Unearthing the Forgotten Flu: Spanish Flu in Clay County
March 1, 2018
-additional research by Mark Peihl & Pamela Burkhardt
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There’s something of a local legend here about Concordia College’s fall quarantine in 1918. The story goes that Concordia’s President J.A. Aasgaard closed the perimeter on October 8, and as a result Concordia’s student body was largely spared from the horrifying pandemic that followed: the 1918 H1N1 influenza pandemic better known as La Grippe or Spanish Flu.
A November issue of the campus newspaper The Crescent noted the quarantine's success and observed the following: “It is evident that our students are so abnormally healthy that even the ‘Flu’ germ shuns them.” The only recorded campus death also seemed to reinforce the wisdom of the decision. Apparently a female student broke quarantine and went home. She contracted the disease at some point during her trip and died shortly thereafter. Erling Rolfsrud included the story in his Cobber Chronicle (1966) without sharing his source and Carroll Engelhardt repeated the story in On Firm Foundation Grounded (1991).
The consensus among scientists and Spanish Flu historians today would support Aasgaard’s choice. Quarantine was about the best available recourse. But, assuming the quarantine was executed as ordered and recorded, it was still probably lifted too early to have made a significant impact on the community’s overall health. The perimeter was opened the same day another Moorhead woman, Esther Anstrup (23), died from the flu. Three additional Moorhead residents, all in their 20s, would die from the flu that month and twenty-nine more people would die in the county after November 7 — when the quarantine was lifted — as the flu moved through smaller towns and rural areas. Twenty-six more would die in December.
By the end of May 1919, Clay County had lost 151 people.
In other words, Concordia may have weathered the storm, but that was more likely due to the peculiarities of Spanish Influenza than an effective quarantine. That is, Spanish Influenza found its most vulnerable hosts in people usually unscathed by influenza: healthy people in their 20s and 30s (just a little older than most college students). In fact, this was one of the clear and more horrifying markers of the disease. Recent work in flu genomics is beginning to explain this peculiarity, as well — but first some history.
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Spanish Influenza had arrived in Minnesota at the end of September, just as the Meuse-Argonne offensive was taking form overseas. The US Surgeon General announced it on September 25 after several Army recruits temporarily housed on the University of Minnesota campus fell ill, but it had broken out at a military funeral in Wells, Minnesota, a week earlier. Walter Paulson was being buried. He’d died of pneumonia serving in the Navy. His brother, Private Raymond Paulson, was among the group watching him go in the ground. Within weeks Raymond, his sister Anna, and the presiding Reverend C.W. Gilman were also dead.
Locals here would have first heard about the flu in news reports about military casualties. When it was apparent the disease was moving through America, some of our area newspapers would note its westward path as it moved toward us in Minnesota. This allowed people in the Red River Valley some time to prepare, but these stories were also lost in war headlines, a mid-term election, a Minnesota wildfire, and yet another liberty loan drive. Even so, not long after its presence was announced in Minnesota, Moorhead Normal School postponed the fall semester.
Then the first cases in Fargo-Moorhead were reported Friday, October 4. On Monday, October 7, infant Selma Johanna Hanson died in Moorhead. She was the first flu casualty in the county. The following day three more women joined her – Maria Letigia Altobelli (28), Ella Anderson (45), and Annie Jane Schilling (25). Moorhead’s city council banned public gatherings and closed schools. On Wednesday, with 2,500 cases reported in Fargo-Moorhead-Dilworth, Concordia closed its perimeter and continued with business as usual – the best they could – within the confines. When they opened those perimeters a month later, they had no idea that the disease would eat at our community for another 15 months.
In Clay County, 174 people died from the flu or flu-related diseases. The population at the time numbered about 21,000 (0.8% of the population died from the flu or flu-related disease). Moorhead lost 68 people (1.2% of the population), Hawley lost 12 people (2.8%), Barnesville and Dilworth lost 10 people (.66% and 1.25%, respectively), and Ulen lost 8 people (1.3%). Outside of the transportation and population centers of Moorhead and Dilworth, the communities of Goose Prairie, Ulen, and Highland Grove townships were particularly hit hard (24 deaths total), but Hawley Township wasn’t far behind (16 deaths). Barnesville’s flu deaths were evenly scattered throughout the pandemic and didn’t begin until October 16.
When the flu fatalities are mapped, it’s fairly clear that the disease made its landing in Fargo-Moorhead-Dilworth, and probably by rail. Many in these communities worked on or with the railroads, including the heavily trafficked Northern Pacific Railway station in Dilworth. The first 15 flu-related deaths of Clay County occurred in Moorhead and Dilworth. The Italian population of Moorhead and Dilworth suffered early and disproportionately, too. Five of the first fifteen deaths appear to have struck Italians. Ethnic and class isolation at the time may explain it. Sex didn’t appear to be a factor: death rates among men and women were about the same.
