The Great Influenza: The Epic Story of the Deadliest Plague in History (Revised Edition)
Author:
Genres: History, Medicine
Book Type: Paperback
Author:
Genres: History, Medicine
Book Type: Paperback
Alice B. reviewed on + 3563 more book reviews
Helpful Score: 1
In the year 1800, the practice of medicine had changed little from that in antiquity. The rapid progress in other sciences in the 18th century had had little impact on medicine, which one historian called âthe withered arm of scienceâ. This began to change as the 19th century progressed. Researchers, mostly in Europe and especially in Germany, began to lay the foundations for a scientific approach to medicine and public health, understanding the causes of disease and searching for means of prevention and cure. The invention of new instruments for medical examination, anesthesia, and antiseptic procedures began to transform the practice of medicine and surgery.
All of these advances were slow to arrive in the United States. As late as 1900 only one medical school in the U.S. required applicants to have a college degree, and only 20% of schools required a high school diploma. More than a hundred U.S. medical schools accepted any applicant who could pay, and many graduated doctors who had never seen a patient or done any laboratory work in science. In the 1870s, only 10% of the professors at Harvard's medical school had a Ph.D.
In 1873, Johns Hopkins died, leaving his estate of US$ 3.5 million to found a university and hospital. The trustees embarked on an ambitious plan to build a medical school to be the peer of those in Germany, and began to aggressively recruit European professors and Americans who had studied in Europe to build a world class institution. By the outbreak of World War I in Europe, American medical research and education, still concentrated in just a few centres of excellence, had reached the standard set by Germany. It was about to face its greatest challenge.
With the entry of the United States into World War I in April of 1917, millions of young men conscripted for service were packed into overcrowded camps for training and preparation for transport to Europe. These camps, thrown together on short notice, often had only rudimentary sanitation and shelter, with many troops living in tent cities. Large number of doctors and especially nurses were recruited into the Army, and by the start of 1918 many were already serving in France. Doctors remaining in private practice in the U.S. were often older men, trained before the revolution in medical education and ignorant of modern knowledge of diseases and the means of treating them.
In all American wars before World War I, more men died from disease than combat. In the Civil War, two men died from disease for every death on the battlefield. Army Surgeon General William Gorgas vowed that this would not be the case in the current conflict. He was acutely aware that the overcrowded camps, frequent transfers of soldiers among far-flung bases, crowded and unsanitary troop transport ships, and unspeakable conditions in the trenches were a tinderbox just waiting for the spark of an infectious disease to ignite it. But the demand for new troops for the front in France caused his cautions to be overruled, and still more men were packed into the camps.
Early in 1918, a doctor in rural Haskell County, Kansas began to treat patients with a disease he diagnosed as influenza. But this was nothing like the seasonal influenza with which he was familiar. In typical outbreaks of influenza, the people at greatest risk are the very young (whose immune systems have not been previously exposed to the virus) and the very old, who lack the physical resilience to withstand the assault by the disease. Most deaths are among these groups, leading to a âbathtub curveâ of mortality. This outbreak was different: the young and elderly were largely spared, while those in the prime of life were struck down, with many dying quickly of symptoms which resembled pneumonia. Slowly the outbreak receded, and by mid-March things were returning to normal. (The location and mechanism where the disease originated remain controversial to this day and we may never know for sure. After weighing competing theories, the author believes the Kansas origin most likely, but other origins have their proponents.)
That would have been the end of it, had not soldiers from Camp Funston, the second largest Army camp in the U.S., with 56,000 troops, visited their families in Haskell County while on leave. They returned to camp carrying the disease. The spark had landed in the tinderbox. The disease spread outward as troop trains travelled between camps. Often a train would leave carrying healthy troops (infected but not yet symptomatic) and arrive with up to half the company sick and highly infectious to those at the destination. Before long the disease arrived via troop ships at camps and at the front in France.
