams per day. These dosages, recommended in medical journals and guidelines, could induce salicylate toxicity, manifesting as , hemorrhages, and exacerbated viral pathology, potentially contributing to mortality rates; pathologist Karen Starko hypothesized this link based on contemporaneous dosing regimens and findings of wet lungs and bleeding. , administered in doses of 5 grains two to four times daily, was used symptomatically for its effects but offered no antiviral benefit. Over-the-counter remedies, including syrups and whiskey, supplemented these but lacked beyond palliation. Vaccine development efforts targeted presumed bacterial causes, yielding polyvalent preparations against H. influenzae and other pathogens, administered to soldiers and civilians in campaigns by pharmaceutical firms and military labs. These vaccines, produced rapidly from autopsied lung cultures, showed mixed results in trials—some reported reduced incidence, but overall they failed to prevent or mitigate viral infection due to erroneous assumptions, with medical literature documenting contradictory efficacy claims. By late , convalescent plasma transfusions from recovered individuals demonstrated promise in lowering mortality for severe cases, but logistical constraints like blood typing limitations and scarcity restricted widespread use. Therapeutic limitations stemmed from diagnostic gaps and the absence of targeted antivirals or broad-spectrum antibiotics, leaving secondary bacterial pneumonias untreated effectively despite some experimental sera. Global research accelerated post-first wave, yet the pandemic's rapid waves outpaced breakthroughs, as the receded before viable interventions emerged; this reactive highlighted medicine's dependence on etiological understanding, which only advanced decades later with viral isolation in . High mortality, particularly from storms in young adults, underscored supportive care's insufficiency against the H1N1 strain's without modern immunomodulators.

Global Mortality and Demographic Impacts

Total Death Toll Estimates and Uncertainties

Estimates of the global death toll from the 1918-1920 , commonly known as the Spanish flu, vary due to incomplete vital registration systems, wartime disruptions, and inconsistent diagnostic criteria, but scholarly reassessments place the figure at approximately 50 million deaths. This estimate, derived by Niall Johnson and Jürgen Mueller in 2002 through compilation of country-level data and adjustments for underreporting, revises earlier projections of 24.7-39.3 million upward, accounting for gaps in records from regions with sparse documentation. Some analyses suggest the total could approach 100 million, particularly when incorporating indirect effects like exacerbated or reduced births, though such higher bounds remain speculative without uniform corroboration across datasets. In the United States, official counts recorded 675,000 influenza-related deaths, a figure adjusted higher in some studies to reflect unverified cases amid overwhelmed reporting. Uncertainties stem primarily from the coincidence with , which suppressed public disclosure of civilian mortality in combatant nations to maintain morale, while neutral countries like faced no such but still suffered from limited for tracking deaths. In British , where the pandemic struck hardest proportionally, estimates hover around 18 million deaths, but these rely on extrapolations from partial provincial reports prone to undercounting due to rural inaccessibility and reliance on local enumerators without standardized verification. African data are even more fragmentary, with colonial records capturing only urban or mission-station fatalities, leaving vast rural and nomadic populations unaccounted for and inviting systematic underestimation. Standard methodologies calculate tolls via excess all-cause mortality—comparing observed deaths in 1918-1920 against pre-pandemic baselines—yet this approach introduces confounders, as wartime conditions like , troop movements, and bacterial co-infections elevated baselines unpredictably, potentially overstating or masking -attributable deaths. Even in well-documented areas, misattribution between , , and other respiratory illnesses compounded errors, given the absence of viral testing until decades later. Contemporary refinements using statistical models and genomic reconstructions of the H1N1 strain offer indirect validation but cannot retroactively resolve archival voids, underscoring persistent debates over true scale.