However, pregnancy was markedly more dangerous than usual. A definitive number doesn’t exist, but medical historian John M. Barry cites studies that put the global fatality rate among infected pregnant women between 23-71%. About 40% of Clay County’s deaths were young adult women, miscarriages, and stillbirths. Little Selma Hanson, the first influenza casualty here, was followed four days later by her mother Rachel (21). At the end of November, Agnes Wilinski was stillborn in Moorhead. Two days later her mother Hattie (26) followed. In March of 1919, Medalia Stockwell (25) died of flu and pneumonia along with the child she was carrying.
Dilworth suffered its 10 fatalities all in the last three weeks of October – though it should be noted that deaths after those first two weeks, even among people in rural areas, were more likely to occur in Fargo-Moorhead hospitals. Dilworth only had one Red Cross nurse, Louise Christensen, and a few volunteers. On October 19, Christensen wrote to her supervisor, “We are very, very busy, have 24 patients in hospital now. Have dismissed about 15, two have died, and perhaps one or two died last night.” Her estimate would have included Louise Rae (45), who had died October 18. Dilworth counted four more deaths in the following ten days.
Though Ulen, Barnesville, Hitterdal, Hawley, and Glyndon closed their schools and banned or limited public gatherings from early October through early November, the disease still spread to more isolated, rural areas. The first rural deaths began in Morken Township on October 14 and Barnesville and Skree Township on October 16. Like the northeastern corner of the county near Ulen, southeastern Skree and Parke townships near Rollag suffered a disproportionate number of flu-related deaths (6 and 4, respectively). Ulen registered its first death on October 18 – even though J.T. Johnson reported that same day from Ulen to the Moorhead Daily News that there was little illness there. Another Ulen death followed on Halloween. The Ulen-Hitterdal area would see 20 more that year.
Hawley held out for a while. Perry Pederson (30) lost his battle on October 25 and an infant, Clarice Aune, died on November 25. There were several deaths in neighboring rural townships, suggesting attempts at quarantine and home care, but December would bring a deadly winter for Hawley. Twelve villagers would die from the flu by May 18, 1919. Ten others would die in the four townships surrounding it (Hawley, Cromwell, Highland Grove, and Eglon). The region was spared from the second wave that began late December, 1919.
The southwestern corner of the county suffered several losses as well, beginning in Holy Cross Township on October 29 with Lynn Peterson (25). Another followed there on November 6, bringing a relatively high concentration of November deaths. Overall, Holy Cross registered 5 deaths during the pandemic, Alliance 3, Elmwood 2, and Kurtz 1. That region suffered during both waves, ending with Valine Larson’s death on February 19, 1920, at the age of 29.
Georgetown appears to have fared well. Though the village reported infection, and census records show a notable population dip in 1920 (likely attributed to war displacement and Prohibition-inspired urban migration), only one death was registered there during the pandemic: Wells Bristol (56), near the very end, on February 24, 1920. The four townships surrounding Georgetown registered only three deaths (2 in Morken and 1 in Kragnes). The old trading post seems to have been isolated enough to withstand the disease.
The final flu casualty in the county occurred on February 29. Leap Day. A child born in Parke Township died only several hours later.
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The result of the prolonged tragedy has been measured in a few sobering ways. There were probably more than 500 million global infections in just under two years (between 25-35% of the population). Though a large majority of those infected experienced nothing more than a few sleepy days of cough and fever, there were probably 50-100 million global deaths (compare this to the 17 million casualties of World War I). This amounted to 2.5-5% of the global population. Much of the developed world lost around 2% of their populations. Fatality rates in underdeveloped countries, particularly those in Asia, were much higher.
Despite similar infection rates, Americans were relatively immune at 675,000 deaths (0.655% of the population), with some wide disparities. For example, a Metropolitan Life Insurance Company study of Americans aged 25 to 45 found that 3.26% of industrial workers and 6% of coal miners died. Life expectancy in the U.S. dropped 12 years in 1918.
In Minnesota, an estimated 250,000 were infected and nearly 12,000 died (0.5% of the state population). More than half of Minnesota’s 3,700 war casualties suffered flu-related deaths (2,300, or 62%). In November of 1918, deaths in the state outnumbered births for the first time.
Clay County endured at least 174 deaths in a population of 21,000 (some were undoubtedly uncounted and/or unreported) during the pandemic's first 18 months. The average age of those who died in Clay County was 26.3 years. Using the life expectancy in the U.S. before the war (about 51 years), that means we lost about 4,333 years of human life in Clay County. Of the 64 Clay County residents who died in the military, 29 died from flu-related illnesses – bringing Clay County’s total flu casualties to 203 people. Our total years lost in the county was closer to 5,000. We lost a lot of life.
The most frequent victims of the Spanish Influenza pandemic were those between 25-35 years old. Many medical researchers have attributed this peculiarity to the strong immune systems of the inflicted. Apparently too strong. When cells in the human body are threatened by pathogens like the Spanish Influenza virus, their first defenses are interferons, cytokine proteins that communicate the need for defense to nearby cells. White blood cells (or leukocytes) follow, disarming/killing/consuming these invaders and infected or dead cells. As you can imagine, all of this activity wreaks havoc on tissues, leaving them inflamed and the host fevered. Inflammation is even part of the defense: if more blood is delivered to the site of infection, more leukocytes are available to fight.
