Disease : Influenza  /    Virus strain :  Strains of A/H1N1   /   Location : Worldwide   /   First outbreak  :  Disputed

Date  :  February 1918 – April 1920

Suspected cases‡  :  500 million (estimate)[2]   /   Deaths  :  17–50+ million (estimate)

The Spanish flu, also known as the 1918 flu pandemic, was an unusually deadly influenza pandemic caused by the H1N1 influenza A virus. Lasting February 1918 to April 1920, it infected 500 million people–about a third of the world's population at the time–in four successive waves. The death toll may have been anything from 17 million to 50 million, and possibly as high as 100 million, making it one of the deadliest pandemics in human history.[3]

The first observations of illness and mortality were documented in the United States (in Fort Riley, Haskell County, Kansas as well as in New York City), France (Brest), Germany and the United Kingdom. To maintain morale, World War I censors minimized these early reports. Newspapers were free to report the epidemic's effects in neutral Spain, such as the grave illness of King Alfonso XIII, and these stories created a false impression of Spain as especially hard hit. This gave rise to the name "Spanish" flu. Historical and epidemiological data are inadequate to identify with certainty the pandemic's geographic origin, with varying views as to its location.

Most influenza outbreaks disproportionately kill the very young and the very old, with a higher survival rate for those in between, but the Spanish flu pandemic resulted in a higher than expected mortality rate for young adults.[4] Scientists offer several possible explanations for the high mortality rate of the 1918 influenza pandemic. Some analyses have shown the virus to be particularly deadly because it triggers a cytokine storm, which ravages the stronger immune system of young adults.[5] In contrast, a 2007 analysis of medical journals from the period of the pandemic found that the viral infection was no more aggressive than previous influenza strains.[6][7] Instead, malnourishment, overcrowded medical camps and hospitals, and poor hygiene, all exacerbated by the recent war, promoted bacterial superinfection. This superinfection killed most of the victims, typically after a somewhat prolonged death bed.[8][9]

The 1918 Spanish flu was the first of two pandemics caused by H1N1 influenza A virus; the second was the 2009 swine flu pandemic.[10]

name stems from the pandemic's spread to Spain from France in November 1918.[11][12] Spain was not involved in the war, having remained neutral, and had not imposed wartime censorship.[13][14] Newspapers were therefore free to report the epidemic's effects, such as the grave illness of King Alfonso XIII, and these widely-spread stories created a false impression of Spain as especially hard hit.[15]

Alternative names were also used at the time of the pandemic. Similar to the name of Spanish flu, many of these also alluded to the purported origins of the disease. In Senegal it was named 'the Brazilian flu', and in Brazil 'the German flu', while in Poland it was known as 'the Bolshevik disease'.[16] In Spain itself, the nickname for the flu, the "Naples Soldier", was adopted from a 1916 operetta, The Song of Forgetting (La canción del olvido) after one of the librettists quipped that the play's most popular musical number, Naples Soldier, was as catchy as the flu.[17]

Nearly a century after the Spanish flu struck in 1918–1920, the World Health Organization (WHO) called on scientists, national authorities and the media to follow best practices in naming new human infectious diseases to minimize unnecessary negative effects on nations, economies and people - this includes a recommendation to no longer name diseases after places.[18][19] More modern terms for this virus include the "1918 influenza pandemic," the "1918 flu pandemic," or variations of these.[20][21][22]

History - Timeline

First wave of early 1918

The pandemic is conventionally marked as having begun on 4 March 1918, with the recording of the case of Albert Gitchell, an army cook at Camp Funston in Kansas, United States, despite there likely having been cases before him.[23] The disease had been observed in Haskell County in January 1918, prompting local doctor Loring Miner to warn the US Public Health Service's academic journal.[24] Within days, 522 men at the camp had reported sick.[25] By 11 March 1918, the virus had reached Queens, New York.[26] Failure to take preventive measures in March/April was later criticised.[27]

As the US had entered World War I, the disease quickly spread from Camp Funston, a major training ground for troops of the American Expeditionary Forces, to other US Army camps and Europe, becoming an epidemic in the Midwest, East Coast, and French ports by April 1918, and reaching the Western Front by the middle of the month.[23] It then quickly spread to the rest of France, Great Britain, Italy, and Spain, and in May reached Wrocław and Odessa.[23] After the signing of the Treaty of Brest-Litovsk, Germany started releasing Russian prisoners of war who then brought the disease to their country.[28] It reached North Africa, India, and Japan in May, and soon after had likely gone around the world as there had been recorded cases in Southeast Asia in April.[29] In June an outbreak was reported in China.[30] After reaching Australia in July, the wave started to recede.[29]

The first wave of the flu lasted from the first quarter of 1918, and was relatively mild.[31] Mortality rates were not appreciably above normal;[32] in the United States ~75,000 flu-related deaths were reported in the first six months of 1918, compared to ~63,000 deaths during the same time period in 1915.[33] In Madrid, Spain, fewer than 1,000 people died from influenza between May and June 1918.[34] There were no reported quarantines during the first quarter of 1918. However, the first wave caused a significant disruption in the military operations of World War I, with three-quarters of French troops, half the British forces, and over 900,000 German soldiers sick.[35]

Seattle police wearing masks in December 1918

Deadly second wave of late 1918

The second wave began in the second half of August, probably spreading to Boston and Freetown, Sierra Leone by ships from Brest, where it had likely arrived with American troops or French recruits for naval training.[35] From the Boston Navy Yard and Camp Devens (later renamed Fort Devens), about 30 miles west of Boston, other U.S. military sites were soon afflicted, as were troops being transported to Europe.[36] Helped by troop movements, it spread over the next two months to all of North America, and then to Central and South America, also reaching Brazil and the Caribbean on ships.[37] From Freetown, the pandemic continued to spread through West Africa along the coast, rivers, and the colonial railways, and from railheads to more remote communities, while South Africa received it in September on ships bringing back members of the South African Native Labour Corps returning from France.[37] From there it spread around Southern Africa and beyond the Zambezi, reaching Ethiopia in November.[38]

From Europe the second wave swept through Russia in a southwest-northeast diagonal front, as well as being brought to Arkhangelsk by the North Russia intervention, and then spread throughout Asia following the Russian Civil War and the Trans-Siberian railway, reaching Iran (where it spread through the holy city of Mashhad), and then later India in September, as well as China and Japan in October.[39] The celebrations of the Armistice of 11 November 1918 also caused outbreaks in Lima and Nairobi, but by December the wave was mostly over.[40]

American Expeditionary Force victims of the Spanish flu at U.S. Army Camp Hospital no. 45 in Aix-les-Bains, France, in 1918

The second wave of the 1918 pandemic was much more deadly than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. October 1918 was the month with the highest fatality rate of the whole pandemic.[41]

Third wave of 1919

In January 1919 a third wave of the Spanish Flu hit Australia, where it killed 12,000 following the lifting of a maritime quarantine, and then spread quickly through Europe and the United States, where it lingered through the Spring and until June 1919.[42][43][44][40] It primarily affected Spain, Serbia, Mexico and Great Britain, resulting in hundreds of thousands of deaths.[45] It was less severe than the second wave but still much more deadly than the initial first wave. In the United States, isolated outbreaks occurred in some cities including Los Angeles,[46] New York City,[47] Memphis, Nashville, San Francisco and St. Louis.[48] Overall American mortality rates were in the tens of thousands during the first six months of 1919.[49]

Fourth wave of 1920

In spring 1920 a very minor fourth wave occurred in isolated areas including New York City,[47] the United Kingdom, Austria, Scandinavia, and some South American islands.[50] Peru experienced a late wave in early 1920, and Japan had one from late 1919 to 1920, with the last cases in March.[51]

American Red Cross nurses tend to flu patients in temporary wards set up inside Oakland Municipal Auditorium, 1918.

History - Potential origins

Despite its name, historical and epidemiological data cannot identify the geographic origin of the Spanish flu.[2] However, several theories have been proposed.

