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Journal of Translational Medicine
Open Access
Commentary
The site of origin of the 1918 influenza pandemic and its public
health implications
John M Barry*
Address: Distinguished Visiting Scholar, the Center for Bioenvironmental Research of Tulane and Xavier Universities, New Orleans, Louisiana, USA
Email: John M Barry* - jbarry@tulane.edu
* Corresponding author
The 1918–1919 influenza pandemic killed more people
than any other outbreak of disease in human history. The
lowest estimate of the death toll is 21 million, while
recent scholarship estimates from 50 to 100 million dead.
World population was then only 28% what is today, and
most deaths occurred in a sixteen week period, from mid-
September to mid-December of 1918.
It has never been clear, however, where this pandemic
began. Since influenza is an endemic disease, not simply
an epidemic one, it is impossible to answer this question
with absolute certainty. Nonetheless, in seven years of
work on a history of the pandemic, this author conducted
an extensive survey of contemporary medical and lay liter-
ature searching for epidemiological evidence – the only
evidence available. That review suggests that the most
likely site of origin was Haskell County, Kansas, an iso-
lated and sparsely populated county in the southwest cor-
ner of the state, in January 1918 [1]. If this hypothesis is
correct, it has public policy implications.
But before presenting the evidence for Haskell County it is
useful to review other hypotheses of the site of origin.
Some medical historians and epidemiologists have theo-
rized that the 1918 pandemic began in Asia, citing a lethal
outbreak of pulmonary disease in China as the forerunner
of the pandemic. Others have speculated the virus was
spread by Chinese or Vietnamese laborers either crossing
the United States or working in France.
More recently, British scientist J.S. Oxford has hypothe-
sized that the 1918 pandemic originated in a British Army
post in France, where a disease British physicians called
"purulent bronchitis" erupted in 1916. Autopsy reports of
soldiers killed by this outbreak – today we would classify
the cause of death as ARDS – bear a striking resemblance
to those killed by influenza in 1918 [2].
But these alternative hypotheses have problems. After the
1918–1919 pandemic, many investigators searched for
the source of the disease. The American Medical Associa-
tion sponsored what is generally considered the best of
several comprehensive international studies of the pan-
demic conducted by Dr. Edwin Jordan, editor of The Jour-
nal of Infectious Disease. He spent years reviewing
evidence from all over the world; the AMA published his
work in 1927.
Since several influenza pandemics in preceding centuries
were already well-known and had come from the orient,
Jordan first considered Asia as the source. But he found no
evidence. Influenza did surface in early 1918 in China,
but the outbreaks were minor, did not spread, and con-
temporary Chinese scientists, trained by Rockefeller Insti-
tute for Medical Research (now Rockefeller University)
investigators, stated they believed these outbreaks were
endemic disease unrelated to the pandemic [3]. Jordan
also looked at the lethal pulmonary disease cited by some
historians as influenza, but this was diagnosed by con-
temporary scientists as pneumonic plague. By 1918 the
plague bacillus could be easily and conclusively identified
in the laboratory [3]. So after tracing all known outbreaks
of respiratory disease in China, Jordan concluded that
none of them "could be reasonably regarded as the true
forerunner" of the pandemic [3].
Jordan also considered Oxford's theory that the "purulent
bronchitis" in British Army camps in 1916 and 1917 was
Published: 20 January 2004
Journal of Translational Medicine 2004, 2:3
Received: 11 January 2004
Accepted: 20 January 2004
This article is available from: http://www.translational-medicine.com/content/2/1/3
© 2004 Barry; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for
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Journal of Translational Medicine 2004, 2 http://www.translational-medicine.com/content/2/1/3
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the source. He rejected it for several reasons. The disease
had flared up, true, but had not spread rapidly or widely
outside the affected bases; instead, it seemed to disappear
[3]. As we now know a mutation in an existing influenza
virus can account for a virulent flare-up. In the summer of
2002, for example, an influenza epidemic erupted in parts
of Madagascar with an extremely high mortality and mor-
bidity; in some towns it sickened an outright majority – in
one instance sixty-seven percent – of the population. But
the virus causing this epidemic was an H3N2 virus that
normally caused mild disease. In fact, the epidemic
affected only thirteen of 111 health districts in Madagas-
car before fading away [4]. Something similar may have
happened in the British base.
Jordan considered other possible origins of the pandemic
in early 1918 in France and India. He concluded that it
was highly unlikely that the pandemic began in any of
them [3].
That left the United States. Jordan looked at a series of
spring outbreaks there. The evidence seemed far stronger.
One could see influenza jumping from Army camp to
camp, then into cities, and traveling with troops to
Europe. His conclusion: the United States was the site of
origin.
A later equally comprehensive, multi-volume British
study of the pandemic agreed with Jordan. It too found no
evidence for the influenza's origin in the Orient, it too
rejected the 1916 outbreak among British troops, and it
too concluded, "The disease was probably carried from
the United States to Europe [5]."
