May 30, 2020
Linda Morse, formerly of Medfield, teaches history at the Foxboro Regional Charter School. This history of the 1918 Spanish flu pandemic, focusing on its impact in Medfield and Millis, will be serialized in The Portal. Her complete article is being published in the New England Journal of History. There are striking parallels between what happened in 1918 and what is now happening a century later with COVID-19.
Introduction
The influenza pandemic of 1918 cruelly informed the population of the newly emerging twentieth century that a tiny enemy could cause more death and disease than the current world war. The newly discovered power of the industrial age was no match for a virus that eliminated at least 21 million people worldwide. A determined medical community knew that battling the virus would require more technological prowess than was available, but they rallied to the cause. Due to the invasion of influenza, health departments around the world realized the importance of tracking contagious diseases and studying bacteria and viruses. Particularly in the United States, communities soon addressed factors of poverty and unsanitary practices in response to the epidemic. People in both urban and rural settings learned that living in squalid conditions influenced the transmission and outcomes of this virus in not only poor communities but everywhere.
Responsibility for health achieved a new importance as communities realized that poor health practices affected everyone. Medfield, Millis and the Medfield State Hospital provide ideal opportunities to analyze the movement of the influenza in both the small, rural towns and a crowded, vulnerable situation such as a State Hospital. Life expectancy rates decreased in both towns confirming similar findings as those experienced around the country. The towns and the hospital responded to the pandemic with a methodology similar to that used in the western world: quarantine, vaccines and medical care.
Humanity was completely unprepared for the death, disruption, and disaster that ensued in every corner of the earth, skipping only the remote volcanic island chain of Tristan da Cunha.[1] Escalated to new heights of mobility during this first modern war, mobilizing troops or citizens working as members of the Red Cross, unknowingly became vulnerable populations as they supported the war effort. People of the world were mixing and mingling as never before and the environment was ripe for a new infectious disease to take hold and explode around the globe.
Symptoms
The respiratory system is highly attractive to the influenza virus, which successfully attaches itself to the cells lining the trachea, nose, throat and lungs.[2] The range of symptoms for the flu included headache, cold symptoms, fever of at least 101º F, cough, back and leg aches, depression for a week or more or, in other words, feeling as though one “had been beaten all over with a club.”[3] The incubation period before coming down with the sickness was about two days, providing plenty of opportunity for socializing and spreading it before realizing that one is ill. Given that one sneeze exudes 85 million bacteria at 152 feet per second, it is not surprising that this virus is extremely efficient at traveling around the world.[4]
The poet and physician William Carlos Williams described the rapidity of disease’s onset by saying, “. . .they’d be sick one day and gone the next, just like that, fill up and die.”[5] The illness struck down people so quickly that “on a Cape Town tram, seven riders, including the conductor and driver, collapsed and died within one three-mile stretch.”[6] The illness is in its acute phase for three to five days, after which the majority of people began to regain their health. The unfortunate five to ten per cent of people who developed pneumonia after the flu had an incredible mortality rate of 60%–70%.[7] Assuming that one was fortunate enough to recover, a long recuperation period was anticipated as in the case of “Alexander J. Pierce, section boss on the N.Y.N.H. & H.R.R. [New York New Haven & Hartford Railroad who] was able to assume his duties last week after an illness of ten weeks with influenza and pneumonia.”[8]
Life of a Virus
Today we know a great deal about the life cycle of the influenza virus. There are three kinds of unrelated influenza viruses, indicating that being ill with one does not give immunity to the others. Virus “A” occurring “naturally in animals,” causes pandemics, virus “B” causes epidemics and is found mainly in children, and virus “C” an uncommon virus.[9] The influenza virus has a short incubation period during which it multiplies in the respiratory tract and is propelled into the air by coughing or sneezing. During this time, a person may still feel perfectly well and be completely unaware of spreading the disease. While the virus is multiplying inside the person, it must also spread quickly to others so that it will not die out as a species.[10] W.I.B. Beveridge, author of Influenza: The Last Great Plague: An Unfinished Story of Discovery, summarizes this theory by stating, “parasites prosper when their hosts become numerous and crowded.”[11]
The majority of pandemics originate in Eurasia, conceivably due to shared living quarters between humans and animals.[12] This intimate contact causes cross-breeding between the virus in animals, particularly birds and pigs, with humans, creating fertile ground for possible pandemics. “For a genetic reassortment to occur, a cell must be simultaneously infected with more than one influenza virus of more than one animal strain.”[13] This theory of how newly emerging viruses develop is called the “hybridization theory.” [14] While hybridization does not frequently occur in humans, it does appear in reservoir populations, i.e., ducks, birds and swine.[15]