United States

The first confirmed cases originated in the United States. Historian Alfred W. Crosby stated in 2003 that the flu originated in Kansas,[52] and popular author John M. Barry described a January 1918 outbreak in Haskell County, Kansas, as the point of origin in his 2004 article.[5]

A 2018 study of tissue slides and medical reports led by evolutionary biology professor Michael Worobey found evidence against the disease originating from Kansas, as those cases were milder and had fewer deaths compared to the infections in New York City in the same time period. The study did find evidence through phylogenetic analyses that the virus likely had a North American origin, though it was not conclusive. In addition, the haemagglutinin glycoproteins of the virus suggest that it originated long before 1918, and other studies suggest that the reassortment of the H1N1 virus likely occurred in or around 1915.[53]

Europe

The major UK troop staging and hospital camp in Étaples in France has been theorized by virologist John Oxford as being at the center of the Spanish flu.[54] His study found that in late 1916 the Étaples camp was hit by the onset of a new disease with high mortality that caused symptoms similar to the flu.[55][54] According to Oxford, a similar outbreak occurred in March 1917 at army barracks in Aldershot,[56] and military pathologists later recognized these early outbreaks as the same disease as the 1918 flu.[57][54] The overcrowded camp and hospital was an ideal environment for the spread of a respiratory virus. The hospital treated thousands of victims of poison gas attacks, and other casualties of war, and 100,000 soldiers passed through the camp every day. It also was home to a piggery, and poultry was regularly brought in from surrounding villages to feed the camp. Oxford and his team postulated that a precursor virus, harbored in birds, mutated and then migrated to pigs kept near the front.[56][57]

A report published in 2016 in the Journal of the Chinese Medical Association found evidence that the 1918 virus had been circulating in the European armies for months and possibly years before the 1918 pandemic.[58] Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza began in Austria in early 1917.[59]

China

In 1993, Claude Hannoun, the leading expert on the 1918 flu at the Pasteur Institute, asserted the precursor virus was likely to have come from China and then mutated in the United States near Boston and from there spread to Brest, France, Europe's battlefields, the rest of Europe, and the rest of the world, with Allied soldiers and sailors as the main disseminators.[60] Hannoun considered several alternative hypotheses of origin, such as Spain, Kansas, and Brest, as being possible, but not likely.[60] In 2014, historian Mark Humphries argued that the mobilization of 96,000 Chinese laborers to work behind the British and French lines might have been the source of the pandemic. Humphries, of the Memorial University of Newfoundland in St. John's, based his conclusions on newly unearthed records. He found archival evidence that a respiratory illness that struck northern China (where the laborers came from) in November 1917 was identified a year later by Chinese health officials as identical to the Spanish flu.[61][62] However, no tissue samples have survived for modern comparison.[63] Nevertheless, there were some reports of respiratory illness on parts of the path the laborers took to get to Europe, which also passed through North America.[63]

One of the few regions of the world seemingly less affected by the 1918 flu pandemic was China, where several studies have documented a comparatively mild flu season in 1918.[64][65][66] (Although this is disputed due to lack of data during the Warlord Period, see Around the globe). This has led to speculation that the 1918 flu pandemic originated in China,[66][65][67][68] as the lower rates of flu mortality may be explained by the Chinese population's previously acquired immunity to the flu virus.[69][66][65]

A report published in 2016 in the Journal of the Chinese Medical Association found no evidence that the 1918 virus was imported to Europe via Chinese and Southeast Asian soldiers and workers and instead found evidence of its circulation in Europe before the pandemic.[58] The 2016 study suggested that the low flu mortality rate (an estimated one in a thousand) found among the Chinese and Southeast Asian workers in Europe meant that the deadly 1918 influenza pandemic could not have originated from those workers.[58] Further evidence against the disease being spread by Chinese workers was that workers entered Europe through other routes that did not result in a detectable spread, making them unlikely to have been the original hosts.[53]

Epidemiology and pathology - Transmission and mutation

As U.S. troops deployed en masse for the war effort in Europe, they carried the Spanish flu with them.

The basic reproduction number of the virus was between 2 and 3.[70] The close quarters and massive troop movements of World War I hastened the pandemic, and probably both increased transmission and augmented mutation. The war may also have reduced people's resistance to the virus. Some speculate the soldiers' immune systems were weakened by malnourishment, as well as the stresses of combat and chemical attacks, increasing their susceptibility.[71][72] A large factor in the worldwide occurrence of the flu was increased travel. Modern transportation systems made it easier for soldiers, sailors, and civilian travelers to spread the disease.[26] Another was lies and denial by governments, leaving the population ill-prepared to handle the outbreaks.[73]

The severity of the second wave has been attributed to the circumstances of the First World War.[74] In civilian life, natural selection favors a mild strain. Those who get very ill stay home, and those mildly ill continue with their lives, preferentially spreading the mild strain. In the trenches, natural selection was reversed. Soldiers with a mild strain stayed where they were, while the severely ill were sent on crowded trains to crowded field hospitals, spreading the deadlier virus. The second wave began, and the flu quickly spread around the world again. Consequently, during modern pandemics, health officials pay attention when the virus reaches places with social upheaval (looking for deadlier strains of the virus).[75] The fact that most of those who recovered from first-wave infections had become immune showed that it must have been the same strain of flu. This was most dramatically illustrated in Copenhagen, which escaped with a combined mortality rate of just 0.29% (0.02% in the first wave and 0.27% in the second wave) because of exposure to the less-lethal first wave.[76] For the rest of the population, the second wave was far more deadly; the most vulnerable people were those like the soldiers in the trenches – adults who were young and fit.[77]

After the lethal second wave struck in late 1918, new cases dropped abruptly – almost to nothing after the peak in the second wave.[78] In Philadelphia, for example, 4,597 people died in the week ending 16 October, but by 11 November, influenza had almost disappeared from the city. One explanation for the rapid decline in the lethality of the disease is that doctors became more effective in prevention and treatment of the pneumonia that developed after the victims had contracted the virus. However, John Barry stated in his 2004 book The Great Influenza: The Epic Story of the Deadliest Plague In History that researchers have found no evidence to support this position.[5] Another theory holds that the 1918 virus mutated extremely rapidly to a less lethal strain. This is a common occurrence with influenza viruses: there is a tendency for pathogenic viruses to become less lethal with time, as the hosts of more dangerous strains tend to die out.[5] Some fatal cases did continue into March 1919, killing one player in the 1919 Stanley Cup Finals.

Epidemiology and pathology - Signs and symptoms

US Army symptomology of the flu.

The majority of the infected experienced only the typical flu symptoms of sore throat, headache, and fever, especially during the first wave.[79] However, during the second wave the disease was much more serious, often complicated by bacterial pneumonia, which was often the cause of death.[79] This more serious type would cause heliotrope cyanosis to develop, whereby the skin would first develop two mahogany spots over the cheekbones which would then over a few hours spread to color the entire face blue, followed by black coloration first in the extremities and then further spreading to the limbs and the torso.[79] After this, death would follow within hours or days due to the lungs being filled with fluids.[79] Other signs and symptoms reported included spontaneous mouth and nosebleeds, miscarriages for pregnant women, a peculiar smell, teeth and hair falling, delirium, dizziness, insomnia, loss of hearing or smell, blurred vision, and impaired color vision.[79] One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred".[80] The severity of the symptoms was believed to be caused by cytokine storms.[81]

The majority of deaths were from bacterial pneumonia,[82][83][84] a common secondary infection associated with influenza. This pneumonia was itself caused by common upper respiratory-tract bacteria, which were able to get into the lungs via the damaged bronchial tubes of the victims.[85] The virus also killed people directly by causing massive hemorrhages and edema in the lungs.[86]Modern analysis has shown the virus to be particularly deadly because it triggers a cytokine storm (overreaction of the body's immune system).[5] One group of researchers recovered the virus from the bodies of frozen victims and transfected animals with it. The animals suffered rapidly progressive respiratory failure and death through a cytokine storm. The strong immune reactions of young adults were postulated to have ravaged the body, whereas the weaker immune reactions of children and middle-aged adults resulted in fewer deaths among those groups.[78][87]

