The Spanish flu was an influenza pandemic caused by an unusually virulent derivative of the influenza virus (subtype AH1N1) that spread in three waves between 1918 – toward the end of World War I – and 1920, claiming between 20 million and 50 million lives in a world population of about 1.8 billion, according to the WHO; estimates range up to 100 million.This means that more people died from the Spanish flu than in World War I (17 million). A total of around 500 million people are thought to have been infected, resulting in a lethality rate of 5 to 10 percent, which was significantly higher than for illnesses caused by other influenza pathogens.
A special feature of the Spanish flu was that it mainly affected people between 20 and 40 years of age, whereas influenza viruses usually posed a particular threat to young children and the elderly. The original reservoir of the pathogen was formed by waterfowl, possibly in recombination with gene segments from swine influenza viruses. Variants of the AH1N1 subtype caused the Russian flu outbreak in 19771978 and the “swine flu” pandemic in 2009. Asian flu (1957) and Hong Kong flu (1968) were based on other subtypes, but the majority of internal genes originated from the Spanish flu virus, which is why it was referred to as the “mother of all pandemics” as recently as 2006.
The name “Spanish flu” arose after the first news about the epidemic came from Spain; as a neutral country, Spain had relatively liberal censorship during World War I, so that reports about the extent of the epidemic were not suppressed there, unlike in other affected countries. The Reuters news agency reported on May 27, 1918, that Spain”s King Alfonso XIII had fallen ill. The Agencia Fabra cabled Reuters in London:
Influenza became fully “Spanish” when, on June 29, 1918, the Spanish health director Martín Salazar announced that he had no reports of a comparable disease in the rest of Europe. From the end of June 1918, the international press increasingly used the term “Spanish flu,” which was also promoted by some warring governments to cover up the actual spread.
In Spain, the disease was initially called Soldado de Nápoles (Soldier of Naples) because it spread as quickly as a song of that name, which was very popular at the time and had first been sung in Madrid on March 1, 1918, shortly before the outbreak of the pandemic, in the zarzuela La canción del olvido (Engl: Song of Forgetfulness, composer: José Serrano Simeón). In contemporary Spanish sources, the term Spanish flu only appeared when authors complained about it. Contemporary Spanish observers probably correctly assumed that the pathogen had been introduced from France, since in the winter of 191718 some 24,000 Spaniards were working in France, 9000 of whom had returned by the time the epidemic broke out. Today, the pandemic in Spain is usually referred to as “Pandemia de gripe de 1918” and rarely as “Gripe española.”
USA and Great Britain
Regardless of the misleading name, most scientists today assume that the pandemic originated in the U.S., but this no longer influenced the naming. The U.S. was in the midst of a massive rearmament process of its pre-war small army in 1918. One of these training camps was Fort Riley in Kansas, where 50,000 men were stationed for military training. This was the place where, on March 4, a soldier was taken to the infirmary with a fever. Within hours, more than a hundred other soldiers fell ill with similar symptoms. In the weeks that followed, the number of cases continued to rise. In April, additional American troop contingents arrived in Europe, bringing the virus with them. The first wave of the pandemic had arrived.The increased mobility due to the war, which was atypical for that time, thus favored the worldwide spread. U.S. soldiers called it three-day fever or purple death (because of the discoloration of the skin), British soldiers called it flu or “Flanders flu” because of the infection in the trenches of Flanders.
Although the German press was not allowed to report on illnesses at the fronts, it was allowed to report on civilian victims from the beginning of June 1918 – even on the first pages of the newspapers. In Germany, it was occasionally called “lightning catarrh” or “Flanders fever.” Other names were Spanish disease, influenza, pneumonia, pneumonic plague.
French military doctors initially spoke in a veiled way of maladie onze (disease eleven). Today, the terms espagnole influenza or pandémie grippale de 1918 are generally used.
Where the Spanish flu first manifested itself is not entirely certain. This is largely to be seen against the background of the First World War. Thousands of soldiers were dying weekly in the fighting in Europe at this time, especially on the Western Front. Both the press and local health authorities therefore focused little on the first cases of influenza in the spring of 1918, especially since only a few people succumbed to the disease during the first wave.
As part of wartime propaganda, the Allied press speculated at the beginning of the pandemic that the infection originated from German submarines and from German prisoners of war, or was even triggered by Germany in a planned manner, for example via the German drug aspirin or via poisoned canned fish. The former was supported, among other things, by illnesses on German submarines interned in Spain, such as on the infamous SM U 39 berthed in Cartagena. The New York Times called for the pandemic to be renamed “German flu.” Moreover, since Germany had begun waging war with poison gas in 1915, suspicions were formulated that it had now also initiated biological warfare and was releasing the “microbes” in a planned manner. When it became clear at the end of June 1918 that German troops were also affected by the pandemic with a time delay, these theses died down.