The genetic makeup of the influenza virus makes it particularly unique for mutability. The ribonucleic acid (RNA) within each virus cell is assembled into eight separate pieces rather than the usual whole that cannot be split apart.[16] These separate pieces allow for easier development of hybrid species of influenza. Each virus has four antigens, or substances that stimulate the creation of antibodies in the host[17], two of which (Haemagglutinin and Neuraminidase) are the most critical for hybridization and attachment to the host’s cell walls. Viruses can either create an antigenic shift in their genetic makeup, causing horrific pandemics due to lack of immunity in the host population (i.e. humans); or evolve into antigenic drift, giving rise to a less disastrous epidemic due to some immunity in the host population.[18]
The 1918 influenza virus has recently been studied extensively by Dr. Jeffrey Taubenberger and his associate Ann Reid. The RNA in lung tissue from Private Roscoe Vaughn, who died in the 1918 pandemic, had been preserved in Washington, D.C. Taubenberger and Reid discovered that the virus’ signature was H1N1, revealing it to be a descendant of a pig virus. Taubenberger’s research provides evidence that the virus had a “common avian ancestor.”[19]
An Unsuspecting World
What would later become known as the Spanish influenza started innocuously enough in the early spring of 1918 at Camp Funston, Fort Riley, Kansas. The soldiers training there became ill shortly after a huge wind and dust storm blew by on Saturday, March 9, 1918.[20] Generally mortality was low, but in certain regions “high mortality rates” were noted “among young adults.”[21] Apparently a community in Haskell, Kansas was not alarmed by the “eighteen severe cases of flu” that led to the deaths of three persons.”[22] The next appearance of the flu occurred in a military camp near Bordeaux, in France, shortly after the American soldiers arrived on April 15.[23] By the end of April, the flu had spread into Spain where it acquired its name “Spanish Influenza.” Obviously, this is a misnomer, but since Spain did monitor its health records at that time, the flu gained worldwide attention and Spain was mistakenly given the credit for the illness.[24] By lingering into the summer, this form of influenza suggested a virulent strain.[25] It has since been determined that when a summer flu occurs, it is generally due to a new strain.[26]
In August, 1918, this new and virulent influenza arrived to infect the innocent people in Boston.[27] In the neighboring communities of Medfield and Millis, citizens marched confidently into the autumn, unaware that they would soon be unwilling participants in an “appalling demonstration of man’s helplessness and ignorance.”[28] The Dedham Transcript newspaper regularly reported on community events available in Medfield and Millis for its citizens to enjoy thus granting insight into how disrupted society became. Thrilling activities included Charles Cox who “pitched his second ‘no hit no run’ [sic] game this season for the Medfield State Hospital nine against the Foxboro State Hospital team at Foxboro last Saturday.”[29] The Medfield Grange sponsored “Neighbors Night” Thursday, August 11, “inviting the Needham and Milton Granges.”[30] The Medfield Civic Association promoted a fundraiser for the Red Cross on Labor Day with activities including baseball, a horse show, dancing, and a variety of sporting events.[31] Medfield supported the Red Cross by raising money with musical concerts, participating with both Millis and Walpole, and sponsoring dancing in the Grange Hall.[32] Reminders of the war infused these small towns as “Company M, 13th Regiment, M.S.G.” came out to participate in a flag raising exercise in Millis on Monday, August 19. The Medfield and Millis schools anticipated opening on Tuesday, September 3, 1918, for their fall term of sixteen weeks.[33]
Characteristics of pandemics differ from those of epidemics. Pandemics begin suddenly, having the ability to spread rapidly around the world, affecting virtually everyone and killing many. Few deaths occur during an epidemic, but those that do are chiefly among those who are elderly or already sick.[34] Scientists today estimate that in the United States in 1918 28% of the population was infected with the influenza. In influenza epidemics where some immunity is found within the population (antigenic drift), there has been a 0.1% mortality rate; in 1918 there was a mortality rate over 2.5% due to the lack of immunity in the population.[35] The more virulent, or second wave of the Spanish flu, circumnavigated the world in four months and by December, 1918, approximately 500,000 people had died leaving 20 million ill.[36] When it was done, the British Ministry of Health suggested there were 21.6 million deaths worldwide.[37] The United States lost approximately 550,000 persons (0.5%) to the Spanish Influenza or slightly more than all military losses from World War I, II, Korea and Vietnam combined.[38]
The Virus Hits