Geographic Disparities in Mortality

Mortality from the 1918 influenza pandemic exhibited stark geographic variations, influenced by factors such as , prior exposure conferring partial immunity, baseline health conditions, and the timing and efficacy of responses. Isolated communities with limited prior contact faced catastrophic losses upon introduction of the virus due to the absence of , while denser urban areas experienced amplified transmission through crowding. Conversely, regions with effective early isolation or measures, or potentially higher pre-existing immunity from earlier strains, recorded comparatively lower rates. These disparities underscore the role of local epidemiological and socioeconomic conditions in modulating impact, independent of viral alone. In the Pacific islands, mortality reached extreme levels in areas with delayed but unchecked spread; Western Samoa reported 19%–22% of its population dying within two months of the virus's arrival in , totaling approximately 8,500 deaths from a pre-epidemic of around 38,000, attributable to rapid person-to-person transmission in close-knit communities lacking immunity. Neighboring averted disaster through stringent maritime enforced from September 1918, resulting in zero deaths among its 8,000 residents. Such contrasts highlight how geographic isolation could either shield populations entirely or exacerbate devastation upon breach. Within the United States, urban centers suffered higher per capita mortality than rural areas, with studies indicating elevated influenza-related death rates in cities due to intensified transmission in crowded settings; for instance, analyses of , , and analogous U.S. patterns showed urban excess mortality surpassing rural by factors linked to density. Indigenous populations, particularly , faced disproportionate tolls, with regional mortality reaching up to 38% in some areas and overall territory excess deaths at 1,672 per 100,000—eight times the rate for non-Natives—reflecting vulnerabilities from , inadequate housing, and limited medical access rather than inherent susceptibility. In , experienced relatively low mortality of approximately 35,000 deaths—or about 0.6% of its 5.8 million population—during the pandemic's three waves, potentially due to a combination of neutral wartime status enabling open reporting and implementation of measures like school closures, alongside possible cross-immunity from milder early strains. Asian regions showed varied patterns, with recording 257,000–481,000 deaths (0.5%–0.9% of ~55 million population) amid high absolute numbers elsewhere like , where estimates suggest 12–17 million fatalities (~4%–6% of ~300 million), though rates were moderated in some areas by rural dispersion and underreporting; overall, lower urban-rural gradients in parts of contrasted with Western patterns, tied to differing immunity profiles and response capacities.

Long-Term Population and Health Consequences

The 1918 influenza pandemic led to a notable decline in rates, particularly evident where birth rates dropped by 5% to 15% in the months following peak mortality, with the occurring approximately 6 to 7 months after the epidemic's height, consistent with increased miscarriages among infected pregnant women. This natality depression contributed to a "" effect, as U.S. census data indicate deficits in the 1919 birth cohort, partly attributed to conception postponement during the crisis and fetal losses, though some analyses suggest the 1920 uptick was not a compensatory boom but rather a return to trend amid broader post-war fertility declines. Cohorts exposed during the exhibited long-term health impairments, including elevated rates of in later adulthood; survivors aged 60 to 82 showed at least 20% excess cardiovascular risk linked to prenatal exposure. Empirical analyses of U.S. Census data from 1960 to 1980 reveal that these fetal-exposed groups faced reduced and 20% higher rates by age 61, supporting fetal origins mechanisms rather than selection effects from immediate mortality. However, evidence for genetic scarring—such as transgenerational inheritance of vulnerabilities—is lacking, with effects primarily attributable to developmental programming during . Among young adult survivors of active , studies indicate modest reductions in , with exposed cohorts showing at most a 20-day decrement overall, though likely smaller after for incidence variations; no consistent postnatal effects on were found beyond . A temporal spike in cases from 1919 to coincided with the , prompting hypotheses of -triggered neurological sequelae or post-viral , but direct causal links remain unproven due to absent virological confirmation and failure to isolate influenza from affected brains. Survivor immunity to subsequent H1N1 strains was partial, as prior exposure could induce dysregulated responses in reinfections, though population-level weakening was not empirically dominant compared to age-specific priming effects.