Possible starting point China
Apart from the propaganda theories, the place of origin was initially suspected to be China. An epidemic had broken out in Harbin in October 1910, with symptoms similar to those of the Spanish flu, as was noticed as early as 1918. In December 1917, there was an outbreak of another respiratory disease in northern China, again with similar symptoms, which lasted until April 1918 and claimed about 16,000 lives. Beginning in late 1916, China sent laborers to Europe for the Allies through the Chinese Labor Corps (CLC), totaling about 185,000 men. The CLC was recruited mainly in the provinces affected by the second outbreak, Shantung, Hopei, and Shanxi, concentrated in barracks camps in the British East China leasehold area of Weihaiwei, and shipped mostly across the Pacific to Canada, by rail to the Canadian East Coast at Halifax, or later to New York and from there to France. Among both the soldiers guarding the Chinese on Vancouver Island and the CLC itself, symptoms of influenza-like infection were observed in increasing numbers, and fatal pneumonias also occurred. In 1918, there were 17 camps in the Nord-Pas de Calais region, numbering up to 96,000 men. The CLC headquarters was at Noyelles-sur-Mer, and the main camps were at Boulogne-sur-Mer, Wimereux, and Etaples, where the Chinese performed the unloading of British ships. However, this theory cannot provide more than circumstantial evidence, especially since it could not be clarified what kind of disease broke out in Shanxi at the end of 1917. Apart from that, the initially relatively low number of victims in the CLC speaks against this hypothesis of origin, which only increased after that of the Allied soldiers stationed nearby.
Possible starting point North France
Another theory is that the epidemic originally broke out in a very large troop camp near the French town of Étaples, where a good 100,000 people were present every day, including Chinese from the CLC. In December 1916, influenza was rampant in this camp and was similarly observed in the military bases at Rouen and Aldershot. Doctors at the time referred to it as “purulent bronchitis,” and autopsies found findings similar to those later seen in Spanish influenza. The delay before the outbreak of the actual pandemic could be explained by the fact that the virus at that time had survived in the context of small, limited epidemics and had developed its high virulence during this period as a result of molecular changes.
Probable starting point United States
The third, currently most probable hypothesis is that the first virulent outbreaks of influenza occurred in the USA in January 1918 and were spread worldwide from there by troop movements – the American Expeditionary Forces in Europe were being massively reinforced at that time. It was established as early as the 1940s by the Australian Nobel Prize winner for medicine Frank Macfarlane Burnet and later extensively substantiated by the U.S. historian Alfred W. Crosby. Research by evolutionary biologist Michael Worobey now also supports this thesis: seven of the virus”s eight genes bear a strong resemblance to influenza genes found in birds in North America. In addition, a genetic link to equine influenza, which was rampant in the U.S. in 1872, among other things, could be identified, which fits in with reports of equine influenza spreading simultaneously with Spanish flu in the cavalry stables of the warring armies.
The main specific symptoms resembled those of other influenza diseases:
Postmortem examinations showed that the respiratory tract was frequently affected in those who died of influenza, occasionally also the mediastinum. Inflammatory foci were found within the lungs, mostly in the lower lobes, and in many the pleural cavity was suppurated. The spleen was often enlarged, more rarely the liver, it and the kidneys sometimes showed damage, the meninges often irritation.
As part of a study at the University of Zurich, 411 autopsy reports on Spanish influenza were evaluated: No reports mentioned visible blood clots, which the authors point out as a major difference from Covid-19: 36 percent of the 75 Covid-19 autopsies published to date report pulmonary artery thrombosis, or pulmonary embolism, even though these patients received thromboprophylaxis.
Diagnosis was not always easy, as the symptoms observed varied, with some patients suffering mainly from pain in the limbs. Due to the severe shivering of many patients, Spanish doctors initially suspected malaria or typhus abdominalis.
Survivors were often marked by severe fatigue and chronic exhaustion for weeks, and it was not uncommon for depression to occur as a consequence. Those who survived pneumonia often faced a long and arduous convalescence.
