Back to the Future: Lessons Learned From the 1918 Influenza Pandemic

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Inside The Swift, Deadly History Of The Spanish Flu Pandemic

Scientist Johan Hultin traveled to Brevig Mission, Alaska, a town of a few hundred souls in the summer of 1997. He was searching for buried bodies, and Alaska's frozen ground was the perfect place to find them. Digging through the permafrost—with permission from the town's authorities—he eventually uncovered a woman who died almost 80 years previously and was in a state of excellent preservation. Hultin then extracted samples of the woman's lung before reinterring her. He intended to use this to decode the genetic sequence of the virus that had killed this Inuit woman along with 90 percent of the town's population.

Brevig Mission was just one place that was part of a global tragedy, one of the worst ever to befall humanity: the influenza pandemic of 1918-19. The outbreak of this influenza virus, also known as Spanish flu, spread with astonishing speed around the world, overwhelming India, and reaching Australia and the remote Pacific islands. In just 18 months at least a third of the world's population was infected. Estimates on the exact number of fatalities vary wildly, from 20 million to 50 million to 100 million deaths. If the upper end of that estimate is accurate, the 1918 pandemic killed more people than both World Wars put together. (Get the facts on influenza.)

The first official cases of the 1918 Spanish flu pandemic were recorded at the U.S. Army's Camp Funston, Kansas, where this emergency influenza ward held treated patients.

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War and pestilence

Several closely related viruses cause influenza, but one strain (type A) is linked to deadly epidemics. The 1918-19 pandemic was caused by an influenza A virus known as H1N1. Despite becoming known as the Spanish flu, the first recorded cases were in the United States in the final year of World War I. (Explore the memorials of World War I.)

A magnified view of the H1N1 virus responsible for the 1918 pandemic.

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By March 1918 the United States had been at war with Germany and the Central Powers for 11 months. During that time America's small, prewar army had grown into a vast fighting force that would eventually send more than two million men to Europe. (How the United States entered World War I.)

American forts experienced a massive expansion as the entire nation mobilized for war. One of these was Fort Riley, Kansas, where a new training facility, Camp Funston, was built to house some of the 50,000 men who would be inducted into the Army. It was here in early March that a feverish soldier reported to the infirmary. Within a few hours more than a hundred other soldiers had come down with a similar condition, and more would fall ill over the following weeks. In April more American troops arrived in Europe and brought the virus with them. The first wave of the pandemic had arrived. (What is the difference between an epidemic and a pandemic?)

Deadly speed

The Spanish flu strain killed its victims with a swiftness never seen before. In the United States stories abounded of people waking up sick and dying on their way to work. The symptoms were gruesome: Sufferers would develop a fever and become short of breath. Lack of oxygen meant their faces appeared tinged with blue. Hemorrhages filled the lungs with blood and caused catastrophic vomiting and nosebleeds, with victims drowning in their own fluids. Unlike so many strains of influenza before it, Spanish flu attacked not only the very young and the very old, but also healthy adults between the ages of 20 and 40.

Biologists at St. Bartholomew's Hospital in London are analyzing brain and lung tissue from victims of the 1918 pandemic as part of global efforts to understand the virus. Here, wax-mounted tissue samples sit on a list of children's names who fell victims to influenza in 1918.

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The principal factor in the virus's spread was, of course, the international conflict then in its last phase. Epidemiologists still dispute the exact origins of the virus, but there is some consensus it was the result of a genetic mutation that perhaps took place in China. But what is clear is that the new strain went global thanks to the massive and rapid movement of troops around the world.

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The drama of the war also served to obscure the unusually high mortality rates of the new virus. At this early stage, the illness was not well understood and deaths were often attributed to pneumonia. Strict wartime censorship meant that the European and North American press were unable to report outbreaks. Only in neutral Spain could the press speak freely about what was happening, and it was from this media coverage that the disease took its nickname.

