THE SPANISH FLU

Today is the 100^th anniversary of the ending of the Spanish Flu.

It is ironic when you think about it.  Most of us who were born after 1918 would not be alive today if our parents died from that particular flu in 1917. 

My father was born in 1906 and my mother was born in 1912 If they had later died from that particular flu just as 50,000 Canadians died and just as many as 20 million people (about one-third of the planet’s population) died world-wide, I and my brother would not have been born. And that goes for our children and grandchildren and eventually, their children and those that follow them.

It is also ironic that if the Spanish Flu didn’t spread around the world like it did, the population today would be more than 8 billion people instead of the current 7 billion since millions of babies would have been born in 1917 when the Spanish flu began circulating world-wide.

That particular flu brought about the fastest and most violent loss of civilian life in modern times just like the Black Death did in the Sixteenth Century.  It began in early 1917 and continued to December 1918.

Canadian soldier, Arthur Lapointe was climbing out of a dugout on the Western Front in Europe when the Spanish Flu struck him with the force of a bullet. “As I reached the top my head, it  swimming with sudden nausea, everything around me whirls, I falter, then fainting, fall headlong to the ground. I feel sick and think I am going to die,” he wrote later. Lapointe was among 45,000 deployed Canadian soldiers stricken with the flu, of whom more than 700 would die. The disease was so brutal that, according to historian Tim Cook, many soldiers compared it to the aftermath of a poison gas attack. Lapointe recovered, but only when he returned home did he discover that three of his brothers and two of his sisters had died of the same disease.

Respiratory symptoms of Spanish influenza include cough, sore throat, runny nose, nasal congestion and breathing problems. Although similar symptoms are seen with all influenza viruses, they are particularly severe with the Spanish influenza. The Spanish influenza was similar to the seasonal influenza, which includes fever, fatigue, muscle and joint pain, headache and lack of appetite. 

When an infected person sneezes or coughs, more than half a million virus particles can be spread to those close by. 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 increased the lethality of the virus. Some speculate hat the soldiers' immune systems were weakened by malnourishment, as well as the stresses of combat and chemical attacks, increasing their susceptibility.

In a 2006 study in the journal Nature, researchers using molecular genetics techniques demonstrated that the Spanish influenza triggered exceptionally high and sustained expression of pro-inflammatory cytokines and chemokines by the immune system, accounting for the relative severity of Spanish influenza symptoms compared to other flu viruses.

What is the role of cytokines in the immune system? They communicate our immune cells by using cytokines, which are a group of proteins secreted by cells of the immune system that act as chemical messengers. Cytokines released from one cell affect the actions of other cells by binding to receptors on their surface. We can think of these receptors as deliverymen.

The flu virus is primarily spread by tiny droplets formed when infected people talk, cough or sneeze. These droplets are either inhaled by others or land in the mouths or noses of nearby people up to 6 feet away.

Scientists offer several possible explanations for the high mortality rate of the Spanish influenza pandemic. Some research suggests that the specific variant of the virus was unusually aggressive. One group of researchers recovered the virus from the bodies of frozen victims, and transfected animals with it, causing a rapidly progressive respiratory failure and death through a cytokine storm (overreaction of the body's immune system). It was postulated that the strong immune reactions of young adults ravaged the body, whereas the weaker immune systems of children and middle-aged adults resulted in fewer deaths among those groups.

In 2007, analysis of medical journals from the period of the 1918 pandemic found that the viral infection itself was not more aggressive than any previous influenza, but that the special circumstances of the epidemic (malnourishment, overcrowded medical camps and hospitals, poor hygiene) promoted bacterial superinfection that killed most of the victims, typically after a somewhat prolonged time in the death bed.

The major troop staging and hospital camp in Étaples, France, was identified as being at the center of the Spanish flu by research published in 1999 by a British team, led by virologist John Oxford. In late 1917, military pathologists reported the onset of a new disease with high mortality that they later recognized as the flu.

The overcrowded camp and hospital which treated thousands of victims of chemical attacks and other casualties of war  was an ideal site for the spreading of a respiratory virus to 100,000 soldiers who were in transit every day. It also was home to a live piggery, and poultry were regularly brought in for food supplies from surrounding villages. Oxford and his team postulated that a significant precursor virus, harbored in birds, mutated so it could migrate to pigs that were kept near the front. 

In 2018, Michael Worobey, an evolutionary biology professor at Arizona University 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 I. Rolland had authored an article in the Lancet (a medical journal) during 1917 about a respiratory illness outbreak beginning in 1916 in Étaples, France.  Worobey traced recent references to that article to family members who had retained slides that Rolland had prepared during that time. Worobey is planning to extract tissue from the slides that may reveal more about the origin of the pathogen.