As a consequence of influenza infection, many people suffered neurological dysfunctions for the rest of their lives; pathologists repeatedly described encephalitis haemorrhagica acuta, at that time called fleabite encephalitis, and its consequences. Furthermore, a notable accumulation of cases of encephalitis lethargica was observed. This is a form of encephalitis that caused lethargy, uncontrolled sleep attacks, and a temporary disorder similar to Parkinson”s disease and, in some cases, permanent postencephalitic parkinsonism. However, a direct association of encephalitis lethargica with Spanish influenza has not been demonstrated; no evidence of influenza virus was found in tissue samples examined by McCall et al. in 2001 and Lo et al. in 2003.
The routes of transmission corresponded to those of influenza in general; the virus entered the body primarily by droplet and contact infection via the mucous membranes of the respiratory tract, mouth, and eyes. The same applies to the environmental stability of the virus; only at temperatures above 22 °C does this decrease significantly, and it is sensitive to detergents and organic solvents.
Spanish influenza occurred in three waves: in the spring of 1918, in the fall of 1918, and in many parts of the world again in the spring of 1919. The first wave of spread in the spring of 1918 did not show a noticeably increased death rate. It was not until the autumn wave of 1918 and the later, third wave in the spring of 1919 that exceptionally high lethality was associated. At the peak of the “autumn wave,” the Prussian and Swiss health authorities estimated that two out of three citizens were ill.
From the fall-winter of 1918, between 20 million and 50 million people died worldwide; conjectures range up to 100 million. This means that more people died from the Spanish flu than in the First World War (17 million).
The world population at that time was about 1.8 billion, so it lost about one and a half to 2.8 percent. As a rough generalization, influenza mortality was lowest in highly industrialized countries, at about 0.5 percent, and more than 0.6 percent in the United States as a starting point. In less economically developed countries in Europe or outside, mortality was usually above one percent, and in Mexico, for example, it was above three percent. In Italy, there were regions with extremely high mortality rates, most notably Lazio, Calabria and Emilia. Most affected were nations that had a high proportion of indigenous people. On some small islands in the Pacific, more than 20 percent of the inhabitants died. Only very small, isolated islands such as St. Helena escaped the pandemic altogether.
The exact number of people who died from the flu can no longer be determined, as it also affected remote regions and in countries such as Russia, the number was not reliably recorded due to the post-war and civil war turmoil. The U.S. Army lost about as many infantry soldiers to influenza as it did to combat operations during World War I. About 675,000 died in the U.S. and about 300,000 in the German Reich. In India alone, 17 to 20 million people are believed to have died from the Spanish flu, which seems well supported by the subsequent 1921 census.
The time span of only one year for the occurrence of three pandemic waves is a peculiarity of Spanish influenza. In other influenza pandemics, such as 188990, intervals of eight to nine months between waves have been observed. The cause of these “compressed” waves is unclear. Numerous anecdotal reports, as well as statistical data from Spain, indicate that people who were ill during the first wave enjoyed relative protection against recurrence in the second wave.
The lethality of this form of influenza virus remains unclear because there are no exact data on the number of people who have become ill; it is thought to be higher than 2.5 percent. Other influenza pandemics have a lethality of less than 0.1 percent.
The baseline epidemic reproduction number was 2 to 3.
The first wave (spring and summer 1918)
The flu epidemic probably began in Haskell County in the U.S. state of Kansas. At the beginning of 1918, the country doctor Loring Miner treated numerous patients there whose flu symptoms were considerably more severe than had previously been known. Miner described the course of the disease as rapid and occasionally fatal. The local paper, the Santa Fe Monitor, reported widespread pneumonia as early as mid-February and, a few days later, that “almost everyone in the country has influenza or pneumonia.” Miner was so concerned about this outbreak of illness that he contacted the United States Public Health Service (PHS), but they did not respond to his request for assistance. However, the report of a form of influenza with an unusually severe course was reflected in the Public Health Reports of the PHS on April 5, 1918: “On March 30, the occurrence of 18 cases of influenza of a severe type was reported from Haskell, Kansas, resulting in 3 deaths.” Thanks to this report, medical history has been able to reconstruct a possible course of infection. Evidence shows that at least three people from Haskell County were drafted to the U.S. Army training camp Camp Funston in late February. On March 4, the kitchen sergeant (mess sergeant) became ill with influenza. He suffered from a sore throat, fever and headache, the typical signs of the flu.Hundreds of other soldiers showed the same symptoms and filled the emergency hospital within hours. Gitchell was not the first patient to be infected by the Spanish flu, but he was the first to be recorded. even though by this time the disease had already reached New York and significantly increased mortality rates from respiratory illnesses had been reported in the U.S. Army since December 1917.
Three weeks later, the training camp, which housed an average of 56,000 recruits, had 1,100 seriously ill and 38 deaths. Soldiers referred to the illness as three-day fever or knock-me-down fever. The disease spread very quickly from the training camp, which was part of the Fort Riley military base.