This was just the first wave. The spring influenza was unusual in the age group it hit most severely, but was not particularly more deadly than typical annual outbreaks. Then in the fall a new form of the disease returned in a much more virulent form. It is theorised that under the chaotic conditions of wartime a mutant form of the virus had emerged and rapidly spread among the troops and then passed into the civilian population. The outbreak rapidly spread around the globe, and few regions escaped. It was particularly devastating to aboriginal populations in remote regions like the Arctic and Pacific islands who had not developed any immunity to influenza.
The pathogen in the second wave could kill directly within a day by destroying the lining of the lung and effectively suffocating the patient. The disease was so virulent and aggressive that some medical researchers doubted it was influenza at all and suspected some new kind of plague. Even those who recovered from the disease had much of their immunity and defences against respiratory infection so impaired that some people who felt well enough to return to work would quickly come down with a secondary infection of bacterial pneumonia which could kill them.
All of the resources of the new scientific medicine were thrown into the battle with the disease, with little or no impact upon its progression. The cause of influenza was not known at the time: some thought it was a bacterial disease while others suspected a virus. Further adding to the confusion is that influenza patients often had a secondary infection of bacterial pneumonia, and the organism which causes that disease was mis-identified as the pathogen responsible for influenza. Heroic efforts were made, but the state of medical science in 1918 was simply not up to the challenge posed by influenza.
A century later, influenza continues to defeat every attempt to prevent or cure it, and another global pandemic remains a distinct possibility. Supportive treatment in the developed world and the availability of antibiotics to prevent secondary infection by pneumonia will reduce the death toll, but a mass outbreak of the virus on the scale of 1918 would quickly swamp all available medical facilities and bring society to the brink as it did then. Even regular influenza kills between a quarter and a half million people a year. The emergence of a killer strain like that of 1918 could increase this number by a factor of ten or twenty.
Influenza is such a formidable opponent due to its structure. It is an RNA virus which, unusually for a virus, has not a single strand of genetic material but seven or eight separate strands of RNA. Some researchers argue that in an organism infected with two or more variants of the virus these strands can mix to form new mutants, allowing the virus to mutate much faster than other viruses with a single strand of genetic material (this is controversial). The virus particle is surrounded by proteins called hemagglutinin (HA) and neuraminidase (NA). HA allows the virus to break into a target cell, while NA allows viruses replicated within the cell to escape to infect others.
What makes creating a vaccine for influenza so difficult is that these HA and NA proteins are what the body's immune system uses to identify the virus as an invader and kill it. But HA and NA come in a number of variants, and a specific strain of influenza may contain one from column H and one from column N, creating a large number of possibilities. For example, H1N2 is endemic in birds, pigs, and humans. H5N1 caused the bird flu outbreak in 2004, and H1N1 was responsible for the 1918 pandemic. It gets worse. As a child, when you are first exposed to influenza, your immune system will produce antibodies which identify and target the variant to which you were first exposed. If you were infected with and recovered from, say, H3N2, you'll be pretty well protected against it. But if, subsequently, you encounter H1N1, your immune system will recognise it sufficiently to crank out antibodies, but they will be coded to attack H3N2, not the H1N1 you're battling, against which they're useless. Influenza is thus a chameleon, constantly changing its colours to hide from the immune system.
Strains of influenza tend to come in waves, with one HxNy variant dominating for some number of years, then shifting to another. Developers of vaccines must play a guessing game about which you're likely to encounter in a given year. This explains why the 1918 pandemic particularly hit healthy adults. Over the decades preceding the 1918 outbreak, the primary variant had shifted from H1N1, then decades of another variant, and then after 1900 H1N1 came back to the fore. Consequently, when the deadly strain of H1N1 appeared in the fall of 1918, the immune systems of both young and elderly people were ready for it and protected them, but those in between had immune systems which, when confronted with H1N1, produced antibodies for the other variant, leaving them vulnerable.