Epidemiology and pathology - Misdiagnosis

Because the virus that caused the disease was too small to be seen under a microscope at the time, there were problems with correctly diagnosing it.[88] The bacterium haemophilus influenzae was instead mistakenly thought to be the cause, as it was big enough to be seen and was present in many, though not all, patients.[88] During the deadly second wave there were also fears that it was in fact plague, dengue fever, or cholera.[89] Another common misdiagnosis was typhus, which was common in circumstances of social upheaval, and was therefore also affecting Russia in the aftermath of the October Revolution.[89] In Chile, the view of the country's elite was that the nation was in severe decline, and therefore the assumption of doctors was that the disease was typhus caused by poor hygiene, and not an infectious one, causing a mismanaged response which did not ban mass gatherings.[89]

Response - Public health management

Coromandel Hospital Board (New Zealand) advice to influenza sufferers (1918)

While systems for alerting public health authorities of infectious spread did exist in 1918, they did not generally include influenza, leading to a delayed response.[90] Nevertheless, actions were taken. Maritime quarantines were declared on islands such as Iceland, Australia, and American Samoa, saving many lives.[90] Social distancing measures were introduced, for example closing schools, theatres, and places of worship, limiting public transportation, and banning mass gatherings.[91] Wearing face masks became common in some places, such as Japan, though there were debates over their efficacy.[91] There was also some resistance to their use, as exemplified by the Anti-Mask League of San Francisco. Vaccines were also developed, but as these were based on bacteria and not the actual virus, they could only help with secondary infections.[91] The actual enforcement of various restrictions varied.[92]

A later study found that measures such as banning mass gatherings and requiring the wearing of face masks could cut the death rate up to 50 percent, but this was dependent on them being imposed early in the outbreak and not being lifted prematurely.[93]

Response - Medical treatment

As there were no antiviral drugs to treat the virus, and no antibiotics to treat the secondary bacterial infections, doctors would rely on a random assortment of medicines with varying degrees of effectiveness, such as aspirin, quinine, arsenics, digitalis, strychnine, epsom salts, castor oil, and iodine.[94] Treatments of traditional medicine, such as bloodletting, ayurveda, and kampo were also applied.[95]

Response - Information dissemination

Due to World War I, many countries engaged in wartime censorship, and suppressed reporting of the pandemic.[96] For example, the Italian newspaper Corriere della Sera was prohibited from reporting daily death tolls.[97] The newspapers of the time were also generally paternalistic and worried about mass panic.[97] Misinformation would also spread along the disease. In Ireland there was a belief that noxious gases were rising from the mass graves of Flanders Fields and being "blown all over the world by winds".[98] There were also beliefs that the Germans were behind it, for example by poisoning the aspirin manufactured by Bayer, or by releasing poison gas from U-boats.[99]

Mortality

Around the globe

Difference between the influenza mortality age-distributions of the 1918 epidemic and normal epidemics – deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911–1917 (dashed line) and the pandemic year 1918 (solid line)[100]

Three pandemic waves: weekly combined influenza and pneumonia mortality, United Kingdom, 1918–1919[101]

The Spanish flu infected around 500 million people, about one-third of the world's population.[2] Estimates as to how many infected people died vary greatly, but the flu is regardless considered to be one of the deadliest pandemics in history.[102][103] An estimate from 1991 states that the virus killed between 25 and 39 million people.[81] A 2005 estimate put the death toll at 50 million (about 3% of the global population), and possibly as high as 100 million (more than 5%).[80][104] However, a reassessment in 2018 estimated the total to be about 17 million,[105] though this has been contested.[106] With a world population of 1.8 to 1.9 billion,[107] these estimates correspond to between 1 and 6 percent of the population.

The disease killed in many parts of the world. Some 12-17 million people died in India, about 5% of the population.[108] The death toll in India's British-ruled districts was 13.88 million.[109] Another estimate gives at least 12 million dead.[110] The decade between 1911 and 1921 was the only census period in which India’s population fell, mostly due to devastation of the Spanish flu pandemic.[111][112]

In Finland, 20,000 died out of 210,000 infected.[113] In Sweden, 34,000 did.[114]

In Japan, 23 million people were affected, with at least 390,000 reported deaths.[115] In the Dutch East Indies (now Indonesia), 1.5 million were assumed to have died among 30 million inhabitants.[116] In Tahiti, 13% of the population died during one month. Similarly, in Western Samoa 22% of the population of 38,000 died within two months.[117]

In New Zealand, the flu killed an estimated 6,400 Pakeha and 2,500 indigenous Maori in six weeks, with Māori dying at eight times the rate of Pakeha.[118][119]

In the U.S., about 28% of the population of 105 million became infected, and 500,000 to 850,000 died (0.48 to 0.81 percent of the population).[120][121][122] Native American tribes were particularly hard hit. In the Four Corners area, there were 3,293 registered deaths among Native Americans.[123] Entire Inuit and Alaskan Native village communities died in Alaska.[124] In Canada, 50,000 died.[125]

In Brazil, 300,000 died, including president Rodrigues Alves.[126]

In Britain, as many as 250,000 died; in France, more than 400,000.[127]

In Ghana, the influenza epidemic killed at least 100,000 people.[128] Tafari Makonnen (the future Haile Selassie, Emperor of Ethiopia) was one of the first Ethiopians who contracted influenza but survived.[129][130] Many of his subjects did not; estimates for fatalities in the capital city, Addis Ababa, range from 5,000 to 10,000, or higher.[131]

The death toll in Russia has been estimated at 450,000, though the epidemiologists who suggested this number called it a "shot in the dark".[81] If it is correct, Russia lost roughly 0.4% of its population, meaning it suffered the lowest influenza-related mortality in Europe. Another study considers this number unlikely, given that the country was in the grip of a civil war, and the infrastructure of daily life had broken down; the study suggests that Russia's death toll was closer to 2%, or 2.7 million people.[132]

Devastated communities

A chart of deaths from all causes in major cities, showing a peak in October and November 1918

Even in areas where mortality was low, so many adults were incapacitated that much of everyday life was hampered. Some communities closed all stores or required customers to leave orders outside. There were reports that healthcare workers could not tend the sick nor the gravediggers bury the dead because they too were ill. Mass graves were dug by steam shovel and bodies buried without coffins in many places.[133]

Bristol Bay, a region of Alaska populated by indigenous people, suffered a death rate of 40 percent of the total population, with some villages entirely disappearing.[134]

Several Pacific island territories were hit particularly hard. The pandemic reached them from New Zealand, which was too slow to implement measures to prevent ships, such as the SS Talune, carrying the flu from leaving its ports. From New Zealand, the flu reached Tonga (killing 8% of the population), Nauru (16%), and Fiji (5%, 9,000 people).[135] Worst affected was Western Samoa, formerly German Samoa, which had been occupied by New Zealand in 1914. 90% of the population was infected; 30% of adult men, 22% of adult women, and 10% of children died. By contrast, Governor John Martin Poyer prevented the flu from reaching neighboring American Samoa by imposing a blockade.[135] The disease spread fastest through the higher social classes among the indigenous peoples, because of the custom of gathering oral tradition from chiefs on their deathbeds; many community elders were infected through this process.[136]

In Iran, the mortality was very high: according to an estimate, between 902,400 and 2,431,000, or 8% to 22% of the total population died.[137] The country was going through the Persian famine of 1917–1919 concurrently.