Outbreaks occurred at other military camps in mid-March, including Camp Forrest in Tullahoma, Tennessee, and Fort Oglethorpe, Georgia. The disease spread from the camps to the civilian population. Of the 1,900 inmates at San Quentin Prison in California, close to 500 fell ill. Flu outbreaks accompanied by life-threatening pneumonia quickly swept the country, and influenza mortality rose markedly in the major cities of the Atlantic coast, in some cases even before the striking outbreaks in the military camps. Thus, already on February 1, 1918, the famous silent film actor Joseph Kaufmann died in New York, and in April his parents.
From the time of the influenza outbreak in Kansas until August 1918, more than a million American soldiers arrived in Europe; there had never before been such heavy traffic between the New and Old Worlds. World War I thus accelerated its global spread. On the other hand, the British naval blockade of Germany and the barrage of the Western Front may have slowed the spread to Germany. In addition, mobility within Europe was severely restricted by the war, especially between Germany and France, but this did not slow the spread of the epidemic from west to east. Possible explanations include spread via neutral states such as Switzerland, which was heavily affected at the time, through hand-to-hand combat, prisoners of war and looting of Allied casualties, or through air currents to the front lines, which were often only a few dozen meters apart at the time.
The disease apparently reached France on U.S. troop ships. For early April 1918, influenza cases are documented from the French port city of Brest, from where it spread both among the civilian population and among soldiers. In French military hospitals, the first flu-stricken soldiers were admitted on April 10. By the end of April, the flu epidemic had reached Paris. In the first two weeks of May 1918, the British Navy reported over 10,000 cases of illness and found itself unable to sail.
In German-speaking countries, the novel disease was reported at the latest in May 1918.
On June 6, 1918, influenza was first noticed among German troops in the front line area at the Ailette: “… the mass cases of influenza, which had hitherto occurred only among the contracting powers, were also spreading to the German troops.” Just one week later, the entire German Western Army was affected, and only two weeks later it spread to the whole of Germany; for example, it had reached Nuremberg on June 28.
In June, numerous cases were reported in India, China, New Zealand and the Philippines. In the port of Manila, more than two-thirds of dock workers fell ill, preventing ships from being unloaded. Global spread was accelerated by migration, troop movements, trade and colonialism.
Denmark and Norway were particularly affected in July; in the Netherlands and Sweden, the peak of the first flu wave was in August. In Australia, 30 percent of Sydney”s population contracted influenza in September.
On July 13, 1918, an article appeared in the British medical journal The Lancet in which three physicians speculated that the current epidemic might not be influenza because the course was so short and very often also without complications. They were apparently unaware at the time that there were already striking exceptions to the largely harmless course. At the end of May 1918, in a small French military camp, almost five percent of the soldiers stationed there died of influenza or its consequences. In Louisville, Kentucky, the pattern that from today”s perspective is one of the characteristic features of the Spanish flu already emerged: a good 40 percent of the fatalities belonged to the 20- to 35-year-old age group.
The wave of influenza, while not decisive in the war, further weakened German troops, who were in many respects badly battered, and can be seen as an accelerant to defeat. The German Spring Offensive of 1918 ran aground, and the final German offensive, after a counterattack on July 18, 1918, brought the final turn of the war in favor of the Allies. Ernst Jünger wrote in Stahlgewittern about the situation on the German front in July 1918: “The young people in particular died away overnight.” German General Erich Ludendorff, de facto head of the Supreme Army Command, cited in his war memoirs for June 13, 1918, that – in addition to the poor supply situation – influenza outbreaks in the troops had been a serious problem.
The second wave (“autumn wave” 1918)
The beginning of the autumn wave can be dated roughly to the second half of August 1918. The virus had undergone a small but momentous change between spring and fall: It was no longer as well adapted to birds but much better adapted to humans. Possibly, the flu first broke out on the Norwegian freighter Bergensfjord, which docked in Brooklyn on August 12, 1918, with 200 crew members ill. Earlier, four people who had died on board had already been turned over to the sea. Outbreaks followed more or less simultaneously in four port cities: Boston in the U.S., Brest (Aug. 22) on France”s Atlantic coast, Dakar in Senegal and Freetown, the capital of the then British colony of Sierra Leone in West Africa. The outbreak in Freetown coincided with the arrival of the British passenger ship HMS Mantua, converted into an auxiliary cruiser, on August 15, and that in Dakar with the arrival of HMS Ebro on August 19. Prior to that, influenza had broken out on both ships. By the end of September, two-thirds of Freetown”s population had contracted influenza. There were three fatalities for every one hundred people who fell ill. Since, according to consistent reports, the disease broke out around the Atlantic on each ship”s arrival, the contemporary impression was that the new wave of influenza had been brewing at sea.