Societal, Economic, and Political Effects

Influence on World War I and Wartime Censorship

The 1918 influenza pandemic significantly impaired military operations during the final months of , particularly affecting Allied forces. In the (AEF), approximately 340,000 soldiers were hospitalized due to , exceeding battle casualties in some periods. The U.S. Army recorded over one million cases among troops in training camps and , with infection rates reaching 25% in the Army and 40% in the Navy. On the Western Front, attack rates among soldiers approximated 40%, contributing to delays in Allied offensives such as the Meuse-Argonne campaign, where troop morbidity reduced combat effectiveness. Wartime censorship in belligerent nations suppressed reporting on the pandemic's scale to preserve morale and operational secrecy, distorting public awareness and hindering coordinated responses. Governments in the United States, Britain, , and minimized flu coverage, with U.S. authorities invoking the and the to prosecute perceived "alarmism" that could undermine the war effort, resulting in thousands of cases broadly targeting dissent. This suppression fostered distrust when outbreaks became undeniable, as empirical evidence of widespread illness eroded confidence in official narratives. Neutral Spain's uncensored press freely reported the pandemic, including King Alfonso XIII's illness in May 1918, leading to the ironic misnomer "Spanish flu" despite the virus's likely origins elsewhere, such as U.S. military camps. The pandemic's toll on troop strength and morale likely hastened the on November 11, 1918, as weakened armies on both sides reduced capacity for prolonged fighting, with some historians attributing the war's abrupt end partly to influenza's debilitating effects.

Economic Disruptions and Recovery Patterns

The 1918 influenza pandemic induced short-term labor shortages across various sectors, particularly in and , due to widespread illness and mortality among working-age adults, which temporarily elevated wages in affected U.S. industries as employers competed for reduced labor supplies. In the sector, a key indicator of industrial activity, labor supply disruptions were sharp but brief, with production recovering rapidly without significant long-term spillovers to other economic areas. City-level analyses in the U.S. indicate that mortality-driven contributed to output dips, yet aggregate GDP contracted by only about 1.5 percent nationally, far less than in many other countries, with non-pharmaceutical interventions imposing minimal additional economic costs relative to lives saved. Agricultural production faced disruptions from elevated rural mortality rates, which reduced the farm labor force by an estimated 8 percent in some regions, though overall output held steady due to prior trends and adaptive reallocations. In developing areas like , influenza deaths correlated with sharp declines in cash crop yields, such as , where mortality spikes exceeded 30 per thousand in peak months, compounding seasonal vulnerabilities. Globally, trade volumes dipped amid port closures and shipping delays, but disentangling flu-specific effects from the concurrent of and I's logistical strains remains challenging, as wartime blockades had already suppressed pre-pandemic commerce. Economic recovery accelerated in , with U.S. real per capita GDP rebounding above pre- trends and stock market indices like the rising 30.5 percent that year, reflecting resilient market adjustments such as labor reallocation and pent-up demand rather than fiscal stimuli. Unlike narratives of severe downturns, the did not precipitate a depression; recessions in 1919–1920 stemmed more from and than influenza, underscoring the economy's capacity for self-correction without modern-style lockdowns.

Social Behaviors and Public Compliance Challenges

Public compliance with non-pharmaceutical interventions during the 1918-1919 influenza pandemic varied widely, with significant defiance undermining official efforts in multiple cities. In , mask mandates enacted in late October 1918 faced immediate resistance, leading to the formation of the Anti-Mask League, which argued that enforced wearing infringed on personal liberties and lacked scientific backing. Noncompliance, termed "slackerism," prompted police enforcement, including arrests for refusing masks on streetcars and public spaces, yet vigilante-like public scolding by citizens supplemented official measures. Religious gatherings often persisted despite closures, correlating with elevated local mortality. In , churches defied bans in September 1918, contributing to over 12,000 deaths in that city alone during the October wave, as congregational transmission accelerated spread among healthy adults. Similar patterns emerged elsewhere, where spiritual resilience prioritized communal worship over isolation, empirically linking higher attendance to excess deaths in affected parishes. Stigma toward sufferers manifested in social avoidance and enforcement, reducing casual contacts but exacerbating isolation. Families predominantly provided care at home, with estimates indicating over 80% of cases managed domestically to avert overload, as institutional capacity collapsed under surges. This approach, while risky for caregivers, distributed burden and preserved systemic function amid scarce professional resources. Following the major waves, denialism surged, with public celebrations like San Francisco's November 1919 mask bonfires symbolizing rejection of prolonged restrictions. Criticisms of mandates as governmental overreach proliferated, fostering long-term toward centralized directives, evidenced by a decade-long decline in compliance post-pandemic. Such reactions highlighted resilience against top-down controls but also perpetuated risks from unheeded empirical lessons on transmission dynamics.