In Ireland, during the worst 12 months, the Spanish flu accounted for one-third of all deaths.[138][139]

In South Africa it is estimated that about 300,000 people amounting to 6% of the population died within six weeks. Government actions in the early stages of the virus' arrival in the country in September 1918 are believed to have unintentionally accelerated its spread throughout the country.[140] Almost a quarter of the working population of Kimberley, consisting of workers in the diamond mines, died.[141] In British Somaliland, one official estimated that 7% of the native population died.[142] This huge death toll resulted from an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.[81]

Less-affected areas

In the Pacific, American Samoa[143] and the French colony of New Caledonia[144] also succeeded in preventing even a single death from influenza through effective quarantines. Australia also managed to avoid the first two waves with a quarantine.[90] Iceland protected a third of its population from exposure by blocking the main road of the island.[90] By the end of the pandemic, the isolated island of Marajó, in Brazil's Amazon River Delta had not reported an outbreak.[145] Saint Helena also reported no deaths.[146]

1919 Tokyo, Japan

Estimates for the death toll in China have varied widely,[147][81] a range which reflects the lack of centralized collection of health data at the time due to the Warlord period. China may have experienced a relatively mild flu season in 1918 compared to other areas of the world.[65][66][69][148] However, some reports from its interior suggest that mortality rates from influenza were perhaps higher in at least a few locations in China in 1918.[132] At the very least, there is little evidence that China as a whole was seriously affected by the flu compared to other countries in the world.[149]

The first estimate of the Chinese death toll was made in 1991 by Patterson and Pyle, which estimated China had a death toll of between 5 and 9 million. However, this 1991 study was subsequently criticized by later studies due to flawed methodology, and newer studies have published estimates of a far lower mortality rate in China.[64][150][65] For instance, Iijima in 1998 estimates the death toll in China to be between 1 and 1.28 million based on data available from Chinese port cities.[151] The lower estimates of the Chinese death toll are based on the low mortality rates that were found in Chinese port cities (for example, Hong Kong) and on the assumption that poor communications prevented the flu from penetrating the interior of China.[147] However, some contemporary newspaper and post office reports, as well as reports from missionary doctors, suggest that the flu did penetrate the Chinese interior and that influenza was severe in at least some locations in the countryside of China.[132] Although medical records from China's interior are lacking, there was extensive medical data recorded in Chinese port cities, such as then British-controlled Hong Kong, Canton, Peking, Harbin and Shanghai. This data was collected by the Chinese Maritime Customs Service, which was largely staffed by non-Chinese foreigners, such as the British, French, and other European colonial officials in China.[152] As a whole, accurate data from China's port cities show astonishingly low mortality rates compared to other cities in Asia.[152] For example, the British authorities at Hong Kong and Canton reported a mortality rate from influenza at a rate of 0.25% and 0.32%, much lower than the reported mortality rate of other cities in Asia, such as Calcutta or Bombay, where influenza was much more devastating.[152][65] Similarly, in the city of Shanghai – which had a population of over 2 million in 1918 – there were only 266 recorded deaths from influenza among the Chinese population in 1918.[152] If extrapolated from the extensive data recorded from Chinese cities, the suggested mortality rate from influenza in China as a whole in 1918 was likely lower than 1% – much lower than the world average (which was around 3–5%).[152] In contrast, Japan and Taiwan had reported a mortality rate from influenza around 0.45% and 0.69% respectively, higher than the mortality rate collected from data in Chinese port cities, such as Hong Kong (0.25%), Canton (0.32%), and Shanghai.[152]

Patterns of fatality

A nurse wears a cloth mask while treating a patient in Washington, DC

The pandemic mostly killed young adults. In 1918–1919, 99% of pandemic influenza deaths in the U.S. occurred in people under 65, and nearly half of deaths were in young adults 20 to 40 years old. In 1920, the mortality rate among people under 65 had decreased sixfold to half the mortality rate of people over 65, but 92% of deaths still occurred in people under 65.[153] This is unusual, since influenza is typically most deadly to weak individuals, such as infants under age two, adults over age 70, and the immunocompromised. In 1918, older adults may have had partial protection caused by exposure to the 1889–1890 flu pandemic, known as the "Russian flu".[154] According to historian John M. Barry, the most vulnerable of all – "those most likely, of the most likely", to die – were pregnant women. He reported that in thirteen studies of hospitalized women in the pandemic, the death rate ranged from 23% to 71%.[155] Of the pregnant women who survived childbirth, over one-quarter (26%) lost the child.[156]Another oddity was that the outbreak was widespread in the summer and autumn (in the Northern Hemisphere); influenza is usually worse in winter.[157]

There were also geographic patterns to the disease's fatality. Some parts of Asia had 30 times higher death rates than some parts of Europe, and generally Africa and Asia had higher rates, while Europe, North America, and Asia had lower ones.[158] There was also great variation within continents, with three times higher mortality in Hungary and Spain compared to Denmark, two to three times higher chance of death in Sub-Saharan Africa compared to North Africa, and possibly up to ten times higher rates between the extremes of Asia.[158] Cities were affected worse than rural areas.[158] There were also differences between cities, which might have reflected exposure to the milder first wave giving immunity, as well as the introduction of social distancing measures.[159]

Another major pattern was that of differences between social classes. In Oslo, death rates were inversely correlated with apartment size, as the poorer people living in smaller apartments died at a higher rate.[160] Social status was also reflected in the higher mortality among immigrant communities, with Italian Americans, a recently arrived group at the time, were nearly twice as likely to die compared to the average Americans.[158] These disparities reflected worse diets, crowded living conditions, and problems accessing healthcare.[158] Paradoxically however, African Americans were relatively spared by the pandemic.[158]

More men than women were killed by the flu, as they were more likely to go out and be exposed, while women would tend to stay at home.[159] For the same reason men also were more likely to have pre-existing tuberculosis, which severely worsened the chances of recovery.[159] However, in India the opposite was true, potentially because Indian women were neglected with poorer nutrition, and were expected to care for the sick.[159]

A study conducted by He et al. (2011) used a mechanistic modeling approach to study the three waves of the 1918 influenza pandemic. They examined the factors that underlie variability in temporal patterns and their correlation to patterns of mortality and morbidity. Their analysis suggests that temporal variations in transmission rate provide the best explanation, and the variation in transmission required to generate these three waves is within biologically plausible values.[161] Another study by He et al. (2013) used a simple epidemic model incorporating three factors to infer the cause of the three waves of the 1918 influenza pandemic. These factors were school opening and closing, temperature changes throughout the outbreak, and human behavioral changes in response to the outbreak. Their modeling results showed that all three factors are important, but human behavioral responses showed the most significant effects.[162]

Impact

World War I

Academic Andrew Price-Smith has made the argument that the virus helped tip the balance of power in the latter days of the war towards the Allied cause. He provides data that the viral waves hit the Central Powers before the Allied powers and that both morbidity and mortality in Germany and Austria were considerably higher than in Britain and France.[59]

Economic

Alberta's provincial board of health poster

Many businesses in the entertainment and service industries suffered losses in revenue, while the healthcare industry reported profit gains.[163] Historian Nancy Bristow has argued that the pandemic, when combined with the increasing number of women attending college, contributed to the success of women in the field of nursing. This was due in part to the failure of medical doctors, who were predominantly men, to contain and prevent the illness. Nursing staff, who were mainly women, celebrated the success of their patient care and did not associate the spread of the disease with their work.[164]

A 2020 study found that US cities that implemented early and extensive non-medical measures (quarantine etc.) suffered no additional adverse economic effects due to implementing those measures,[165] when compared with cities that implemented measures late or not at all.[166]

Long-term effects

A 2006 study in the Journal of Political Economy found that "cohorts in utero during the pandemic displayed reduced educational attainment, increased rates of physical disability, lower income, lower socioeconomic status, and higher transfer payments received compared with other birth cohorts."[167] A 2018 study found that the pandemic reduced educational attainment in populations.[168] The flu has also been linked to the outbreak of encephalitis lethargica in the 1920s.[169]

Legacy

Despite the high morbidity and mortality rates that resulted from the epidemic, the Spanish flu began to fade from public awareness over the decades until the arrival of news about bird flu and other pandemics in the 1990s and 2000s.[170] This has led some historians to label the Spanish flu a "forgotten pandemic".[52]

1918 influenza epidemic burial site in Auckland, New Zealand

There are various theories of why the Spanish flu was "forgotten". The rapid pace of the pandemic, which, for example, killed most of its victims in the United States within less than nine months, resulted in limited media coverage. The general population was familiar with patterns of pandemic disease in the late 19th and early 20th centuries: typhoid, yellow fever, diphtheria and cholera all occurred near the same time. These outbreaks probably lessened the significance of the influenza pandemic for the public.[171] In some areas, the flu was not reported on, the only mention being that of advertisements for medicines claiming to cure it.[172]

Additionally, the outbreak coincided with the deaths and media focus on the First World War.[173] Another explanation involves the age group affected by the disease. The majority of fatalities, from both the war and the epidemic, were among young adults. The number of war-related deaths of young adults may have overshadowed the deaths caused by flu.[153]

When people read the obituaries, they saw the war or postwar deaths and the deaths from the influenza side by side. Particularly in Europe, where the war's toll was high, the flu may not have had a tremendous psychological impact or may have seemed an extension of the war's tragedies.[153] The duration of the pandemic and the war could have also played a role. The disease would usually only affect a particular area for a month before leaving[citation needed]. The war, however, had initially been expected to end quickly but lasted for four years by the time the pandemic struck.