Countless military hospitals and clinics around the world lacked nursing staff and space for beds. Fresh bedding was scarce, so the sick lay in dirty and bloodstained sheets. The dead piled up in the corridors of the morgue, and there was barely enough time to bury them.
In an attempt to contain the disease, senior military physicians tried to ensure that only the most necessary ship movements were allowed. Before leaving port, ships were to undergo quarantine to prevent sick people from being on board. However, the military physicians did not succeed in enforcing this measure. They received insufficient support either from Surgeon General of the United States Rupert Blue, who headed the U.S. Public Health Service, or from their own organization. The U.S. military successfully resisted this measure because troops fighting in Europe desperately needed reinforcements. This decision carried a high risk for the soldiers being shipped. For every 100 soldiers who fell ill on board a ship while transporting troops to Europe, six died: this meant that the lethality of those who fell ill on the ship was more than twice as high as on land.
Despite the quarantine measures initiated, the disease spread very rapidly. The number of deaths in the U.S. attributable to this flu epidemic rose from 2800 in the month of August to at least 12,000 deaths in September. Doctors from already affected cities in eastern North America sent grim reminders to their colleagues in the West:
In less than four weeks, the disease had spread to New Orleans, Seattle and San Francisco. The outbreak of influenza could occur very quickly. In a military base in Georgia, only two cases were reported on one day in September 1918, but 716 were reported the next day. One of the most severely affected cities in the U.S. was Philadelphia, where 711 people fell victim to the disease on a single day in October 1918. Since the city morgue was designed for a maximum of 36 dead, the dead had to be stored in four rows in corridors and rooms. A large military parade was still held in Philadelphia in the early fall of 1918, drawing large numbers of citizens to the streets and squares. The situation was similar in Boston. Within a week afterward, nearly 5,000 people died in Philadelphia, and 3,500 in Boston by mid-October. After six weeks, the number in Philadelphia was more than 12,000, more than eight times as many as in restrictive St. Louis, where authorities had relied on restrictions on public life and quarantine. Thus, schools, movie theaters, libraries and churches were closed. This St. Louis strategy is still cited as a successful method today.
According to a 2007 study in the Journal of the American Medical Association (JAMA) of interventions in 43 U.S. cities during the second wave in the fall of 1918spring of 1919, combinations of public interventions (nonpharmaceutical interventions, NPI), particularly school closures and bans on public gatherings (church, theater, and others), in effect for an average of four weeks, were associated with reductions in peak mortality rates and total deaths (excess mortality). This study reportedly played a role in the March 2020 measures taken in Germany against the Covid 19 pandemic, most notably on the decision to close schools.
Another 2007 study also showed that those U.S. cities that had taken a consistent combination of several different public policies early in the epidemic had half the peak mortality rate compared with cities that had not. Individual measures were not associated with a comparable lower rate. In many cases, face masks were also required to be worn. Violation was punishable by fines, for example. In San Francisco, an officer even shot a citizen for refusing to wear a mask.
During the week of October 17-23, 1918, 21,000 people died of influenza in the United States, which, with other deaths, resulted in the highest mortality ever recorded in a single week in the United States, an excess mortality of 63 percent. The Spanish flu burned itself into the collective memory of U.S. Americans: A total of about 675,000 civilians died in the United States, more citizens than U.S. soldiers on the battlefields of both world wars. In Montreal, Canada, where 201 people succumbed to the flu on October 21, priests administered last rites in the open street.
As in North America, the disease spread worldwide. The effects in Europe were followed less closely. As before, the First World War was more in the focus of the press and public attention.