Deadly Contact

Native Americans treat patients infected by European diseases in this 1591 engraving by Theodor de Bry.

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Epidemics are as old as civilization: Signs of smallpox appear on 12th-century B.C. Egyptian mummies. Increased contact led to the spread of disease. In the sixth century A.D. The Plague of Justinian moved along trade routes, killing 25 million people across Asia, Africa, Arabia, and Europe. Eight centuries later, the Black Death wiped out 60 percent of Europe's population. When Europeans settled in the Americas in the 16th and 17th centuries, they introduced smallpox, influenza, and measles to the native peoples, killing an estimated 90 percent of the population. Here, Native Americans treat patients infected by European diseases in a 1591 engraving by Theodor de Bry.

The second wave

The overcrowded trenches and encampments of the First World War became the perfect hosts for the disease. As troops moved, so the infection traveled with them. The wave that had first appeared in Kansas abated after a few weeks, but this was only a temporary reprieve. By September 1918 the epidemic was ready to enter its most lethal phase.

Flu: The Story Of The Great Influenza Pandemic Of 1918 And The Search For The Virus That Caused It

Farrar, Straus and Giroux, 256 pages, $25.00, 1999 0374157065ISBN: 0-374-15706-5

There is a cemetery in a small railroad town in northern Ohio where I grew up that tells a sliver of the story of the great 'Spanish' influenza pandemic of 1918. One section of the cemetery is full of simple, rough, limestone markers that tilt willy-nilly in the perpetually damp sod of the graveyard. These unembellished memorials mark the graves of unfortunate souls who died one week during the fall of 1918 from the flu. In other towns all over the country there are similar hastily prepared grave sites. At least 10,000 people died in the city of Philadelphia during one three-week period during the month of October, overwhelming doctors, hospitals and undertakers.

The pandemic occurred just at the moment in history when the nightmare of World War I was finally ending, and it killed far more than the Great War itself. The death toll from the flu of 1918 was more than a half-million people in the United States, and more than 20 million people worldwide. This modern day plague is the topic of a new book by Gina Kolata, a science writer for the New York Times. Although the subject of the 1918 flu pandemic is certainly compelling stuff, there is little in this new book that has not already been said better by others, most notably by Alfred Crosby in a book entitled America's Forgotten Pandemic, originally written in the 1970s but since updated. In that book the student of flu can find the primary data underlying many of Kolata's generalizations.

It is unfortunate that much of the book reads like a newspaper article written on a tight deadline. The reader often feels that only the most lurid anecdotes are mentioned, apparently precluding any in-depth description of our burgeoning understanding of the structure and function of the virus itself. The virus is, after all, the 'mass murderer' in this detective story. There are no thoughts here about how viruses propagate or kill or evolve. There is not a word about the molecular virology underlying the phenomena of antigenic drift (a change in surface protein, usually resulting from a base pair mutation) or antigenic shift (which for flu is usually the acquisition of a whole new segment of RNA). Any scientist or physician interested in the influenza virus itself, and all its fascinating efficiencies and complexities, will be sorely disappointed with this book.

The author does, however, vividly illustrate how the great devastation wrought by the flu pandemic continues to affect more recent history. Two chapters of ten in this new book concern the swine flu fiasco of 1976. A series of unfortunate events was started with the death of a single soldier at Fort Dix, New Jersey. The causative agent in the soldier's case was determined to be an influenza virus of a type that normally infects pigs. Because of work in the decades after the 1918 flu pandemic that suggested a link between flu in humans and flu in pigs, scientists feared that the soldier's case was only the first in a deadly pandemic that could engulf the nation and the world. Using scant evidence, and what seems in retrospect to be numerology, a small group of prominent vaccinologists convinced President Gerald Ford to immunize the entire nation. The swine flu epidemic never occurred, but 43 million Americans were vaccinated, leading to scores of lawsuits of patients who claim to have been injured after being immunized.