But when that defense is moving too strong in too concentrated of an area, it damages necessary human tissues in what’s called a ‘cytokine storm’ (the war analogy here might be friendly fire or total annihilation). Spanish Influenza triggered these cytokine storms and left a battlefield in the lungs, spaces now filled with liquid and dead tissues and offering little respiration or defense. In fatal cases, the flu killed by hypoxia. In other words, people drowned to death in their own fluids. This is why several fatalities were marked by what was called “heliotrope cyanosis,” a bluing of the skin from oxygen deprivation.
However, dangers lay ahead even for those who were able to shake the flu virus. When other pathogens — like Streptococcus Pneumoniae — that would otherwise be routinely destroyed in the upper respiratory system came upon this battlefield, they were be able to stroll right through it to the deeper tissues of the lower lungs. The secondary infections that followed flu infection, typically viral and bacterial pneumonia, are widely believed to have killed more people than the flu itself.
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Given the impact of the pandemic and the continued threat we face from influenza, scientists are still searching for answers. Consensus is out on the question of locating the outbreak’s “spill-over event” or “patient zero.” There was so much movement on this planet at the time, it’s an almost impossible task. Some point to a 1916 English outbreak of “Purulent Bronchitis.” Others to a 1917 outbreak in France, possibly carried to the Western Front by the Chinese Labor Corps. The strongest case seems to point to Haskell County, Kansas, where a rural outbreak moved to the Army’s nearby Camp Funston and filled the hospital and barracks with sick soldiers in March, 1918. As journalist and historian Laura Spinney puts it, about the only real consensus is that this was a deadly pandemic that picked up its name because neutral Spain was the only place journalists were willing to report on it.
However, the abandoned Ph.D. of a Swedish virology student at the University of Iowa in 1951 has recently become a touchstone moment in better understanding the Spanish Influenza. Johan Hultin was looking for a dissertation idea when a guest lecturer offhandedly remarked that someone should travel north and find a frozen (preserved) sample of Spanish Influenza in the North American permafrost. Hultin accepted the challenge, flew to Alaska, found two destroyed graveyards, trekked 6 miles through soggy tundra, and came to a third at Brevig Mission. Here the flu had killed 72 people. All but three children. But the graveyard looked promising.
After consulting the village’s matriarch and council, Hultin was given permission to dig through the mass grave that had been filled thirty-three years prior. He promised that the villagers’ sacrifice would help prevent the tragedy again. He found his sample six feet down, frozen, and took it back to Iowa. Then, after several tests, he ran out of tissues. The sample was gone and he abandoned his Ph.D. After some time off he returned to earn an M.D.
Forty five years later, Jeffrey Taubenberger at the Armed Forces Institute of Pathology was making waves in the world of virology. He’d sequenced segments of Spanish Infleunza that had been preserved in the National Tissue Repository, but he’d encountered the same problem: not enough tissues. Fortunately, Hultin was still cued into the medical world and he reached out to Taubenberger. With the Institute’s funding, Hultin returned to Brevig Mission in August, 1997, to conduct a second excavation. The village had known of his previous attempt and the village matriarch was the granddaughter of the woman he’d appealed to in 1951. Once again, the council gave him permission; and, once again, Hultin found his sample. He took a larger piece.
In 2005, the full genome was sequenced, including that of the virus’s important surface H- and N- glycoproteins (Hemagglutinen and Neuraminidase are the flu’s primary weapons in both entering and leaving human cells; the proteins' different strains are identified with numbers). Taubenberger and his team determined that Spanish Influenza, an H1N1 virus, was likely the progenitor of current human and swine influenza A strains (H1N1 and H3N2), as well as the extinct H2N2 virus that circulated in the 1950s and ‘60s. They also confirmed earlier hypotheses that the pathogen had made a zoonotic leap, mutating from an animal strain and spilling over into the human population. This was valuable information, of course, but many didn’t see a smoking gun. Still not much to explain the pandemic’s origin or virulence.
Then, over the last decade, Dr. Michael Worobey took the problem from a different perspective. Instead of searching within the flu’s genome, he set it beside other flu genomes to determine its rate of mutation and isolate the divergences or branches on its phylogenetic tree. His process, using “molecular clocks” and thousands of flu gene sequences, is leading to a new understanding of the flu, particularly in understanding the importance of childhood exposure and immunities. The 1918 H1N1 flu had been so lethal to 20- and 30-year olds because their early exposures had been to a flu of markedly different surface proteins: H3N8. Other demographics, like teens and older adults, had some defense following their childhood exposure to an H1N8 flu.
As elderly Americans at the time had grown up with a separate H1N1 flu, they had in many ways already fought the battle.
-Davin Wait, HCSCC
-additional research by Mark Peihl, HCSCC