In Germany, this was even more true. Since 1914, the German armies had been fighting unsuccessfully against the Allies, and the arrival of American soldiers on the continent massively changed the balance of power on the Western Front. In Germany, influenza was seen as a minor issue, because the poor supply situation with famine winters and political uncertainty also added to the problem. German physicians quickly noticed that a conspicuously large number of 20- to 40-year-olds were dying without symptoms of deficiency. This gave rise to the theory of an overreaction of the immune system in this inherently resistant group of people. This overreaction, now called “cytokine storm,” often triggers rapid death by suffocation. In the fall of 1918, Germany experienced considerable restrictions affecting the postal system, telecommunications offices and public transportation. “Flu vacations” in German schools were also widespread. Mines, factories, and agriculture were shut down, but responsibility for action was left to local governments, as regions were affected very differently. Assemblies, restaurant operations, and religious services were not suppressed throughout the German Reich. On October 9, 1918, General Erich Ludendorff blamed the looming defeat on the supply situation, the overwhelming superiority of the Allies, and the low fighting morale and poor condition of his troops, among other things, to Reich Chancellor Max von Baden, who himself had fallen ill with Spanish flu shortly thereafter. He named the rampant wave of influenza as one of several causes for the last two points. Although Ludendorff”s statements were primarily intended to distract attention from his strategic missteps by creating a legend, other reports also show that although the wave of influenza affected the German army less than, for example, the American forces, it had a greater impact due to the desolate situation of the German army. Between 500,000 and 708,000 German soldiers fell ill with the flu.
The Spanish flu hit Austria-Hungary when the monarchy was on the verge of collapse. Toward the end of World War I, many people were malnourished, undernourished, exhausted, depressed, demoralized or traumatized, making them vulnerable to infectious diseases. There was a shortage of medicines, doctors, and nurses. Public institutions were not fully capable of acting. In Austria, the pandemic killed about 21,000 people in 191819. Most of the Spanish flu fatalities were in the 15- to 40-year-old age group. The second wave was most severe in OctoberNovember 1918. In Austria, as the only and first country in Europe, Emperor Karl ordered the creation of a separate Ministry of Public Health in the fall of 1917. But it was not until July 30, 1918 that Johann Horbaczewski, a Ruthenian professor of medicinal chemistry at the Bohemian University in Prague, was appointed Minister of Public Health. Horbaczewski tried to appease, claiming that this epidemic was not pneumonic plague and generally took a benign course. His few activities showed all the powerlessness and helplessness at that time.
The first wave of influenza affected the Swiss population from July to August, the second wave from September to December 1918. According to official statistics, 24,449 people died of Spanish influenza in Switzerland between July 1918 and the end of June 1919. This corresponds to 0.62 percent of the total population in 1918. In national historiography, the Spanish flu appeared mainly in connection with the national strike in November 1918 and the casualties among the soldiers. In the absence of compulsory medical reporting, it is assumed that the number of unreported cases was high.
South America, Asia, Africa and the Pacific islands were severely affected. The pandemic claimed more than half of its victims in Asia. In India, the lethality rate was particularly high, with an estimated five deaths per hundred people infected. The death toll in India was estimated at up to 20 million people. This was exacerbated by the fact that India was ravaged by famine at the time. Many people moved from the rural regions to the larger cities in the hope of finding better supplies there. In the cramped conditions, the risk of infection was particularly high. The death toll in China was estimated at over nine million. In the areas of present-day Tanzania, Zambia and Mozambique, which had been damaged by the colonial wars and the world war, the epidemic also raged very strongly.
New Zealand was hit by the flu epidemic especially in Black November 1918, when the first troops returned. In New Zealand, 8573 people died of the disease, more than twice as many as New Zealand soldiers had died in the First World War. At the height of the crisis, all public life came to a standstill. The Māori were particularly hard hit by the flu epidemic. In remote Māori communities, the disease outbreak usually came without any warning. Often, so many were affected that no one was available to care for the sick or bury the dead. The course was similarly dramatic in Samoa, where one-fifth of the population, or 7500 people, died. The Samoa Islands aroused the interest of scientists insofar as in Western Samoa the population was reduced by 22 percent within a few weeks, while in American Samoa, about 70 kilometers away, the flu was practically non-existent, probably because of the rigid quarantine measures there.
The third wave (local flock 1919-1920)
In February 1919, another wave of influenza occurred, first in Great Britain and then, from May 1919, in other countries. It hit the USA mainly in the spring of 1920, but its course was not as deadly as the second one. Since it was mainly younger people who died, it is classified as Spanish flu.
End of the pandemic
During 1920, the virus became much less lethal and has since caused only normal seasonal influenza.
Subsequent influenza waves – for example, in Germany in the winter of 193233 – were of lesser magnitude and characterized by a different age distribution, so that they are no longer associated with Spanish influenza.
Quarantine measures had already been initiated by the health authorities in some countries at a very early stage. As early as the second half of August 1918, the Surgeon General of the United States had ordered health authorities in the USA to quarantine ships with sick people on board in all ports. However, because of the war effort, this proved almost impossible to carry out. In Toronto, Dr. Hastings, a health department employee, published advice on how to avoid infection. This included the recommendation to avoid crowds, to keep one”s mouth, skin, and clothes clean at all times, and to leave windows open as much as possible. People were to keep cool when walking and warm when driving or sleeping. Hands should be washed before eating and food should be chewed well. The accumulation of digestive products in the body should be avoided, and one should drink a glass or two of water directly after getting up. Towels, napkins and cutlery used by others should be avoided. Likewise, one should refrain from wearing too tight clothing, shoes or gloves.