The most original part of the book is where the author describes recent efforts Jeffery Taubenberger and his team at the Armed Forces Institute of Pathology to sequence the 1918 influenza virus using polymerase chain reaction (PCR)-based techniques. These careful workers have successfully isolated fragments of RNA from the 1918 influenza virus. The acquisition of the tissues for these experiments, either from paraffin-embedded specimens recovered from a government warehouse or from snippets of tissue obtained from bodies buried in the permafrost, is the stuff of high drama.

Even after the latest round of PCR analysis of the flu genome, it remains a mystery why the flu virus of 1918 was so deadly. The most pressing question remains: Can such a deadly virus ever emerge again? On one hand it seems unlikely, given the rapid advances in our medical knowledge. New drugs, such as zanamivir (Relenza), can inhibit the ability of the flu virus to proliferate by blocking the activity of the neuraminidase enzyme. When the Spanish flu pandemic hit, doctors around much of the globe were still using venesection as a treatment.

On the other hand, drug-resistant variants of the flu virus could emerge. Furthermore, the flu virus of 1918 killed quickly—there are many cases of documented mortality in under 48 hours. A large-scale epidemic could overwhelm our modern, sophisticated medical system. Because our overcrowded cities are massively interconnected by commerce and travel, an emerging virus could be spread today at a rate that is orders of magnitude faster than the rate of spread eight decades ago.

So the questions remain: Can such a pandemic happen again? How will we deal with the deadly viruses that will undoubtedly emerge in the future? Greater knowledge about what happened in the 1918 flu pandemic and a deeper understanding of the virus that caused it would be useful. And although Kolata's book provides a lot of heat, it does not shed much light on the questions that really matter.

Lessons Should Have Been Learned From Previous Pandemics

Source: Anna Shvets / Pexels

By Emma Collins

In December 2024, on the International Day of Epidemic Preparedness, UN-Secretary-General Antonio Guterres stated: "The COVID-19 crisis may have passed, but a harsh lesson remains: The world is woefully unprepared for the next pandemic."

Global pandemics are not a new phenomenon, with one of the first documented being the Black Death in the 1300s and, in more recent history, the Spanish Flu of 1918. So why were we not fully prepared to limit the impact of COVID-19?

There remain many current causes of concern such as the highly pathogenic avian influenza A (H5N1) virus. Indeed, since the 1980s, at least 30 new infectious disease threats have emerged (Buchy et al, 2021)—for example, HIV (1981), SARS-CoV-1 (2003), swine influenza (2009), MERS-CoV (2012), West African Ebola virus (2013), and Zika (2015).

The aim of declaring a pandemic is to create a global alert, for people to be aware of the risks that a virus or disease may pose and what they can do to protect themselves and others from it. Reflecting on the worldwide response to two of those: SARS and MERS—two potentially severe acute respiratory infections both caused by coronaviruses, we ask what lessons should have been learned from the recent COVID-19 pandemic and these past coronavirus outbreaks and pandemics.

SARS

SARS stands for severe acute respiratory syndrome. From late 2002 to 2003, illness caused by the coronavirus SARS-CoV-1 caused more than 700 deaths (World Health Organization [WHO], 2006) during the first outbreak. Emerging in China, it then spread to several other countries. Currently, no cure is available, and researchers continue to study and develop vaccines for it.

The virus spread quickly internationally due to its high transmission rate. The WHO coordinated an international investigation and provided support to bring the virus under control (WHO, 2020). There were arguments made at the time for the development of novel surveillance techniques and cooperation between public health and academic institutions, to ensure there were enough scientists with the time and interest to improve tests to apply in an emergency (Weiss, 2004).

Without a vaccine or cure, timely identification and isolation of individuals with SARS over several days was vital, and it was recommended that the public should take personal measures such as good hygiene and workers in high-risk roles provided with sufficient personal protection equipment (PPE).

