The Anatomy of a Pandemic: What went wrong during the 1918 influenza outbreak?

by Ruth Riedl

The flu is generally accepted to be a seasonal occurrence that most people don’t worry much about, except to get a flu shot. Odds are that if you’re a healthy adult who has had a flu shot, you’ll be fine, unless things go wrong and the virus mutates so that vaccines are not fully effective or cause more infections, such as during the 2009 “swine flu” pandemic. In a typical year, 5-20% of Americans will contract the flu and 3,000-49,000 people will die; however, during a pandemic, the number of infections and deaths can soar, which is what occurred during the 1918 influenza pandemic. Although the virus spread worldwide, in America, about a quarter of the population were infected and nearly 600,000 people died [1].

For years, historians and scientists alike have puzzled over why this outbreak became a worldwide pandemic, but a lack of genetic evidence and incomplete medical and death records have made it difficult to identify a specific reason for the high mortality rate. Was it that this novel strain of influenza was more lethal or more contagious than previous strains? Did public health measures fail to stop the spread of infection? Did the movement of soldiers during World War I spread the virus to previously isolated populations? And why did so many young adults die in the 1918 outbreak when they were usually the least likely to die from disease? The question of what causes a pandemic has become even more salient in light of this year’s outbreak of influenza A, as cases soared during the winter months. If we are to anticipate and prevent future pandemics, we need to know what in 1918 went wrong so as to create the largest pandemic since the Bubonic Plague.

The American outbreak of influenza began during the spring of 1918 in military camps in the Midwest and Southwest [2]. Normally, an epidemic in a relatively isolated military training camp would burn itself out after a few weeks; however, the movement of recruits between different training camps facilitated the inadvertent spread of influenza within military camps and later, to the general public [3].

By increasing circulation of the virus within the American public, the military unintentionally exacerbated another difficulty associated with the United States’ involvement in World War I. Nearly one third of American physicians and a large number of nurses were overseas assisting the wounded [4]; thus the influenza outbreak added additional strain to an already strained medical network. This deficiency in physicians and nurses coupled with the large numbers of influenza cases meant that people who were sick were often not able to be seen in hospitals and clinics, contributing to the high fatality rate observed in 1918 [5].

Along with a breakdown in the American medical system, historians have questioned the role of public health or a lack thereof in the mortality rate during the influenza outbreak. Public health in 1918 was in its infancy by today’s standards, but officials had had some experience with controlling other infectious diseases, namely tuberculosis [6]. Some of the common public health measures taken included social distancing, wearing masks, shutting down public gathering areas, and citizen education [7]. As the influenza pandemic raged on, fear of the disease increased. Fear and public health endorsement of the practice of minimizing contact with others led people to participate in social distancing, which was effective at slowing the spread of the pandemic. Death rates from cities observing strict public health measures demonstrate the efficacy of this practice and also highlight the consequences of not implementing social distancing. In Philadelphia, gathering areas were not closed until after the peak of the epidemic, resulting in high mortality rates. Cities such as Chicago and New York enacted social distancing measures as soon as influenza cases were detected. Consequently, they noted lower death rates compared to Philadelphia [8]. This further indicates that cities that didn’t immediately recognize influenza as a public health emergency and enact social distancing measures had higher mortality rates than those cities that did, thus contributing to the high mortality associated with the 1918 influenza outbreak.

One controversial public health measure enacted by a few cities such as New York, Chicago, and New Haven was the refusal to close schools [9]. During the early 1900s, physicians made rounds within school districts, examining children for illness. The rationale was that by keeping schools open, cities would ensure that children who were ill would be identified and treated. Additionally, officials thought that keeping the schools open would minimize a child’s risk of contact with an infected adult and vice versa [10]. This likely backfired because it was often children who first became ill and were the source of secondary bacterial infections that often killed those who had been weakened by influenza [11]. Although the cites that did not close their public schools didn’t see a huge spike in mortality, not closing schools likely facilitated the spread of influenza among school children, who brought the disease home to the rest of their family, thus continuing the chain of infection.

Historians and scientists have also proposed that race and economic status played important roles in the high mortality observed in 1918, since in the early 1900s, the health outcomes of minorities and those of lower economic status were generally much worse than the health outcomes of upper class, white Americans. The literature does not support the claim that race influenced mortality [12]. Economic status, on the other hand, did play a part in the high death rate seen with influenza. Although the influenza pandemic of 1918 was often said to be an equalizer, infecting people regardless of their class status, surveys of Americans who contracted influenza in 1918 indicate that those of lower economic status fared worse during the pandemic than those of high economic status [13]. This trend was even more apparent when looking at different age groups, as people over the age of 65 who were of low economic status showed a significantly higher risk of mortality than any other age group. The elderly were at risk for death due to various health complications, and their poor health was exacerbated by a lack of access to health care, nutritious food, and sanitary living conditions. Ultimately, the lack of access to both medical resources as well as basic necessities helped turn a common illness into a pandemic.