In New York, spitting in the street was made a punishable offense. About 500 people were arrested for violating it. Other cities mandated the wearing of mouth guards and threatened fines for those who violated them. The New York Health Board underscored the requirement with the slogan “Better be ridiculous than dead.”
The non-drug treatment methods, which included dietary, physical and naturopathic measures, plus hot air and electric light baths, sweating and Prießnitz cures, baths, packs and compresses, were mostly ineffective. The same was true of the multitude of questionable medicines recommended to the medical profession in numerous essays: Malafebrin, Vioform, Sublimate, Creosote. In view of the culminating health catastrophe, there was no time for critical drug testing.
Since effective specific remedies were not available, physicians concentrated on alleviating symptoms: antipyretic therapy was already in the foreground during influenza in 188990, and many a febrifuge experienced an astonishing renaissance in 191819, not only the old familiar quinine, but also the pharmaceutical specialties antipyrine, salipyrine, antifebrine and phenacetin. Since the 1890s, pyramidone and acetylsalicylic acid have been triumphant. The latter now became the central drug in the fight against Spanish flu. If a strong sedative and antineuralgic effect was desired in severe cases, the physicians of 1918 resorted to substances such as opium, morphine, heroin or cocaine.
For the annoying, often agonizing irritating cough, narcotic and anesthetic cough suppressants were available, such as codeine, the subcutaneously injectable opium extract Pantopon, or glycerin preparations for inhalation. Camphorbenzoe, eucalyptus oil or ipecacuanha powder were prescribed as expectorants. A guiding principle of symptomatic influenza treatment was the maintenance of cardiovascular function, especially in cases of life-threatening pneumonia, for which digitalis, strophanthin, caffeine, strychnine, and camphor were used, and in special cases adrenaline. Oxygen inhalation was used to relieve respiratory distress, but its side effects limited its value. Advertisements in newspapers touted fig syrup or eucalyptus ointments as remedies. Antiseptic sprays were supposed to keep the mouth and nose clean.
Great, but ultimately vain, hopes were placed in specifically effective chemotherapeutics such as the syphilis drug Salvarsan and its successor Neosalvarsan, in colloidal silver preparations such as Kollargol, Septargol, Elektrargol and Fulmargin, and finally in the diuretic Urotropin, which had proven its worth in urology and whose germicidal effect on staphylococcal and streptococcal infections was beyond question. The quinine derivatives eukupin, optochin and vuzin were widely used, but without resounding success.
A secondary study of 55 publications in the British Medical Journal between July 1918 and October 1920 showed, among other things, that a mixture of three different bacterial vaccines was effective against the then still unknown pathogen of Spanish influenza; complications and deaths from influenza actually caused by a virus fell significantly. This can be explained by the fact that the severe courses were mostly characterized by secondary bacterial infections.
Answers to these questions are sought, among others, in the previous influenza exposure of the different age groups. One possible explanation for the anomalies is a virus circulating before 1889 that may have caused partial immunization. One problem with this conjecture, however, is that this precursor virus would have disappeared around 1889 but reappeared nearly 30 years later. Another explanation is based on the doctrine that the immune system responds particularly effectively to the first variant of a virus with which it is confronted, and is thus less well adapted to different strains of pathogens. If the so-called Russian flu of 1889-1895 was indeed not based on the coronavirus HCoV-OC43 but on the influenza virus subtype AH3N8 (see above), and people belonging to the age group between 20 and 40 years in 1918 came into contact with influenza for the first time at that time, then they would not have had an adequate immune defense against the Spanish flu. The very elderly, on the other hand, may have had relative protection because they had previously been exposed to influenza more similar to Spanish influenza. However, clear evidence for this is lacking.
According to Gibbs et al. in Spektrum der Wissenschaft of January 2006, one factor in the unusual distribution was also the atypically strong cytokine activity induced by the virus. The overreaction of the immune system in the form of a cytokine storm induces defense cells to attack lung tissue. Since the group of 20- to 40-year-olds has a particularly active immune system, the expression of the cytokine storm is especially strong here. The cytokine storm would be a parallel to COVID-19 disease, which is just as easily transmissible, but in February 2020 was still estimated to be one step lower in clinical severity than Spanish flu. It is now thought to be potentially equivalent in clinical severity as well. Both diseases are viral zoonoses of the respiratory tract that were or are spread primarily by droplet infection. The pathophysiologic mechanisms are related; both pathogens bind to the same ACE-2 receptors in respiratory and intestinal mucosa. However, in contrast to Spanish influenza, Covid-19 has so far shown no reduction in lethality in older age groups, but a significant increase.