With no medical defence against or cure for influenza even today, the only effective response in the case of an outbreak of a killer strain is public health measures such as isolation and quarantine. Influenza is airborne and highly infectious: the gauze face masks you see in pictures from 1918 were almost completely ineffective. The government response to the outbreak in 1918 could hardly have been worse. After creating military camps which were nothing less than a culture medium containing those in the most vulnerable age range packed in close proximity, once the disease broke out and reports began to arrive that this was something new and extremely lethal, the troop trains and ships continued to run due to orders from the top that more and more men had to be fed into the meat grinder that was the Western Front. This inoculated camp after camp. Then, when the disease jumped into the civilian population and began to devastate cities adjacent to military facilities such as Boston and Philadelphia, the press censors of Wilson's war machine decided that honest reporting of the extent and severity of the disease or measures aimed at slowing its spread would impact âmoraleâ and war production, so newspapers were ordered to either ignore it or print useless happy talk which only accelerated the epidemic. The result was that in the hardest-hit cities, residents confronted with the reality before their eyes giving to lie to the propaganda they were hearing from authorities retreated into fear and withdrawal, allowing neighbours to starve rather than risk infection by bringing them food.
As was known in antiquity, the only defence against an infectious disease with no known medical intervention is quarantine. In Western Samoa, the disease arrived in September 1918 on a German steamer. By the time the disease ran its course, 22% of the population of the islands was dead. Just a few kilometres across the ocean in American Samoa, authorities imposed a rigid quarantine and not a single person died of influenza.
We will never know the worldwide extent of the 1918 pandemic. Many of the hardest-hit areas, such as China and India, did not have the infrastructure to collect epidemiological data and what they had collapsed under the impact of the crisis. Estimates are that on the order of 500 million people worldwide were infected and that between 50 and 100 million died: three to five percent of the world's population.
Researchers do not know why the 1918 second wave pathogen was so lethal. The genome has been sequenced and nothing jumps out from it as an obvious cause. Understanding its virulence may require recreating the monster and experimenting with it in animal models. Obviously, this is not something which should be undertaken without serious deliberation beforehand and extreme precautions, but it may be the only way to gain the knowledge needed to treat those infected should a similar wild strain emerge in the future. (It is possible this work may have been done but not published because it could provide a roadmap for malefactors bent on creating a synthetic plague. If this be the case, we'll probably never know about it.)
Although medicine has made enormous strides in the last century, influenza, which defeated the world's best minds in 1918, remains a risk, and in a world with global air travel moving millions between dense population centres, an outbreak today would be even harder to contain. Let us hope that in that dire circumstance authorities will have the wisdom and courage to take the kind of dramatic action which can make the difference between a regional tragedy and a global cataclysm.
All of these advances were slow to arrive in the United States. As late as 1900 only one medical school in the U.S. required applicants to have a college degree, and only 20% of schools required a high school diploma. More than a hundred U.S. medical schools accepted any applicant who could pay, and many graduated doctors who had never seen a patient or done any laboratory work in science. In the 1870s, only 10% of the professors at Harvard's medical school had a Ph.D.
In 1873, Johns Hopkins died, leaving his estate of US$ 3.5 million to found a university and hospital. The trustees embarked on an ambitious plan to build a medical school to be the peer of those in Germany, and began to aggressively recruit European professors and Americans who had studied in Europe to build a world class institution. By the outbreak of World War I in Europe, American medical research and education, still concentrated in just a few centres of excellence, had reached the standard set by Germany. It was about to face its greatest challenge.
With the entry of the United States into World War I in April of 1917, millions of young men conscripted for service were packed into overcrowded camps for training and preparation for transport to Europe. These camps, thrown together on short notice, often had only rudimentary sanitation and shelter, with many troops living in tent cities. Large number of doctors and especially nurses were recruited into the Army, and by the start of 1918 many were already serving in France. Doctors remaining in private practice in the U.S. were often older men, trained before the revolution in medical education and ignorant of modern knowledge of diseases and the means of treating them.
In all American wars before World War I, more men died from disease than combat. In the Civil War, two men died from disease for every death on the battlefield. Army Surgeon General William Gorgas vowed that this would not be the case in the current conflict. He was acutely aware that the overcrowded camps, frequent transfers of soldiers among far-flung bases, crowded and unsanitary troop transport ships, and unspeakable conditions in the trenches were a tinderbox just waiting for the spark of an infectious disease to ignite it. But the demand for new troops for the front in France caused his cautions to be overruled, and still more men were packed into the camps.