And, yet, 2020 saw global healthcare systems overwhelmed with COVID-19, and healthcare workers disproportionally exposed to the virus with lives lost due to insufficient PPE (Davis, 2021). SARS-CoV-2 (the virus that causes COVID-19) and SARS-CoV-1 (the virus that causes SARS) have highly similar gene sequences and behaviour patterns (Liu et al., 2020 ). Similar suffering will be experienced if we do not learn from past experiences.

MERS

MERS, the Middle East respiratory syndrome coronavirus (MERS-CoV) emerged in Saudi Arabia. Records show more than 2,600 lab-confirmed cases of MERS and more than 900 deaths (WHO, 2024). As with SARS, scientists are still looking to develop a vaccine to prevent the virus.

MERS is classed as a "zoonotic" virus, reflecting its spread between animals and people. It has been identified in dromedary camels in several countries in the Middle East, Africa, and South Asia, spreading to 27 countries since 2012 (WHO, 2022). Human-to-human transition is possible but rare and is found particularly in care settings, again highlighting the need for good hygiene.

The social and economic impact of MERS put stress on healthcare systems resulting in high levels of mortality and morbidity. From this loss, lessons could and perhaps should have been learned. This included the importance of quick case identification and reporting, efficient infection prevention and control, community-based interventions, and clear, consistent risk communication to the public (Salomon, 2024).

A global, cooperative approach to fighting these diseases is needed more than ever, particularly where vaccines are not yet available.

The importance of this was shown with the COVID-19 vaccine. Highly contagious diseases like MERS, SARS, and COVID-19 significantly impact those with underlying health conditions or in high-risk age groups (Liu et al., 2020), making vaccines even more critical.

COVID-19: Did History Repeat Itself?

Had we invested more into understanding past coronaviruses and how they could have been better managed, we arguably would have been better prepared to respond to and manage COVID-19.

COVID-19 is caused by the coronavirus SARS-COV-2. Most people experienced mild to moderate respiratory symptoms, but, for others, it was devastating, especially in older people or those with pre-existing conditions, although anyone was at risk of serious illness or death (WHO, 2023).

Initial national and global advice centred around good hygiene, staying at home, and, if you needed to go outside, wearing masks and distancing yourself from others. Advice later focused on receiving the COVID-19 vaccine.

More unique to COVID-19 was the accessibility of television and social media. Instant reports from individuals with potentially no clinical or scientific expertise could rapidly "go viral." WHO labeled it an "infodemic" that paralleled the pandemic (Gwendolyn 2020). This increased the prevalence of misinformation; however, government agencies and public health authorities also took advantage of social media to share helpful advice (Pergolizzi 2021).

Despite the huge achievement in the development of the COVID-19 vaccine, significant barriers remain to achieving worldwide delivery of these vaccines to all countries and all age groups. Nevertheless, the COVID-19 vaccine approach needs to be employed alongside active surveillance of emerging variants and pathogens (Buchy et al., 2021). Relative to other infections such as influenza, little is known about the origin and cross-species transmission of COVID-19. Although healthcare services, drug availability, and lab testing have improved significantly since the 20th century, our experience with COVID-19 has flagged gaps (Buchy et al., 2021).

COVID-19 has surpassed previous coronavirus outbreaks in terms of total deaths and the number of affected individuals (Pandey et al., 2020) with more than 700 million cases and 7 million deaths worldwide. COVID-19 has raised calls for humans to interact differently with each other and the environment. Issues such as climate change, urbanisation, our proximity to animals, vaccine hesitancy, and so much more all play their part (Peeri et al., 2020; Buchy et al., 2021).

Conclusion: Pandemics Are Inevitable, and Lessons Must Be Learned

Future pandemics are inevitable, so we need to be better prepared. The ultimate goal is to pre-empt and prevent future pandemics. History has shown this requires a wide range of interventions and government support of public and private research on an international scale (Coccia 2023). Financial and healthcare support also must be prioritised in low-to-middle-income countries, which will undoubtedly be at a higher risk, suffer a greater burden of disease, and experience less vaccine equity and access.

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