In 1951, Johan Hultin, then a doctoral student and later a pathologist, had exhumed tissue samples from a mass grave of influenza victims in the permafrost of Alaska, but was unable to detect influenza viruses. In 1997, he obtained permission from the community, located on the Seward Peninsula, to exhume again. Samples of lung tissue were taken from four of the dead, and fragments of the influenza virus genes were isolated from one of them. Finally, it was possible to sequence the complete genome of the Spanish flu pathogen. The same group of researchers at the U.S. Armed Forces Institute of Pathology in Rockville, under the direction of Jeffery Taubenberger, also isolated portions of the influenza virus from various tissue samples preserved by the U.S. Army from World War I in 1996 and 1997.
In 2003, Reid et al. confirmed that the virus belonged to the influenza A viruses. In 2004, Gamblin et al. showed how the Spanish flu virus binds to human cells by structural analysis of hemagglutinin H1.
In October 2005, U.S. scientists led by Jeffery Taubenberger reported that they had reconstructed the 1918 virus in a high-security laboratory at the CDC (Centers for Disease Control and Prevention) in Atlanta. Taubenberger and his team published their research, which began in 1995, in a series of articles beginning in 1997 and culminating in the publication of the complete gene sequence in the journals Science and Nature in 2005.
Based on their analyses, the researchers concluded that the RNA polymerase of the human influenza virus was directly derived from an avian influenza virus and that the transition to humans probably occurred just before the pandemic began. Because of the close resemblance to known avian influenza variants, they further argue that the virus achieved its dangerousness as a result of a few mutations and not through an exchange of genetic material with previously existing human influenza variants, i.e., not through reassortment (see also antigenic shift in influenza viruses).
In animal experiments, the reconstructed virus proved to be extremely aggressive (as expected from the high death rates of the 1918 epidemic): it killed mice more rapidly than any other human influenza virus known to date and – unlike most human influenza viruses – was also lethal to chicken embryos. Unlike other experiments with mice, the reconstructed virus did not have to be adapted to mice for this purpose. This shows that the proteins hemagglutinin as well as possibly the neuraminidase of the virus contain virulence factors for mice. Its polymerase genes were similar to those of AH5N1 and other avian influenza viruses. It also proved to be highly proliferative in epithelial cells from human bronchi, which would lead to pneumonia in the functioning organ. In addition, unlike influenza viruses circulating today, it is able to replicate without trypsin, which requires a previously unknown mechanism of neuraminidase that facilitates cleavage of hemagglutinin.
Previously, the active virus had been made available only to a scientist at the CDC. Since late October 2005, the Centers for Disease Control and Prevention has been shipping the Spanish flu virus to all interested Biological Protection Level 3 laboratories.
In 2007, it was revealed by researchers at St. Jude Children”s Hospital, Memphis, Tennessee, that a viral protein only 90 amino acids in size, designated PB1-F2, appears to be responsible for the unusually high lethality.
Since the publication of the results of the study by Taubenberger and his colleagues in 2005, virologists have been increasingly warning of a new pandemic that could surpass the Spanish flu many times over due to the incomparably higher spatial mobility compared to 191820.
Among the fatalities of the Spanish flu were Egon Schiele and his wife Edith, Max Weber and Frederick Trump, Donald Trump”s grandfather, as well as Mehmed V, Sultan and thus head of state of the Ottoman Empire, and the last Emperor of Austria Karl I. Franz Kafka”s pulmonary tuberculosis, which had been largely dormant in 1918, may have been given its fatal twist by the Spanish flu.
Effects on political and historical events included the illnesses of President Woodrow Wilson and his advisor Edward Mandell House during the deliberations on the Versailles Peace Treaty, since Wilson, unlike representatives of other victorious powers, was anxious for a settlement, and that of Max von Baden, the last Chancellor of the German Empire, which led to a delay in important political decisions at a particularly critical time.
In October 2019, the first monument erected in Germany to commemorate the Spanish flu was unveiled in Wiesloch (Baden-Württemberg). The focal point is the old gravestone of the victim Anna Katharina Ritzhaupt, who died in 1918 at the age of 24.
The speed at which the Spanish flu spread was reflected in the nursery rhyme “A bird named Enza.”