Early in 1918, a doctor in rural Haskell County, Kansas began to treat patients with a disease he diagnosed as influenza. But this was nothing like the seasonal influenza with which he was familiar. In typical outbreaks of influenza, the people at greatest risk are the very young (whose immune systems have not been previously exposed to the virus) and the very old, who lack the physical resilience to withstand the assault by the disease. Most deaths are among these groups, leading to a âbathtub curveâ of mortality. This outbreak was different: the young and elderly were largely spared, while those in the prime of life were struck down, with many dying quickly of symptoms which resembled pneumonia. Slowly the outbreak receded, and by mid-March things were returning to normal. (The location and mechanism where the disease originated remain controversial to this day and we may never know for sure. After weighing competing theories, the author believes the Kansas origin most likely, but other origins have their proponents.)
That would have been the end of it, had not soldiers from Camp Funston, the second largest Army camp in the U.S., with 56,000 troops, visited their families in Haskell County while on leave. They returned to camp carrying the disease. The spark had landed in the tinderbox. The disease spread outward as troop trains travelled between camps. Often a train would leave carrying healthy troops (infected but not yet symptomatic) and arrive with up to half the company sick and highly infectious to those at the destination. Before long the disease arrived via troop ships at camps and at the front in France.
This was just the first wave. The spring influenza was unusual in the age group it hit most severely, but was not particularly more deadly than typical annual outbreaks. Then in the fall a new form of the disease returned in a much more virulent form. It is theorised that under the chaotic conditions of wartime a mutant form of the virus had emerged and rapidly spread among the troops and then passed into the civilian population. The outbreak rapidly spread around the globe, and few regions escaped. It was particularly devastating to aboriginal populations in remote regions like the Arctic and Pacific islands who had not developed any immunity to influenza.
The pathogen in the second wave could kill directly within a day by destroying the lining of the lung and effectively suffocating the patient. The disease was so virulent and aggressive that some medical researchers doubted it was influenza at all and suspected some new kind of plague. Even those who recovered from the disease had much of their immunity and defences against respiratory infection so impaired that some people who felt well enough to return to work would quickly come down with a secondary infection of bacterial pneumonia which could kill them.
All of the resources of the new scientific medicine were thrown into the battle with the disease, with little or no impact upon its progression. The cause of influenza was not known at the time: some thought it was a bacterial disease while others suspected a virus. Further adding to the confusion is that influenza patients often had a secondary infection of bacterial pneumonia, and the organism which causes that disease was mis-identified as the pathogen responsible for influenza. Heroic efforts were made, but the state of medical science in 1918 was simply not up to the challenge posed by influenza.
A century later, influenza continues to defeat every attempt to prevent or cure it, and another global pandemic remains a distinct possibility. Supportive treatment in the developed world and the availability of antibiotics to prevent secondary infection by pneumonia will reduce the death toll, but a mass outbreak of the virus on the scale of 1918 would quickly swamp all available medical facilities and bring society to the brink as it did then. Even regular influenza kills between a quarter and a half million people a year. The emergence of a killer strain like that of 1918 could increase this number by a factor of ten or twenty.
Influenza is such a formidable opponent due to its structure. It is an RNA virus which, unusually for a virus, has not a single strand of genetic material but seven or eight separate strands of RNA. Some researchers argue that in an organism infected with two or more variants of the virus these strands can mix to form new mutants, allowing the virus to mutate much faster than other viruses with a single strand of genetic material (this is controversial). The virus particle is surrounded by proteins called hemagglutinin (HA) and neuraminidase (NA). HA allows the virus to break into a target cell, while NA allows viruses replicated within the cell to escape to infect others.