Legacy, Comparisons, and Contemporary Research

Cultural Representations and Historical Memory

Literature from the era and shortly after captured the personal devastation of the Spanish flu, often intertwining it with broader themes of isolation and mortality. Katherine Anne Porter's 1939 novella Pale Horse, Pale Rider draws from her own near-fatal illness during the pandemic, portraying a young woman's and loss amid wartime reporting in , emphasizing individual fragility over collective chaos. Earlier works, such as ' The Enormous Room (1922), reference the flu's intrusion into prisoner-of-war experiences, highlighting its indiscriminate disruption. These fictional accounts prioritize anecdotal human suffering, contrasting with factual records of widespread societal adaptation. Visual arts provided stark, contemporaneous depictions, as seen in Edvard Munch's 1919 self-portrait showing his emaciated figure post-infection, symbolizing the flu's physical toll on artists and intellectuals. Spanish satirical cartoons from November 1918 likened the pandemic to a "tragic game of football" between war and influenza, personifying the dual afflictions devastating Earth. Films rarely addressed the flu directly during its peak due to censorship and production halts; British silent cinema, for instance, features only one surviving informational reel, while later portrayals like the 1985 film 1918 romanticized community resilience in Texas towns, focusing on endurance rather than horror. Historical memory of the Spanish flu remains selective and subdued, with public memorials scarce until the early ; a 2018 granite marker in , commemorates over 50 million global deaths, one of few dedicated sites amid thousands of war monuments. This oversight stems partly from the pandemic's eclipse by World War I's narrative dominance and the absence of tangible, enduring symbols like battlefields, leading to cultural forgetting despite its higher death toll compared to later events. In contrast to COVID-19's pervasive media documentation, the 1918 event lacks similar archival visibility, fostering a gap between factual records of rapid societal recovery and romanticized victimhood in retrospective lore. Oral histories from survivors underscore community solidarity, revealing acts of neighborly aid that sustained isolated families, as in accounts where unaffected residents delivered food and care during household outbreaks. interviews from the 1970s-2000s describe mutual support networks forming organically, countering emphases on helplessness in some cultural retellings by evidencing pragmatic resilience without reliance on medical interventions. ethnographic collections preserve folk narratives of everyday heroism, such as volunteers nursing strangers, which align with empirical data on localized compliance and recovery patterns rather than pervasive despair. These firsthand accounts highlight a factual legacy of adaptive human agency, often downplayed in favor of war-centric historical focus.