The past four influenza pandemics of the 20th century have been caused by either the emergence of a novel influenza strain or the genetic reshuffling of currently circulating strains. These changes are known as antigenic drift and antigenic shift and often occur when viruses mutate within an animal host, such as pigs or birds. Influenza viruses are characterized by two proteins that allow the virus to bind to human cells, hemagglutinin and neuraminidase, and when the virus undergoes antigenic shift or repeated antigenic drift, a person’s immune system doesn’t recognizes the virus and they can become infected. This is almost certainly what happened in 1918. Prior to 1918, an influenza virus of subtype H3NX was the primary subtype in circulation, meaning that the majority of people alive did not have immunity to the H1N1 influenza strain [14]. Additionally, exposure to the H3NX strain between 1875 and 1901 resulted in individuals who were significantly more likely to exhibit severe immune responses to the H1N1 and bacterial infections [15]. This was characterized by what is know as ‘cytokine storm’, in which too many immune cells are activated in a specific area of the body. When this occurs in the lungs, it can predispose an individual to lung infections, such as bacterial pneumonia, which was commonly observed during the 1918 influenza pandemic. Those individuals most likely to suffer from this cytokine storm would have been 17-43 years of age during 1918, directly correlating with the spike in mortality seen in young adults during this pandemic [16]. Exposure to the H3NX influenza appears to be one of the most important determinations of mortality for the 1918 influenza and this along with a lack of immunity to H1N1 transformed the 1918 outbreak into a full-blown pandemic.

Ultimately, a variety of factors played a part in influencing the mortality rate in 1918. The movement of soldiers between military camps likely exacerbated the spread of influenza between cities as did well-intentioned public health practices such as not closing schools. Cities that did not enact social distancing practices and individuals of low socioeconomic status who could not access healthcare suffered higher rates of infection and mortality, and a shortage of doctors and medical care intensified the mortality rate. However, the most important factors in turning influenza in to a pandemic were exposure to the H3NX strain present during the previous 40 years and lack of immunity to H1N1.

What does this mean for future pandemics? We have better vaccines and treatments for those infected, but looking back on the 1918 influenza demonstrates that we need to be aware that vaccines alone cannot protect us, especially if novel strains of influenza appear. We need to have measures in place to provide healthcare for a large number of people and be prepared to enact public health measures to prevent the spread of illness. 1918 provides us with a better understanding of what these medical and public health measures may be.
Further reading:
“Flu (Influenza).” Antigenic Shift Illustration, How the Flu Virus Changes. NIAID, NIH. January 11, 2011. Accessed April 30, 2015. http://www.niaid.nih.gov/topics/flu/research/basic/pages/antigenicshiftillustration.aspx

Kolata, Gina. Flu: The Story of the Great Influenza Pandemic of 1918 and the Search for the Virus That Caused It. New York, NY: Farrar, Straus and Giroux, 1999.

World Health Organization. “Influenza Virus Infections in Humans.” Influenza at the Human-Animal Interface. February 1, 2014. Accessed April 30, 2015. http://www.who.int/influenza/human_animal_interface/virology_laboratories_and_vaccines/influenza_virus_infections_humans_feb14.pdf

Garrett, Laurie. “The Year of the Flu.” Council on Foreign Relations. February 4, 2015. Accessed April 30, 2015. http://www.cfr.org/public-health-threats-and-pandemics/year-flu/p36079

References:
[1] Nancy Bristow, American Pandemic: The Lost Worlds of the 1918 Influenza Epidemic. (Oxford and New York: Oxford University Press, 2012).
[2] Monica Schoch-Spana, “Implications of Pandemic Influenza for Bioterrorism Response.” Clinical Infectious Diseases (2000): 1409-1413.
[3] Sandra Opdycke, The Flu Epidemic of 1918: America’s Experience in the Global Health Crisis. (London: Routledge, 2014).
[4] Schoch-Spana. “Implications.”
[5] Opdycke. The Flu Epidemic of 1918.
[6] Ibid.
[7] Francesco Aimone, “The 1918 Influenza Epidemic in New York City: A Review of the Public Health Response.” Public Health Reports (2010): 71-79.
[8] Opdycke. The Flu Epidemic of 1918.
[9] Aimone. “New York City”; Alexandra M. Stern, Mary B. Reilly, Martin S. Cetron, and Howard Markel, “’Better Off in School’: School Medical Inspection as a Public Health Strategy During the 1018-1919 Influenza Pandemic in the United States.” Public Health Reports (2010): 63-70.
[10] Stern, et. al., “’Better Off in School.’”
[11] Stephen Schoenbaum, “Transmission of, and protection agains, influenza: Epidemioloic observations beginning with the 1918 pandemic and their implications.” In The Spanish Influenza Pandemic of 1918-19: New perspectives. Ed. Howard Phillips and David Killingray. London: Routledge, 2003. 242-251. Print.
[12] Vanessa Northington Gamble, ““There Wasn’t a Lot of Comforts in Those Days:” African Americans, Public Health, and the 1918 Influenza Epidemic.” Public Health Reports 125.3 (2010): 114.
[13] Edgar Sydenstricker, “The incidence of influenza among persons of different economic status during the epidemic of 1918.” Public Health Reports (1896-1970) (1931): 154-170.
[14] G. Dennis Shanks, and John F. Brundage. “Pathogenic responses among young adults during the 1918 influenza pandemic.” Emerg Infect Dis 18.2 (2012): 201-207.
[15] David M. Morens, and Anthony S. Fauci. “The 1918 Influenza Pandemic: Insights for the 21st Century.” The Journal of Infectious Diseases (2007): 1018-1028.
[16] Morens. “Insights for the 21st Century.”

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