What makes creating a vaccine for influenza so difficult is that these HA and NA proteins are what the body's immune system uses to identify the virus as an invader and kill it. But HA and NA come in a number of variants, and a specific strain of influenza may contain one from column H and one from column N, creating a large number of possibilities. For example, H1N2 is endemic in birds, pigs, and humans. H5N1 caused the bird flu outbreak in 2004, and H1N1 was responsible for the 1918 pandemic. It gets worse. As a child, when you are first exposed to influenza, your immune system will produce antibodies which identify and target the variant to which you were first exposed. If you were infected with and recovered from, say, H3N2, you'll be pretty well protected against it. But if, subsequently, you encounter H1N1, your immune system will recognise it sufficiently to crank out antibodies, but they will be coded to attack H3N2, not the H1N1 you're battling, against which they're useless. Influenza is thus a chameleon, constantly changing its colours to hide from the immune system.
Strains of influenza tend to come in waves, with one HxNy variant dominating for some number of years, then shifting to another. Developers of vaccines must play a guessing game about which you're likely to encounter in a given year. This explains why the 1918 pandemic particularly hit healthy adults. Over the decades preceding the 1918 outbreak, the primary variant had shifted from H1N1, then decades of another variant, and then after 1900 H1N1 came back to the fore. Consequently, when the deadly strain of H1N1 appeared in the fall of 1918, the immune systems of both young and elderly people were ready for it and protected them, but those in between had immune systems which, when confronted with H1N1, produced antibodies for the other variant, leaving them vulnerable.
With no medical defence against or cure for influenza even today, the only effective response in the case of an outbreak of a killer strain is public health measures such as isolation and quarantine. Influenza is airborne and highly infectious: the gauze face masks you see in pictures from 1918 were almost completely ineffective. The government response to the outbreak in 1918 could hardly have been worse. After creating military camps which were nothing less than a culture medium containing those in the most vulnerable age range packed in close proximity, once the disease broke out and reports began to arrive that this was something new and extremely lethal, the troop trains and ships continued to run due to orders from the top that more and more men had to be fed into the meat grinder that was the Western Front. This inoculated camp after camp. Then, when the disease jumped into the civilian population and began to devastate cities adjacent to military facilities such as Boston and Philadelphia, the press censors of Wilson's war machine decided that honest reporting of the extent and severity of the disease or measures aimed at slowing its spread would impact âmoraleâ and war production, so newspapers were ordered to either ignore it or print useless happy talk which only accelerated the epidemic. The result was that in the hardest-hit cities, residents confronted with the reality before their eyes giving to lie to the propaganda they were hearing from authorities retreated into fear and withdrawal, allowing neighbours to starve rather than risk infection by bringing them food.
As was known in antiquity, the only defence against an infectious disease with no known medical intervention is quarantine. In Western Samoa, the disease arrived in September 1918 on a German steamer. By the time the disease ran its course, 22% of the population of the islands was dead. Just a few kilometres across the ocean in American Samoa, authorities imposed a rigid quarantine and not a single person died of influenza.
We will never know the worldwide extent of the 1918 pandemic. Many of the hardest-hit areas, such as China and India, did not have the infrastructure to collect epidemiological data and what they had collapsed under the impact of the crisis. Estimates are that on the order of 500 million people worldwide were infected and that between 50 and 100 million died: three to five percent of the world's population.
Researchers do not know why the 1918 second wave pathogen was so lethal. The genome has been sequenced and nothing jumps out from it as an obvious cause. Understanding its virulence may require recreating the monster and experimenting with it in animal models. Obviously, this is not something which should be undertaken without serious deliberation beforehand and extreme precautions, but it may be the only way to gain the knowledge needed to treat those infected should a similar wild strain emerge in the future. (It is possible this work may have been done but not published because it could provide a roadmap for malefactors bent on creating a synthetic plague. If this be the case, we'll probably never know about it.)
Although medicine has made enormous strides in the last century, influenza, which defeated the world's best minds in 1918, remains a risk, and in a world with global air travel moving millions between dense population centres, an outbreak today would be even harder to contain. Let us hope that in that dire circumstance authorities will have the wisdom and courage to take the kind of dramatic action which can make the difference between a regional tragedy and a global cataclysm.
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