In 2019, the first dedicated monument to the memory of the pandemic was unveiled in Wiesloch in Germany.[174]

• [...]

Comparison with other pandemics

This flu killed more people in 24 weeks than HIV/AIDS killed in 24 years.[78] However, it killed a much lower percentage of the world's population than the Black Death, which lasted for many more years.[175]Notes

1. ^ Not necessarily pandemic, but included for comparison purposes.

Research

Main article: Spanish flu research .. see next .. 

An electron micrograph showing recreated 1918 influenza virions

The origin of the Spanish flu pandemic, and the relationship between the near-simultaneous outbreaks in humans and swine, have been controversial. One hypothesis is that the virus strain originated at Fort Riley, Kansas, in viruses in poultry and swine which the fort bred for food; the soldiers were then sent from Fort Riley around the world, where they spread the disease.[197] Similarities between a reconstruction of the virus and avian viruses, combined with the human pandemic preceding the first reports of influenza in swine, led researchers to conclude the influenza virus jumped directly from birds to humans, and swine caught the disease from humans.[198][199] Others have disagreed,[200] and more recent research has suggested the strain may have originated in a nonhuman, mammalian species.[201] An estimated date for its appearance in mammalian hosts has been put at the period 1882–1913.[202] This ancestor virus diverged about 1913–1915 into two clades (or biological groups), which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates to between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, they were suggested as the original recipients of the virus, passing the virus to humans sometime between 1913 and 1918.

At the Centers for Disease Control and Prevention, Terrence Tumpey examines a reconstructed version of the 1918 flu.

An effort to recreate the 1918 flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology, the USDA ARS Southeast Poultry Research Laboratory, and Mount Sinai School of Medicine in New York City. The effort resulted in the announcement (on 5 October 2005) that the group had successfully determined the virus's genetic sequence, using historic tissue samples recovered by pathologist Johan Hultin from an Inuit female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers[203] Roscoe Vaughan and James Downs.[204][205]

On 18 January 2007, Kobasa et al. (2007) reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from cytokine storms[206] – an overreaction of the immune system. This may explain why the 1918 flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.[207]

On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hoped had helped preserve the virus.[208] The coffin was found to be split and the cadaver badly decomposed; nonetheless, samples of lung and brain tissue were taken.[209]

In December 2008, research by Yoshihiro Kawaoka of the University of Wisconsin linked the presence of three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from 1918 flu samples to the ability of the flu virus to invade the lungs and cause pneumonia. The combination triggered similar symptoms in animal testing.[210]

In June 2010, a team at the Mount Sinai School of Medicine reported the 2009 flu pandemic vaccine provided some cross-protection against the 1918 flu pandemic strain.[211]

One of the few things known for certain about the influenza in 1918 and for some years after was that it was, except in the laboratory, exclusively a disease of human beings.[212]

In 2013, the AIR Worldwide Research and Modeling Group "characterized the historic 1918 pandemic and estimated the effects of a similar pandemic occurring today using the AIR Pandemic Flu Model". In the model, "a modern day 'Spanish flu' event would result in additional life insurance losses of between US$15.3–27.8 billion in the United States alone", with 188,000–337,000 deaths in the United States.[213]

In 2018, Michael Worobey, an evolutionary biology professor at the University of Arizona who is examining the history of the 1918 pandemic, revealed that he obtained tissue slides created by William Rolland, a physician who reported on a respiratory illness likely to be the virus while a pathologist in the British military during World War One.[214] Rolland had authored an article in the Lancet during 1917 about a respiratory illness outbreak beginning in 1916 in Étaples, France.[215][216] Worobey traced recent references to that article to family members who had retained slides that Rolland had prepared during that time. Worobey extracted tissue from the slides to potentially reveal more about the origin of the pathogen.[citation needed]

Spanish flu research concerns scientific research regarding the causes and characteristics of the "Spanish flu," a variety of influenza that in 1918 was responsible for the worst influenza pandemic in modern history. Many theories about the origins and progress of the Spanish flu persisted in the literature, but it was not until 2005, when various samples were recovered from American World War I soldiers and an Inuit woman buried in the Alaskan tundra, that significant research was made possible.

Origin of virus

There are two prevailing theories usually postulated.[citation needed] One theory by Alfred W. Crosby is that the virus strain originated at Fort Riley, Kansas, by two genetic mechanisms – genetic drift and antigenic shift – in viruses in poultry and swine which the fort bred for local consumption. Though initial data from a recent reconstruction of the virus suggested that it jumped directly from birds to humans, without traveling through swine,[a] this has since been cast into doubt. One researcher published in 2004 argued that the disease was found in Haskell County, Kansas, as early as January 1918.[2] A similar and even more deadly virus had been seen earlier at British camps in France and at Aldershot.[3]

Earlier investigative work published in 2000 by a team led by British virologist, John Oxford[4] of St Bartholomew's Hospital and the Royal London Hospital, suggested that a principal British troop staging camp in Étaples, France, was at the center of the 1918 flu pandemic or at least a significant precursor virus to it. There had been a mysterious respiratory infection at the military base during the winter of 1915–1916.[5]

Discovery of viral genomes

Dr. Jeffery Taubenberger and Dr. Ann Reid reviewing a genetic sequence from the 1918 Spanish flu virus.

Centers for Disease Control and Prevention as Dr. Terrence Tumpey examines a reconstructed version of the 1918 flu.

In February 1997, Johan Hultin recovered samples of the 1918 influenza from the frozen corpse of a Native Alaskan woman buried for nearly eight decades in permafrost near Brevig Mission, Alaska.[6] He brought the samples to a team[where?] led by Jeffery Taubenberger of the US Armed Forces Institute of Pathology (AFIP). Brevig Mission lost approximately 85% of its population to the 1918 flu in November 1918. One of the four recovered samples contained viable genetic material of the virus. This sample provided scientists a first-hand opportunity to study the virus, which was inactivated with guanidinium thiocyanate before transport. This sample and others found in AFIP archives allowed researchers to completely analyze the critical gene structures of the 1918 virus.

"We have now identified three cases: The Brevig Mission case and two archival cases that represent the only known sources of genetic material of the 1918 influenza virus," said Taubenberger, chief of AFIP's molecular pathology division and principal investigator on the project.[7][b]

The archived autopsy samples had been taken from WWI Army privates Roscoe Vaughan and James Downs.[9]

Wikinews has related news:

• Scientists recreating the 1918 flu virus suggest that it may have come from birds

The 6 February 2004 edition of Science magazine reported that two research teams, one led by Sir John Skehel, director of the National Institute for Medical Research in London, another by professor Ian Wilson of The Scripps Research Institute in San Diego, had managed to synthesize the hemagglutinin protein responsible for the flu outbreak of 1918. They did this by piecing together DNA from a lung sample from an Inuit woman buried in the Alaskan tundra and a number of preserved samples from American soldiers of the First World War. The teams had analyzed the structure of the gene and discovered how subtle alterations to the shape of a protein molecule had allowed it to move from birds to humans with such devastating effects.

On 5 October 2005, Tumpey and other researchers at the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, and the Mount Sinai School of Medicine in New York, announced that the (~13 kbp) genetic sequence of the 1918 flu strain, a subtype of avian strain H1N1, had been reconstructed using historic tissue samples and a small part of the RNA from a modern strain.[10][11][12]

Characteristics of virus

Influenza viruses have a relatively high mutation rate that is characteristic of RNA viruses. The H5N1 virus has mutated into a variety of types with differing pathogenic profiles; some pathogenic to one species but not others, some pathogenic to multiple species.[13] The ability of various influenza strains to show species-selectivity is largely due to variation in the hemagglutinin genes. Genetic mutations in the hemagglutinin gene that cause single amino acid substitutions can significantly alter the ability of viral hemagglutinin proteins to bind to receptors on the surface of host cells. Such mutations in avian H5N1 viruses can change virus strains from being inefficient at infecting human cells to being as efficient in causing human infections as more common human influenza virus types.[14]

In July 2004, researchers led by H. Deng of the Harbin Veterinary Research Institute, Harbin, China, and Robert Webster of the St. Jude Children's Research Hospital, Memphis, Tennessee, reported results of experiments in which mice had been exposed to 21 isolates of confirmed H5N1 strains obtained from ducks in China between 1999 and 2002. They found "a clear temporal pattern of progressively increasing pathogenicity."[15] Results reported by Webster in July 2005 reveal further progression toward pathogenicity in mice and longer virus shedding by ducks.