Australian Nobel laureate MacFarlane Burnet spent most
of his scientific career working on influenza and studied
the pandemic closely. He too concluded that the evidence
was "strongly suggestive" that the disease started in the
United States and spread with "the arrival of American
troops in France [6]."
Before dismissing the conclusions of these contemporary
investigators who lived through and studied the pan-
demic, one must remember how good many of them
were. They were very good indeed.
The Rockefeller Institute, whose investigators were inti-
mately involved in the problem, alone included extraordi-
nary people. By 1912 its head Simon Flexner – his brother
wrote the "Flexner report" that revolutionized American
medical education – used immune serum to bring the
mortality rate for meningococcal meningitis down from
over 80% to 18%; by contrast, in the 1990s at Massachu-
setts General Hospital a study found a 25% mortality rate
for bacterial meningitis. Peyton Rous won the Nobel Prize
in 1966 for work he did at the institute in 1911; he was
that far ahead of the scientific consensus. By 1918 Oswald
Avery and others at Rockefeller Institute had already pro-
duced both an effective curative serum and a vaccine for
the most common pneumococcal pneumonias. At least
partly because of the pandemic, Avery would spend the
rest of his career studying pneumonia. That work led
directly to his discovery of the "transforming principle" –
his discovery that DNA carries the genetic code.
The observations of investigators of this quality cannot be
dismissed lightly. Jordan was of this quality.
More evidence against Oxford's hypothesis comes from
Dr. Jeffrey Taubenberger, well-known for his work extract-
ing samples of the 1918 virus from preserved tissue and
sequencing its genome. He initially believed, based on
statistical analysis of the rate of mutation of the virus that
it existed for two or three years prior to the pandemic. But
further work convinced him that the virus emerged only a
few months prior to the pandemic (personal communica-
tion with the author from J Taubenberger, June 5
th
2003).
So if the contemporary observers were correct, if American
troops carried the virus to Europe, where in the United
States did it begin?
Both contemporary epidemiological studies and lay histo-
ries of the pandemic have identified the first known out-
break of epidemic influenza as occurring at Camp
Funston, now Ft. Riley, in Kansas. But there was one place
where a previously unknown – and remarkable – epi-
demic of influenza occurred.
Haskell County, Kansas, lay three hundred miles to the
west of Funston. There the smell of manure meant civili-
zation. People raised grains, poultry, cattle, and hogs.
Sod-houses were so common that even one of the
county's few post offices was located in a dug-out sod
home. In 1918 the population was just 1,720, spread over
578 square miles. But primitive and raw as life could be
there, science had penetrated the county in the form of Dr.
Loring Miner. Enamored of ancient Greece – he periodi-
cally reread the classics in Greek – he epitomized William
Welch's comment that "the results [of medical education]
were better than the system." His son was also a doctor,
trained in fully scientific ways, serving in the Navy in Bos-
ton.
In late January and early February 1918 Miner was sud-
denly faced with an epidemic of influenza, but an influ-
enza unlike any he had ever seen before. Soon dozens of
his patients – the strongest, the healthiest, the most robust
people in the county – were being struck down as sud-
denly as if they had been shot. Then one patient pro-
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gressed to pneumonia. Then another. And they began to
die. The local paper Santa Fe Monitor, apparently worried
about hurting morale in wartime, initially said little about
the deaths but on inside pages in February reported, "Mrs.
Eva Van Alstine is sick with pneumonia. Her little son Roy
is now able to get up... Ralph Lindeman is still quite sick...
Goldie Wolgehagen is working at the Beeman store during
her sister Eva's sickness... Homer Moody has been
reported quite sick... Mertin, the young son of Ernest
Elliot, is sick with pneumonia... Pete Hesser's children are
recovering nicely... Ralph McConnell has been quite sick
this week (Santa Fe Monitor, February 14
th
, 1918)."
The epidemic got worse. Then, as abruptly as it came, it
disappeared. Men and women returned to work. Children
returned to school. And the war regained its hold on peo-
ple's thoughts.
The disease did not, however, slip from Miner's thoughts.
Influenza was neither a reportable disease, nor a disease
that any state or federal public health agency tracked. Yet
Miner considered this incarnation of the disease so dan-
gerous that he warned national public health officials
about it. Public Health Reports (now Morbidity and Mor-
tality Weekly Report), a weekly journal produced by the
U.S. Public Health Service to alert health officials to out-
breaks of communicable diseases throughout the world,
published his warning. In the first six months of 1918,
this would be the only reference in that journal to influ-
enza anywhere in the world.
Historians and epidemiologists have previously ignored
Haskell most likely because his report was not published
until April and it referred to deaths on March 30, after
influenza outbreaks elsewhere. In actuality, by then the
county was free of influenza. Haskell County, Kansas, is
the first recorded instance anywhere in the world of an
outbreak of influenza so unusual that a physician warned
public health officials. It remains the first recorded
instance suggesting that a new virus was adapting, vio-
lently, to man.
