It was a global catastrophe – this airborne virus affected every continent, including the Arctic and remote Pacific Islands, and between the first recorded case in March 1918 and the last in March 1920 an estimated 500 million people were infected worldwide (around one third of the world’s population) and 50 – 100 million people died (three to five percent of the global population). The virus killed more than the First World War, likely even more than the Second World War and possibly even more than the two wars combined. It is believed that more people died of influenza in the single year of 1918 than in the four years of the Black Death from 1347 to 1351.
Whereas most influenza outbreaks occur in the winter and disproportionately kill juvenile, elderly or already at risk and weakened patients, by contrast the 1918 pandemic was worst in the summer and autumn and predominantly killed previously healthy young adults. Those aged 75 or above had the lowest death rate of all. Some postulate that the strong immune reactions of young adults ravaged the body, whereas the weaker immune systems of children and the middle-aged or older resulted in fewer deaths amongst these groups.
The pandemic first appeared in late 1917 and early 1918, near the end of the First World War. Whilst the origins and causes of the outbreak are still debated, the consequences of war – malnourishment, overcrowding, overloaded medical camps and hospitals and poor hygiene – are one of the explanations for the spread of the virus. The most recent investigations have determined that the viral infection itself was not any more aggressive than previous influenzas, but that these special circumstances promoted bacterial superinfection. Spread by an infected person sneezing or coughing, the close quarters and huge troop movements of World War I hastened the pandemic. Soldiers were especially susceptible as their immune systems would likely have been weakened by malnourishment and the stresses of combat and chemical attacks.
Troops travelling home by boat and train at the end of the war then took the flu into the cities, where it began to spread to the countryside as a result of increased travel and mobility. Modern transportation systems in the early 20th century and greater international trading made it easier for soldiers, sailors and civilian travellers to spread the disease.
Once the virus struck, onset was devastatingly quick. Within hours of the first symptoms of fatigue, fever and headache, some victims would develop pneumonia and start turning blue as a result of a lack of oxygen. They would then struggle for air until they suffocated to death.
There is little unanimity about the source of the outbreak. Some believe that the flu originated in the US when a feverish soldier, Albert Gitchell, reported to the infirmary at training facility Camp Funston in Fort Riley, Kansas in March 1918. By noon the same day 107 patients had been admitted with similar symptoms and within five weeks 1,127 out of 26,000 men in the camp were infected. However, others report there had already been a wave of influenza through at least 14 US military camps by late 1917 and an outbreak of influenza in Haskell County, Kansas, so severe that local physician Loring Miner alerted the US Public Health Service.
Another influential inquiry pinpoints a major troop staging and hospital camp in Étaples, France as being the origin of 1918’s flu pandemic. The conditions at the overcrowded camp and hospital – which treated thousands of casualties of war and victims of chemical attacks – was ideal for the spread of a respiratory virus as over 100,000 soldiers were in transit every day. It was also home to a live piggery and poultry was regularly brought in from the surrounding villages, giving rise to the hypothesis that a significant precursor virus, harboured in birds, mutated to migrate to pigs that were kept near the front line and eventually passed to human beings.
Others suggested that the flu originated in East Asia, Brest in France and Austria, as early as 1917. Most recently, in 2014, historian Mark Humphries put forward the theory that source of the pandemic could have been the mobilisation of 96,000 Chinese labourers to work behind British and French lines on the Western Front – a similar respiratory illness had struck northern China in November 1917.
In April 1918, American troops arrived in Europe. Around this time soldiers in the trenches in France started becoming ill with ‘la grippe’, complaining of sore throats, headaches and a loss of appetite. Although highly infectious, recovery was, at first, swift with doctors calling it ‘three-day-fever’. But it quickly became clear that this was no ordinary flu. The first wave of what would eventually become a pandemic had arrived.
The drama of the war served to obscure the unusually high mortality rates as at this stage the illness was not very well understood and deaths were often attributed to pneumonia.