Nevertheless, there have been persistent claims that the epidemic originated in the United States. Historian Alfred Crosby claimed that the flu originated in Kansas, and popular author John Barry described Haskell County, Kansas, as the point of origin. It has also been claimed that, by late 1917, there had already been a first wave of the epidemic in at least 14 US military camps.

Earlier hypotheses put forward varying points of origin for the epidemic. Some hypothesized that the flu originated in East Asia, a common area for transmission of disease from animals to humans because of dense living conditions. Claude Hannoun, the leading expert on the 1918 flu for the Pasteur Institute, asserted the former virus was likely to have come from China, mutating in the United States near Boston and spreading to Brest, France, Europe's battlefields, Europe, and the world via Allied soldiers and sailors as the main spreaders.^[31] He considered several other hypotheses of origin, such as Spain, Kansas in the United States and Brest as being possible, but not likely.

Political scientist Andrew Price-Smith published data from the Austrian archives suggesting that the influenza had earlier origins, beginning in Austria in early 1917.

In 2014, historian Mark Humphries of the Memorial University of Newfoundland in St.John's stated that newly unearthed records confirmed that one of the side stories of the war, the mobilization of 96,000 Chinese laborers to work behind the British and French lines on World War I's western front, might have been the source of the pandemic. In the report, Humphries found archival evidence that a respiratory illness that struck northern China in November 1917 was identified a year later by Chinese health officials as identical to the "Spanish" flu. 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. It found evidence that the virus had been circulating in the European armies for months and possibly years before the 1918 pandemic occurred.

In the United States, the disease was first observed in Haskell County, Kansas, in January 1918, prompting local doctor Loring Miner to warn the U.S. Public Health Service's academic journal. On 4^thof March 1918, company cook Albert Gitchell reported sick at Fort Riley, an American military facility that at the time was training American troops during World War I, making him the first recorded victim of the flu. Within days, 522 men at the camp had reported sick. By 11 March 1918, the virus had reached Queens, New York. Failure to take preventive measures in March/April was later determined to be a stupid failure.

In August 1918, a more virulent strain appeared simultaneously in Brest, France; in Freetown, Sierra Leone; and in the U.S. in Boston, Massachusetts. The Spanish flu also spread through Ireland, carried there by returning Irish soldiers. The Allies of World War I came to call it the Spanish flu, primarily because the pandemic received greater press attention after it moved from France to Spain in November 1918. Spain was not involved in the war and had not imposed wartime censorship so it can ‘t be shown that the flu started oin that country.

 It has been said that this flu killed more people in 24 weeks than AIDS killed in 24 years, and more in a year than the Black Death killed in a century, although the Black Death killed a much higher percentage of the world's smaller population at the time.

The disease killed people in every area of the Globe. As many as 17 million people died in India, about 5% of the population. The death toll in India's British-ruled districts alone was 13.88 million.

In Japan, of the 23 million people who were affected, 390,000 died. In the Dutch East Indies (now Indonesia), 1.5 million were assumed to have died among 30 million people living there. In Tahiti 13% of the population died during one month. Similarly, in Samoa22% of the population of 38,000 died within two months.

In Iran, the mortality was very high: according to an estimate, between 902,400 and 2,431,000, or 8.0% to 21.7% of the total population died.

In the U.S., about 28% of the population became infected, and 500,000 to 675,000 died.^[55] Native American tribes were particularly hard hit. In the Four Corners area alone, 3,293 deaths were registered among Native Americans. Entire Inute and Alaskan Native village communities died in Alaska.  In Canada 50,000 died. In Brazil, 300,000 died, including president Rodrigues Alves In Britain, as many as 250,000 died; in France, more than 400,000. In West Africa the influenza epidemic killed at least 100,000 people in Ghana.^[61] Tafari Makonnen (the future Haile Selassie, Emperor of Ethiopia) was one of the first Ethiopians who contracted influenza but survived. Many of his subjects did not; estimates for fatalities in the capital city, Addis Ababa, range from 5,000 to 10,000, or higher. In British Somaliland, one official estimated that 7% of the native population died.

A large factor in the worldwide occurrence of this flu was increased travel. Modern transportation systems made it easier for soldiers, sailors, and civilian travelers to spread the disease in other countries.

Think about what follows. Back in 1917 and 1918, there weren’t as many planes traveling world-wide like there is in this century. If the flu like the Spanish Flu occurred in this era, , it is possible that more than twice the number of deaths would be the result since there are more people on Earth today than there was back in 1917 and 1918.