Parallels and Differences with Modern Pandemics

The basic reproductive number (R0) for the 1918 H1N1 influenza virus has been estimated at 1.4 to 2.8, comparable to the original strain's R0 of approximately 2 to 3, indicating similar inherent transmissibility in the absence of interventions. Both pathogens spread primarily via respiratory droplets and aerosols, leading to rapid global dissemination, though 1918 occurred amid troop movements that accelerated transmission without modern air travel equivalents. Mortality patterns diverged sharply by age: the Spanish flu exhibited a W-shaped distribution, with excess deaths among young adults aged 20-40 years—often healthy individuals succumbing to a hyperinflammatory "" response—contrasting COVID-19's J-shaped curve concentrated in those over 70, driven by comorbidities and rather than robust immune overreactions in youth. Pathogenetically, secondary bacterial coinfections, such as with or , contributed to over 90% of 1918 fatalities via superimposed on viral damage, whereas deaths more often stemmed from direct endothelial and alveolar injury with less frequent bacterial superinfections, occurring in under 10% of severe cases. Non-pharmaceutical interventions (NPIs) like school closures, public gathering bans, and mask mandates proved effective short-term in both pandemics, reducing peak transmission by up to 50% in 1918 U.S. cities implementing layered measures early; analogous analyses confirmed NPIs delayed waves and lowered case rates, though adherence waned over time in both eras. Unlike 's prolonged lockdowns extending months or years in some regions, 1918 responses emphasized transient NPIs lasting 2-8 weeks per wave, correlating with faster societal resumption and minimal long-term economic scarring—U.S. GDP dipped modestly in 1918-1919 before rebounding by 1920, versus 's sharper contractions exceeding 10% in major economies with slower recoveries tied to extended restrictions. The 1918 pandemic lacked global coordination, relying on fragmented national or local efforts without organizations like the WHO, whereas modern incorporates 1918-derived lessons such as rapid viral sequencing—enabled by post-1918 advances—and stockpiled antivirals, though critiques highlight overreliance on predictive models that underestimated 1918's bacterial cofactors and overestimated uniform NPI scalability amid varying compliance.

Advances in Virology and Preparedness Lessons

The reconstruction of the 1918 H1N1 influenza virus marked a pivotal advance in , beginning with efforts in 1996 by Jeffrey Taubenberger and colleagues at Forces of , who extracted from preserved lung tissues of victims. By 2005, the full sequence was completed, revealing unique adaptations such as mutations in the (HA) and genes that enhanced replication efficiency and triggered excessive responses, contributing to the virus's lethality. This avian-origin strain's characterization via systems enabled safe laboratory recreation of the virus for controlled studies, elucidating mechanisms like the PB1-F2 protein's role in secondary bacterial infections and immune dysregulation. These insights directly informed vaccine development, as recombinant vaccines incorporating the 1918 HA protein demonstrated protection in animal models against lethal challenge, informing strategies for universal vaccines targeting conserved epitopes across H1N1 variants. Antiviral testing confirmed oseltamivir's efficacy; in models, the drug reduced viral loads and prevented severe disease from the reconstructed 1918 strain, though resistance mutations could emerge under selective pressure, underscoring the need for stockpiling and combination therapies. Such facsimile-based research has accelerated preclinical evaluation of broad-spectrum antivirals and adjuvanted vaccines, enhancing preparedness for zoonotic threats. Key preparedness lessons from the 1918 pandemic emphasize robust of viruses in animal reservoirs and human populations to detect antigenic shifts early, as coordinated monitoring informs and prepandemic production. While international cooperation through networks like the WHO's Global Surveillance and Response System is essential for and strain distribution, historical and recent politicization—such as delayed reporting or origin disputes—has eroded trust, highlighting the causal importance of transparent, apolitical mechanisms to avoid amplifying transmission via withheld information. Empirical analyses of 1918 responses affirm the mortality benefits of non-pharmaceutical interventions (NPIs) like school closures, public gathering bans, and when implemented early and in layers, as evidenced by lower peak death rates in U.S. cities such as compared to . Recent 2020s studies, revisiting these data, indicate NPIs flattened mortality curves without imposing lasting economic penalties; cities with stringent measures experienced similar medium-term recoveries to those without, countering claims of inevitable trade-offs and supporting evidence-based calibration over indiscriminate shutdowns or panic-driven policies. This underscores causal realism: pandemics inherently depress output via workforce morbidity, but targeted NPIs mitigate deaths while preserving resilience through adaptive enforcement.

References

  1. https://www.[ancestry.com](/page/Ancestry.com)/c/ancestry-blog/the-killer-flu-how-did-the-1918-pandemic-affect-your-family
  2. https://www.[researchgate](/page/ResearchGate).net/publication/267908581_Estimate_of_the_Reproductive_Number_for_the_1918_Influenza_Pandemic
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