If the virus did not originate in Haskell, there is no good
explanation for how it arrived there. There were no other
known outbreaks anywhere in the United States from
which someone could have carried the disease to Haskell,
and no suggestions of influenza outbreaks in either news-
papers or reflected in vital statistics anywhere else in the
region. And unlike the 1916 outbreak in France, one can
trace with perfect definiteness the route of the virus from
Haskell to the outside world.
All Army personnel from the county reported to Funston
for training. Friends and family visited them at Funston.
Soldiers came home on leave, then returned to Funston.
The Monitor reported in late February, "Most everybody
over the country is having lagrippe or pneumonia (Santa
Fe Monitor, February 21
st
1918)." It also noted, "Dean
Nilson surprised his friends by arriving at home from
Camp Funston on a five days furlough. Dean looks like
soldier life agrees with him." He soon returned to the
camp. Ernest Elliot left to visit his brother at Funston as
his child fell ill. On February 28, John Bottom left for Fun-
ston. "We predict John will make an ideal soldier," said
the paper (Santa Fe Monitor February 28
th
, 1918).
These men, and probably others unnamed by the paper,
were exposed to influenza and would have arrived in Fun-
ston between February 26 and March 2. On March 4 the
first soldier at the camp reported ill with influenza at sick
call. The camp held an average of 56,222 troops. Within
three weeks more than eleven hundred others were sick
enough to require hospitalization, and thousands more –
the precise number was not recorded – needed treatment
at infirmaries scattered around the base.
Whether or not the Haskell virus did spread across the
world, the timing of the Funston explosion strongly sug-
gests that the influenza outbreak there did come from
Haskell. Meanwhile Funston fed a constant stream of men
to other American locations and to Europe, men whose
business was killing. They would be more proficient at it
than they knew.
Soldiers moved uninterrupted between Funston and the
outside world, especially to other Army bases and France.
On March 18, Camps Forrest and Greenleaf in Georgia
saw their first cases of influenza and by the end of April
twenty-four of the thirty-six main Army camps suffered an
influenza epidemic [3]. Thirty of the fifty largest cities in
the country also had an April spike in excess mortality
from influenza and pneumonia [7]. Although this spring
wave was generally mild – the killing second wave struck
in the fall – there were still some disturbing findings. A
subsequent Army study said, "At this time the fulminating
pneumonia, with wet hemorrhagic lungs, fatal in from 24
to 48 hours, was first observed [8]." (Pathology reports
suggest what we now call ARDS.) The first recorded
autopsy in Chicago of an influenza victim was conducted
in early April. The pathologist noted, "The lungs were full
of hemorrhages." He found this unusual enough to ask
the then-editor of The Journal of Infectious Diseases "to
look over it as a new disease" [3].
By then, influenza was erupting in France, first at Brest, the
single largest port of disembarkation for American troops.
By then, as MacFarlane Burnet later said, "It is convenient
to follow the story of influenza at this period mainly in
regard to the army experiences in America and Europe
[6]."
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The fact that the 1918 pandemic likely began in the
United States matters because it tells investigators where
to look for a new virus. They must look everywhere.
In recent years the World Health Organization and local
public health authorities have intervened several times
when new influenza viruses have infected man. These
interventions have prevented the viruses from adapting to
man and igniting a new pandemic. But only 83 countries
in the world – less than half – participate in WHO's sur-
veillance system (WHO's flunet website http://
rhone.b3e.jussieu.fr/flunet/www/docs.html). While some
monitoring occurs even in those countries not formally
affiliated with WHO's surveillance system, it is hardly ade-
quate. If the virus did cross into man in a sparsely popu-
lated region of Kansas, and not in a densely populated
region of Asia, then such an animal-to-man cross-over can
happen anywhere. And unless WHO gets more resources
and political leaders move aggressively on the diplomatic
front, then a new pandemic really is all too inevitable.
References
1. Barry JM: The Great Influenza: the Epic Story of the Deadliest Plague in
History Firstth edition. New York: Viking; 2004.
2. Oxford JS: The so-called Great Spanish Influenza Pandemic of
1918 may have originated in France in 1916. Philos Trans R Soc
Lond B Biol Sci 2001, 356:1857-1859.
3. Jordan E: Epidemic influenza Firstth edition. Chicago: AMA; 1927.
4. Outbreak of influenza, Madagascar, July-August 2002. Euro
Surveill 2002, 7:172-174.
5. Thomson D, Thomson R: Influenza. Annals of the Pickett-Thomson
Research Laboratory Firstth edition. Baltimore: Williams and Wilkens;
1934.
6. Burnet FM, Clark E: Influenza: a survey of the last fifty years Melbourne.:
Macmillan Co; 1942.
7. Collins SD, Frost WH, Gover M, Sydenstricker E: Mortality from influ-
enza and pneumonia in the 50 largest cities of the United States Firstth
edition. Washington: U.S. Government Printing Office; 1930.
8. Ireland MW: Medical Department of the United States Army in the World
War – Communicable diseases Firstth edition. Washington: U.S. Govern-
ment Printing Office; 1928.