In August 1918 a more virulent strain appeared simultaneously in Brest, France; in Freetown, Sierra Leone; and in Boston, Massachussetts in the US. It also spread through Ireland, carried there by returning Irish soldiers. This second wave was far more deadly than the first, having mutated to a much deadlier form. Again, this was attributed to the circumstances of the First World War. In civilian life, natural selection favours a mild strain as those who get ill stay at home and those who are mildly ill continue with their lives, preferentially spreading the milder form. In the Western Front trenches, however, natural selection was reversed. Soldiers with a mild strain stayed where they were whereas the severely sick were sent on crowded trains to field hospitals, spreading the deadlier strain. By September 1918 the pandemic was about to enter its most lethal phase – the 13 weeks between September and December 1918 would prove to be the costliest in lives, with October 1918 the most deadly month of the whole pandemic.
New cases dropped abruptly after the lethal second wave struck in 1918 – theories for this range from the virus mutating again rapidly to a less lethal strain, or that doctors got better at treating and preventing the pneumonia that developed after victims contracted the virus. Either way, the disease which had wreaked such havoc disappeared almost as quickly as it had arrived. Despite a third wave striking in early 1919, it died away swiftly.
Spanish Flu was NOT so-called because the flu was first recorded in Spain (contrary to reports at the time). Although Spain was seriously affected as the illness swept Europe – one of the earliest casualties was the King of Spain and it left an estimated eight million people dead – Spain being especially hard hit was a false impression. To maintain morale during wartime censors minimised reports of illness and mortality in the United Kingdom, Germany, France and the United States. As Spain was neutral, papers were free to report the virus’s effects, thereby giving rise to the pandemic’s nickname ‘Spanish Flu’ which was first used in a British Medical Journal paper. Offended by this slander, Spaniards referred to the illness as the ‘Naples soldier’. The German army called it ‘Blitzkatarrh’ and British troops referred to it as the ‘Flanders grippe’ or ‘Spanish lady’.
In Britain, the port of Glasgow was the first place to record the flu in May 1918. Young women, especially those working in factories were the worst affected. Within weeks the illness had spread south reaching London by June. Although by August it seemed to be a spent force, it returned with a vengeance in October and spread at an alarming rate. Not restricted by location, gender or class, anyone could catch it – Prime Minister David Lloyd George contracted it, but survived. So did war poet Robert Graves, although when he returned from Limerick to his home in Hove, he promptly infected his entire household.
Although recognised as contagious Spanish Flu was not mentioned in parliament until October 1918, and there was no strategy for tackling it. Back then there was no National Health Service, so the response was decentralised and uncoordinated.
Local authorities and the press did offer some advice to prevent its spread, such as catching later trains to avoid crowds, wearing extra layers, thoroughly washing drinking glasses, giving up shaking hands and giving up kissing. The focus was on minimising the risk of infection through contact. Posters were displayed in towns, health visitors and school nurses distributed leaflets, buildings were disinfected and fumigated, schools were closed and public spaces, such as cinemas, were required to be ventilated at regular intervals. Some theatres even banned children and removed all carpets.
Nevertheless, some advice (such as ‘clean your teeth regularly’, ‘eat plenty of porridge’) was useless and often recommendations were difficult to put into practice. Overcrowding and insanitary conditions made isolation, ventilation and cleanliness virtually impossible.
The spread of the disease was compounded further by several other factors. A vast number of medical staff had been diverted by the First World War and those not in military service (usually over 50 years old and often lacking up-to-date training) were run off their feet. Hospitals were overwhelmed and medical students were drafted in to help, yet there was little they could do as there were no treatments for the flu and no antibiotics to treat the pneumonia. Furthermore, a shortage of undertakers and gravediggers led to bodies lying unburied for days at a time and many funerals taking place at night – the flu really could not have struck at a worse time.
By the end of summer 1919 when the pandemic had subsided a quarter of the British population had been affected and 228,000 people in Britain had died.