In December 2008, research by Yoshihiro Kawaoka of University of Wisconsin showed the presence of the three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from the H1N1 1918 flu samples was enough to trigger similar symptoms in animal testing.[16]

Research of viral pathogenesis

Recent research of Taubenberger et al. has suggested that the 1918 virus, like H5N1, could have arisen directly from an avian influenza virus.[11] However, researchers at University of Virginia and Australian National University have suggested that there may be an alternative interpretation of the data used in the Taubenberger et al. paper.[17][18] Taubenberger et al. responded to these letters and defended their original interpretation.[19]

Other research by Tumpey and colleagues who reconstructed the H1N1 virus of 1918 came to the conclusion that it was most notably the polymerase genes and the HA and NA genes that caused the extreme virulence of this virus.[12] On 18 January 2007, Kobasa et al. reported that infected monkeys (Macaca fascicularis) exhibited classic symptoms of the 1918 pandemic and died from a cytokine storm.[20]

The sequences of the polymerase proteins (PA, PB1, and PB2) of the 1918 virus and subsequent human viruses differ by only 10 amino acids from the avian influenza viruses. Viruses with 7 of the 10 amino acids in the human influenza locations have already been identified in currently circulating H5N1. This has led some researchers to suggest that other mutations may surface and make the H5N1 virus capable of human-to-human transmission.

Another important factor is the change of the HA protein to a binding preference for alpha-2,6 sialic acid (the major form found in the human respiratory tract). In avian virus the HA protein preferentially binds to alpha-2,3 sialic acid, which is the major form in the avian enteric tract. It has been shown that only a single amino acid change can result in the change of this binding preference. Altogether, only a handful of mutations may need to take place in order for H5N1 avian flu to become a pandemic virus like the one of 1918. However it is important to note that likelihood of mutation does not indicate the likelihood for the evolution of such a strain, since some of the necessary mutations may be constrained by stabilizing selection.

Blood plasma as an effective treatment

In the event of another pandemic, US military researchers have proposed reusing a treatment from the deadly pandemic of 1918 in order to blunt the effects of the flu: Some military doctors injected severely afflicted patients with blood or blood plasma from people who had recovered from the flu. Data collected during that time indicates that the blood-injection treatment reduced mortality rates by as much as 50 percent.[21]

Navy researchers have launched a test to see if the 1918 treatment will work against deadly Asian bird flu. Results thus far have been inconclusive.[citation needed] Human H5N1 plasma may be an effective, timely, and widely available treatment for the next flu pandemic.[citation needed] A new international study using modern data collection methods, would be a difficult, slow process. Citing the months-long wait for a vaccine for the next pandemic, many flu experts are of the opinion that the 1918 method is something to consider.[22]

In the worldwide 1918 flu pandemic, "physicians tried everything they knew, everything they had ever heard of, from the ancient art of bleeding patients, to administering oxygen, to developing new vaccines and sera (chiefly against what we now call Hemophilus influenzae – a name derived from the fact that it was originally considered the etiological agent – and several types of pneumococci). Only one therapeutic measure showed any hint of success: Transfusing blood from recovered patients to new victims."[23]

The “Spanish Flu” killed an estimated 50-100 million people during a pandemic 1918-19. What if the story  we have been told about this pandemic isn’t true?

What if, instead, the killer infection was neither the flu nor Spanish in origin?

Newly analyzed documents reveal that the “Spanish Flu” may have been a military vaccine experiment gone awry.

In looking back on the 100th anniversary of the end of World War I, we need to delve deeper to solve this mystery.

Summary

• The reason modern technology has not been able to pinpoint the killer influenza strain from this pandemic is because influenza was not the killer.

• More soldiers died during WWI from disease than from bullets.

• The pandemic was not flu. An estimated 95% (or higher) of the deaths were caused by bacterial pneumonia, not influenza/a virus.

• The pandemic was not Spanish. The first cases of bacterial pneumonia in 1918 trace back to a military base in Fort Riley, Kansas.

• From January 21 – June 4, 1918, an experimental bacterial meningitis vaccine cultured in horses by the Rockefeller Institute for Medical Research in New York was injected into soldiers at Fort Riley.

• During the remainder of 1918 as those soldiers – often living and traveling under poor sanitary conditions – were sent to Europe to fight, they spread bacteria at every stop between Kansas and the frontline trenches in France.

• One study describes soldiers “with active infections (who) were aerosolizing the bacteria that colonized their noses and throats, while others—often, in the same “breathing spaces”—were profoundly susceptible to invasion of and rapid spread through their lungs by their own or others’ colonizing bacteria.” (1)

• The “Spanish Flu” attacked healthy people in their prime.  Bacterial pneumonia attacks people in their prime. Flu attacks the young, old and immunocompromised.

• When WW1 ended on November 11, 1918, soldiers returned to their home countries and colonial outposts, spreading the killer bacterial pneumonia worldwide.

• During WW1, the Rockefeller Institute also sent the antimeningococcic serum to England, France, Belgium, Italy and other countries, helping spread the epidemic worldwide.

During the pandemic of 1918-19, the so-called “Spanish Flu” killed 50-100 million people, including many soldiers.

Many people do not realize that disease killed far more soldiers on all sides than machine guns or mustard gas or anything else typically associated with WWI.

I have a personal connection to the Spanish Flu.  Among those killed by disease in 1918-19 are members of both of my parents’ families.

On my father’s side, his grandmother Sadie Hoyt died from pneumonia in 1918. Sadie was a Chief Yeoman in the Navy.  Her death left my grandmother Rosemary and her sister Anita to be raised by their aunt. Sadie’s sister Marian also joined the Navy.  She died from “the influenza” in 1919.

On my mother’s side, two of her father’s sisters died in childhood. All of the family members who died lived in New York City.

I suspect many American families, and many families worldwide, were impacted in similar ways by the mysterious Spanish Flu.

In 1918, “influenza” or flu was a catchall term for disease of unknown origin.  It didn’t carry the specific meaning it does today.

It meant some mystery disease which dropped out of the sky.  In fact, influenza is from the Medieval Latin “influential” in an astrological sense, meaning a visitation under the influence of the stars.

WHY IS WHAT HAPPENED 100 YEARS AGO IMPORTANT NOW?

Between 1900-1920, there were enormous efforts underway in the industrialized world to build a better society.  I will use New York as an example to discuss three major changes to society which occurred in NY during that time and their impact on mortality from infectious diseases.

1.    Clean Water and Sanitation

In the late 19th century through the early 20th century, New York built an extraordinary system to bring clean water to the city from the Catskills, a system still in use today.  New York City also built over 6000 miles of sewer to take away and treat waste, which protects the drinking water. The World Health Organization acknowledges the importance of clean water and sanitation in combating infectious diseases. (2)

2.    Electricity

In the late 19th century through the early 20th century, New York built a power grid and wired the city so power was available in every home.  Electricity allows for refrigeration. Refrigeration is an unsung hero as a public health benefit. When food is refrigerated from farm to table, the public is protected from potential infectious diseases.  Cheap renewable energy is important for many reasons, including combating infectious diseases.

3.     Pharmaceutical

In the late 19th century through the early 20th century, New York became the home of the Rockefeller Institute for Medical Research (now Rockefeller University).  The Institute is where the modern pharmaceutical industry was born. The Institute pioneered many of the approaches the pharmaceutical industry uses today, including the preparation of vaccine serums, for better or worse.  The vaccine used in the Fort Riley experiment on soldiers was made in horses.

US Mortality Rates data from the turn of the 20th century to 1965 clearly indicates that clean water, flushing toilets, effective sewer systems and refrigerated foods all combined to effectively reduce mortality from infectious diseases BEFORE vaccines for those diseases became available.