During the summer of 1918, the North American continent was free of the flu.[39] However, the flu was apparently hiding before simultaneously erupting in Brest, France, Boston, Massachusetts, and Freetown, Sierra Leone in late August 1918.[40] These were sites where great human movement and crowding existed, an ideal situation for a contagious illness. Boston that year was very dry, having received only 8.13 inches of rain in four months, far below the average rainfall. The city was filled with soldiers, sailors and shipyard workers working and living in close contact.[41] Sanitation was a serious problem. Camp Devens, Massachusetts, was where the influenza made its first appearance on August 22.[42] Before long, the illness spread to the civilian population around Boston, with the first case reported from a Boston hospital on September 3. The seriousness of the illness had yet to be recognized, for Boston still held its “Win-the-War-for Freedom” parade that same day.[43]
The illness continued its rapid spread into Boston and surrounding communities, and on September 5, 1918 the Massachusetts Department of Health decided to inform the newspapers of the arrival of the epidemic.[44] Newspapers reported that the spread of the flu into the local population followed army camp movements in the region with the peak of illness among civilians appearing about two weeks after the disease was found among military personnel.[45] Due to a greater age variety and less crowded conditions in the general population, it took longer for the peak of the pandemic to develop.[46] The State Board of Health reported that the flu reached Springfield, Massachusetts by September 23.[47] As the flu moved in a whirlwind around the globe, alarmed doctors at the Massachusetts Department of Health worried about “the explosive nature of the pandemic, our ignorance as to etiology, mode of transmission and excessive death rate made the problem extremely difficult to handle.”[48] Across the Commonwealth the incidence of influenza, recorded from October 4 through December was 145,262 people with 40,222 cases in 1919. The incidence of lobar pneumonia across the state was 13,374 (compared to 1756 reported in 1917, the first year for available records). Because influenza was not on the list of diseases dangerous to the public health until September 30, 1918, actual reporting by the community did not occur until several days later.[49] Most cases of lobar pneumonia were reported during the flu epidemic and it is impossible to discern whether influenza or some other cause brought on the pneumonia.
The virus moved in three waves, with varying degrees of virulence. In the spring, the virus was considered mild. When the flu began in Camp Funston, Kansas, the soldiers were unwell for two to three days, but returned quickly to work. Shortly thereafter, a pneumonia epidemic arose infecting 233 and killing 48. At the time, physicians considered this an acceptable mortality rate.[50]When the aggressive autumn wave began, physicians were deeply concerned over the camp’s health facilities. Camp Devens in Massachusetts held 45,000 men, which meant it was overcrowded by 10,000 men.[51] It is no wonder that by the end of October more than 17,000 men at Devens had experienced the flu and/or pneumonia and 787 men died.[52] For more specific statistics of September, reports from Camp Devens from September 4 to October 29, revealed 2817 cases of influenza-pneumonia resulting in 787 deaths, with a mortality percentage of 27.9. There were 231 occurrences of influenza-pneumonia from October 2 through 29 at Camp Devens, with 127 fatalities, leaving an incredibly high fatality rate of 54.9%.[53] Warren Vaughan of Harvard Medical School, expressed his concern in the American Journal of Epidemiology, when he wrote,
“Compared with epidemics for which we have fairly accurate statistics the death rate at Camp Sherman in the fall of 1918 is surpassed only by that of plague in London in 1665 and that of yellow fever in Philadelphia in 1793. The plague killed 14 per cent of London’s population in seven months’ time. Yellow fever destroyed 10 per cent of the population of Philadelphia in four months. In seven weeks, influenza and pneumonia killed 3.1 per cent of the strength at Camp Sherman. If we consider the time factor, these three instances are not unalike in their lethality. The plague killed 2 per cent of the population in a month, yellow fever 2.5 per cent, and influenza and pneumonia 1.9 per cent.”[54]
In the general population of Massachusetts, approximately 7.6% of those who reportedly contracted influenza subsequently died (records were not kept during September or early October).[55] A third wave, occurring in January and February of 1919, was not as virulent.[56] It was noted that persons and regions “suffered less severely in the fall” if the flu had visited their area in the spring, perhaps affording them some form of immunity. In whatever season it visited, by the end of January 1919, the “fall virus had reached virtually every inhabited place on earth.”[57]
The Spanish Influenza deeply alarmed the world due to its particularly unusual habit of striking down robust and young adults, a stark contrast to the average flu. The typical pattern of influenza mortality strikes the very young and the elderly. This influenza struck heavily among the 21-to-29-year-old-group, displaying a “W” shape on a graph. During the spring epidemic, the pathologist Edwin R. LeCount of Chicago noted that upon autopsy there was “widespread hemorrhagic and edematous process in the lungs,” and unfortunately, only after the devastating fall epidemic erupted did he comprehend this significant finding.[58]
To be continued…
[1] A. A. Hoehling, The Great Epidemic: When the Spanish Influenza Struck. (Boston: Little Brown and Company, 1961), 8.