Have doctors and the pharmaceutical manufacturers taken credit for reducing mortality from infectious disease which rightfully belongs to sandhogs, plumbers, electricians and engineers?

If hubris at the Rockefeller Institute in 1918 led to a pandemic disease which killed millions of people, what lessons can we learn and apply to 2018?

THE DISEASE WAS NOT SPANISH

While watching an episode of American Experience on PBS a few months ago,  I was surprised to hear that the first cases of “Spanish Flu” occurred at Fort Riley, Kansas in 1918.  I thought, how is it possible this historically important event could be so badly misnamed 100 years ago and never corrected?

Why “Spanish”?

Spain was one of a few countries not involved in World War I.  Most of the countries involved in the war censored their press.

Free from censorship concerns, the earliest press reports of people dying from disease in large numbers came from Spain.  The warring countries did not want to additionally frighten the troops, so they were content to scapegoat Spain. Soldiers on all sides would be asked to cross no man’s land into machine gun fire, which was frightening enough without knowing that the trenches were a disease breeding ground.

One hundred years later, it’s long past time to drop “Spanish” from all discussion of this pandemic.  If the flu started at a United States military base in Kansas, then the disease could and should be more aptly named.

In order to prevent future disasters, the US (and the rest of the world) must take a hard look at what really caused the pandemic.

It is possible that one of the reasons the Spanish Flu has never been corrected is that it helps disguise the origin of the pandemic.

If the origin of the pandemic involved a vaccine experiment on US soldiers, then the US may prefer calling it Spanish Flu instead of The Fort Riley Bacteria of 1918, or something similar.  The Spanish Flu started at the location this experimental bacterial vaccine was given making it the prime suspect as the source of the bacterial infections which killed so many.

It would be much more difficult to maintain the marketing mantra of “vaccines save lives” if a vaccine experiment originating in the United States during the years of primitive manufacturing caused the deaths of  50-100 million people.

“Vaccines save lives … except we may have killed 50-100 million people in 1918-19” is a far less effective sales slogan than the overly simplistic “vaccines save lives.”

THE DISEASE WHICH KILLED SO MANY WAS NOT FLU OR A VIRUS.  IT WAS BACTERIAL.

During the mid-2000’s there was much talk about “pandemic preparedness.”  Influenza vaccine manufacturers in the United States received billions of taxpayer dollars to develop vaccines to make sure that we don’t have another lethal pandemic “flu,” like the one in 1918-19.

Capitalizing on the “flu” part of Spanish flu helped vaccine manufacturers procure billion dollar checks from governments, even though scientists knew at the time that bacterial pneumonia was the real killer.

It is not my opinion that bacterial pneumonia was the real killer – thousands of autopsies confirm this fact.

According to a 2008 National Institute of Health paper, bacterial pneumonia was the killer in a minimum of 92.7% of the 1918-19 autopsies reviewed.  It is likely higher than 92.7%.

The researchers looked at more than 9000 autopsies, and “there were no negative (bacterial) lung culture results.”

“… In the 68 higher-quality autopsy series, in which the possibility of unreported negative cultures could be excluded, 92.7% of autopsy lung cultures were positive for ≥1 bacterium. … in one study of approximately 9000 subjects who were followed from clinical presentation with influenza to resolution or autopsy, researchers obtained, with sterile technique, cultures of either pneumococci or streptococci from 164 of 167 lung tissue samples.

There were 89 pure cultures of pneumococci; 19 cultures from which only streptococci were recovered; 34 that yielded mixtures of pneumococci and/or streptococci; 22 that yielded a mixture of pneumococci, streptococci, and other organisms (prominently pneumococci and nonhemolytic streptococci); and 3 that yielded nonhemolytic streptococci alone. There were no negative lung culture results.” (3)

Pneumococci or streptococci were found in “164 of (the) 167 lung tissue samples” autopsied.  That is 98.2%. Bacteria was the killer.

WHERE DID THE SPANISH FLU BACTERIAL PNEUMONIA OF 1918-19 ORIGINATE?

When the United States declared war in April 1917, the fledgling Pharmaceutical industry had something they had never had before – a large supply of human test subjects in the form of the US military’s first draft.

Pre-war in 1917, the US Army was 286,000 men. Post-war in 1920, the US army disbanded, and had 296,000 men.

During the war years 1918-19, the US Army ballooned to 6,000,000 men, with 2,000,000 men being sent overseas.  The Rockefeller Institute for Medical Research took advantage of this new pool of human guinea pigs to conduct vaccine experiments. 

" A REPORT ON ANTIMENINGITIS VACCINATION AND OBSERVATIONS ON AGGLUTININS IN THE BLOOD OF CHRONIC MENINGOCOCCUS CARRIERS by Frederick L. Gates  (From the Base Hospital, Fort Riley, Kansas, and The Rockefeller Institute for Medical Research, New York.  /   Received 1918 Jul 20 )  " See  [HG005A][GDrive]  

(Author note:  Please read this Fort Riley paper in its entirety so you can appreciate the carelessness of the experiments conducted on these troops.)

Between January 21st and June 4th of 1918, []reports on an experiment where soldiers were given 3 doses of a bacterial meningitis vaccine.  Those conducting the experiment on the soldiers were just spitballing dosages of a vaccine serum made in horses.

The vaccination regime was designed to be 3 doses.  4,792 men received the first dose, but only 4,257 got the 2nd dose (down 11%), and only 3702 received all three doses (down 22.7%).

A total of 1,090 men were not there for the 3rd dose.  What happened to these soldiers? Were they shipped East by train from Kansas to board a ship to Europe?  Were they in the Fort Riley hospital? [The report from [Dr. Frederick Lamont Gates (born 1886)] report doesn’t tell us.

An article accompanying the American Experience broadcast I watched sheds some light on where these 1,090 men might be.  [Dr. Frederick Lamont Gates (born 1886)] began his experiments in January 1918.

By March of that year, “100 men a day” were entering the infirmary at Fort Riley.

Are some of these the men missing from Dr. Gates’ report – the ones who did not get the 2nd or 3rd dose?

“… Shortly before breakfast on Monday, March 11, the first domino would fall signaling the commencement of the first wave of the 1918 influenza.

Company cook Albert Gitchell reported to the camp infirmary with complaints of a “bad cold.”

Right behind him came Corporal Lee W. Drake voicing similar complaints.

By noon, camp surgeon Edward R. Schreiner had over 100 sick men on his hands, all apparently suffering from the same malady…” (5)

[Dr. Frederick Lamont Gates (born 1886)] does report that several of the men in the experiment had flu-like symptoms: coughs, vomiting and diarrhea after receiving the vaccine.

These symptoms are a disaster for men living in barracks, travelling on trains to the Atlantic coast, sailing to Europe, and living and fighting in trenches.

The unsanitary conditions at each step of the journey are an ideal environment for a contagious disease like bacterial pneumonia to spread.

From Dr. Gates’ report:

“Reactions.– … Several cases of looseness of the bowels or transient diarrhea were noted. This symptom had not been encountered before. Careful inquiry in individual cases often elicited the information that men who complained of the effects of vaccination were suffering from mild coryza, bronchitis, etc., at the time of injection.”

“Sometimes the reaction was initiated by a chill or chilly sensation, and a number of men complained of fever or feverish sensations during the following night.

Next in frequency came nausea (occasionally vomiting), dizziness, and general “aches and pains” in the joints and muscles, which in a few instances were especially localized in the neck or lumbar region, causing stiff neck or stiff back. A few injections were followed by diarrhea.

The reactions, therefore, occasionally simulated the onset of epidemic meningitis and several vaccinated men were sent as suspects to the Base Hospital for diagnosis.”(4)

According to [Dr. Frederick Lamont Gates (born 1886)], they injected random dosages of an experimental bacterial meningitis vaccine into soldiers. Afterwards, some of the soldiers had symptoms which “simulated” meningitis, but Dr. Gates advances the fantastical claim that it wasn’t actual meningitis.