[2] W. I. B. Beveridge, Influenza: The Last Great Plague: An Unfinished Story of Discovery. (New York: Prodist, 1977), 12.
[3] Alfred W. Crosby, America’s Forgotten Pandemic: The Influenza of 1918. (Cambridge: Cambridge University Press, 1989), 5, 39; Beveridge, 11-12.
[4] Richard Collier, The Plague of the Spanish Lady: The Influenza Pandemic of 1918-1919. (New York: Atheneum, 1974), 11.
[5] Crosby, 216.
[6] Jack Fincher. “America’s Deadly Rendezvous with the ‘Spanish Lady,’ Smithsonian 19 January 1989, 135.
[7] Crosby, 79.
[8] Dedham Transcript. December 21, 1918, 2.
[9] Beveridge, 9; 70.
[10] Beveridge, 9; 70.
[11] Beveridge, 111.
[12] Beveridge, 91.
[13] R. M. Henig, “Flu Pandemic,” New York Times Magazine 29 November 1992, 31.
[14] Beveridge, 84.
[15] Henig, 31.
[16] Beveridge, 74.
[17] Dorland’s Illustrated Medical Dictionary, s.v. “antigen”
[18] Beveridge, 68-72
[19] Jeffrey Taubenberger, et al., “Initial genetic Characterization of the 1918 ‘Spanish’ Influenza Virus,” Science 21, 275, no. 5307 (March 1997): 1793. , 1795.
[20] Hoehling, 11.
[21] K. David Patterson and Gerald F. Pyle. “The Geography and Mortality of the 1918 Influenza Pandemic,” Bulletin of the History of Medicine, 65m no. 1 (1991): 8.
[22] Crosby, 18.
[23] Crosby, 25.
[24] Crosby, 26.
[25] Patterson and Pyle, 8.
[26] Beveridge, 44.
[27] Crosby, 38.
[28] Hoehling, 194.
[29] “Medfield,” Dedham Transcript, August 24, 1918, 2.
[30] Dedham Transcript, August 13, 1918, 2.
[31] Dedham Transcript, August 24, 1918, 2.
[32] Dedham Transcript, September 7, 1918, 2.
[33] Dedham Transcript, August 24, 1918, 2.
[34] Beveridge, 18.
[35] Taubenberger, 1793.
[36] Crosby, 28; Hoehling, 3.
[37] Patterson and Pyle, 7.
[38] Beveridge, 31; Patterson and Pyle, 17.
[39] Crosby, 30.
[40] Crosby, 37.
[41 Hoehling, 23.
[42] Crosby, 4.
[43] Crosby, 40.
[44] Crosby, 40.
[45] Crosby, 62.
[46] Crosby 62-3.
[47] Fourth Annual Report of the State Department of Health of Massachusetts. Public Document No. 34, 1918, (Boston: Boston Wright and Potter Printing Co. State Printers, 1919), 198.
[48] Department of Health 1918, 197.
[49] Department of Health 1918, 188-189.
[50] Crosby, 11.
[51] Crosby, 4, 19; Hoehling, 13.
[52] Crosby, 11.
[53] Department of Health 1918, 199.
[54] Beveridge, 32.
[55] Department of Health 1918, 197.
[56] Beveridge, 21; Crosby, 203; Patterson and Pyle, 4.
[57] Patterson and Pyle, 4; 11.
[58] Crosby, 21.