The soldiers developed flu-like symptoms.  Bacterial meningitis, then and now, is known to mimic flu-like symptoms. (6)

Perhaps the similarity of early symptoms of bacterial meningitis and bacterial pneumonia to symptoms of flu is why the vaccine experiments at Fort Riley have been able to escape scrutiny as a potential cause of the Spanish Flu for 100 years and counting.

HOW DID THE “SPANISH FLU” SPREAD SO WIDELY SO QUICKLY?

There is an element of a perfect storm in how the [Dr. Frederick Lamont Gates (born 1886)]  bacteria spread.  WWI ended only 10 months after the first injections. Unfortunately for the 50-100 million who died, those soldiers injected with horse-infused bacteria moved quickly during those 10 months.

An article from 2008 on the CDC’s website describes how sick WWI soldiers could pass along the bacteria to others by becoming “cloud adults.”

“Finally, for brief periods and to varying degrees, affected hosts became “cloud adults” who increased the aerosolization of colonizing strains of bacteria, particularly pneumococci, hemolytic streptococci, H. influenzae, and S. aureus.

For several days during local epidemics—particularly in crowded settings such as hospital wards, military camps, troop ships, and mines (and trenches)—some persons were immunologically susceptible to, infected with, or recovering from infections with influenza virus.

Persons with active infections were aerosolizing the bacteria that colonized their noses and throats, while others—often, in the same “breathing spaces”—were profoundly susceptible to invasion of and rapid spread through their lungs by their own or others’ colonizing bacteria.” (1)

Three times in his report on the Fort Riley vaccine experiment, [Dr. Frederick Lamont Gates (born 1886)] states that some soldiers had a “severe reaction” indicating “an unusual individual susceptibility to the vaccine”.

While the vaccine made many sick, it only killed those who were susceptible to it.  Those who became sick and survived became “cloud adults” who spread the bacteria to others, which created more cloud adults, spreading to others where it killed the susceptible, repeating the cycle until there were no longer wartime unsanitary conditions, and there were no longer millions of soldiers to experiment on.

The toll on US troops was enormous and it is well documented.  Dr. Carol Byerly describes how the “influenza” traveled like wildfire through the US military.  (substitute “bacteria” for Dr. Byerly’s “influenza” or “virus”):

“… Fourteen of the largest training camps had reported influenza outbreaks in March, April, or May, and some of the infected troops carried the virus with them aboard ships to France …

As soldiers in the trenches became sick, the military evacuated them from the front lines and replaced them with healthy men.

This process continuously brought the virus into contact with new hosts—young, healthy soldiers in which it could adapt, reproduce, and become extremely virulent without danger of burning out.

… Before any travel ban could be imposed, a contingent of replacement troops departed Camp Devens (outside of Boston) for Camp Upton, Long Island, the Army’s debarkation point for France, and took influenza with them.

Medical officers at Upton said it arrived “abruptly” on September 13, 1918, with 38 hospital admissions, followed by 86 the next day, and 193 the next.

Hospital admissions peaked on October 4 with 483, and within 40 days, Camp Upton sent 6,131 men to the hospital for influenza. Some developed pneumonia so quickly that physicians diagnosed it simply by observing the patient rather than listening to the lungs…” (7)

The United States was not the only country in possession of the Rockefeller Institute’s  experimental bacterial vaccine.

A 1919 report from the Institute states: “Reference should be made that before the United States entered the war (in April 1917) the Institute had resumed the preparation of antimeningococcic serum, in order to meet the requests of England, France, Belgium Italy and other countries.”

The same report states:  “In order to meet the suddenly increased demand for the curative serums worked out at the Institute, a special stable for horses was quickly erected …” (8)

An experimental antimeningoccic serum made in horses and injected into soldiers who would be entering the cramped and unsanitary living conditions of war … what could possibly go wrong?

Is the bacterial serum made in horses at the Rockefeller Institute which was injected into US soldiers and distributed to numerous other countries responsible for the 50-100 million people killed by bacterial lung infections in 1918-19?

The Institute says it distributed the bacterial serum to England, France, Belgium, Italy and other countries during WWI. Not enough is known about how these countries experimented on their soldiers.

I hope independent researchers will take an honest look at these questions.

THE ROAD TO HELL IS PAVED WITH GOOD INTENTIONS

I do not believe that anyone involved in these vaccine experiments was trying to harm anyone.

Some will see the name Rockefeller and yell. “Illuminati!” or “culling the herd!”

I do not believe that’s what happened.

I believe standard medical hubris is responsible – doctors “playing God”, thinking they can tame nature without creating unanticipated problems.

With medical hubris, I do not think the situation has changed materially over the past 100 years.

WHAT NOW?

The vaccine industry is always looking for human test subjects.  They have the most success when they are able to find populations who not in a position to refuse.

Soldiers (9), infants, the disabled, prisoners, those in developing nations – anyone not in a position to refuse.

Vaccine experimentation on vulnerable populations is not an issue of the past.  Watch this video clip of Dr. Stanley Plotkin where he describes using experimental vaccines on orphans, the mentally retarded, prisoners, and those under colonial rule.

The deposition was in January 2018. The hubris of the medical community is the same or worse now than it was 100 years ago.

Watch as Dr. Plotkin admits to writing:

“The question is whether we are to have experiments performed on fully functioning adults and on children who are potentially contributors to society or to perform initial studies in children and adults who are human in form but not in social potential.”

Please watch the horrifying video clip.(10)  :   "Dr. Stanley "Human-in-Form" Plotkin, re: experiments on orphans/mentally retarded/prisoners"  /  Video - [HV006O][GDrive]  

[...]

References

1. Deaths from Bacterial Pneumonia during 1918–19 Influenza Pandemic

John F. Brundage*  and G. Dennis Shanks†

Author affiliations: *Armed Forces Health Surveillance Center, Silver Spring, Maryland, USA; †Australian Army Malaria Institute, Enoggera, Queensland, Australia

https://wwwnc.cdc.gov/eid/article/14/8/07-1313_article

2.  World Health Organization: Unsafe drinking water, sanitation and waste management  

http://www.who.int/sustainable-development/cities/health-risks/water-sanitation/en/

3. J Infect Dis. 2008 Oct 1; 198(7): 962–970.

Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness

David M. Morens, Jeffery K. Taubenberger, and Anthony S. Fauci

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2599911/

5. American Experience, “The First Wave”, PBS

https://www.pbs.org/wgbh/americanexperience/features/influenza-first-wave/

6. Mayo Clinic:  Meningitis

www.mayoclinic.org/diseases-conditions/meningitis/symptoms-causes/syc-20350508

7. Public Health Rep. 2010; 125(Suppl 3): 82–91.

The U.S. Military and the Influenza Pandemic of 1918–1919

Carol R. Byerly, PhD

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862337/

8.  Rockefeller Institute pamphlet PDF (1919) - [HI0011][GDrive]  

9.  Is Military Research Hazardous to Veterans’ Health? Lessons Spanning Half a Century, A Staff Report Prepared for the Committee on Veterans’ Affairs, United States Senate, December 1994

https://www.hsdl.org/?abstract&did=438835

[...]

In Part 1 (1) ( See [HW002Z][GDrive]  ), I asked if medical products made in horses may have played a role in the new disease which killed millions worldwide in the pandemic of 1918-19.

The December 1917 issue of Popular Mechanics magazine  is BELOW - sheds light on the vaccine manufacturing process of 100 years ago.

The feature article, “How New York City’s Health Department Makes Serums and Vaccines for the United States Army” describes processes in place in 1917:

“After the horse has been inoculated with the disease poison in gradually increasing doses he is bled and his serum is found to be antitoxin.

This is administered to human beings and renders them immune to the disease …. Some horses give more antitoxin serum than others.

The same horse may be used at several different times for the preparation of distinctly different antitoxins … Horses are used in the preparation of diphtheria, tetanus antitoxin and antimeningococcus serum. “

It is difficult to believe that they used the same horses to make multiple disease serums, but they did.

If safety had been a concern, perhaps certain horses would have been dedicated to producing serum for one disease (or “poison” as the article calls it), but safety does not appear to be on the list of concerns.

These muddled and potentially contaminated serums were then given to soldiers (and to the public).

SPECIES JUMP?

Were pathogens transferred from these horses to humans in mass quantities in ways they had never transferred before?

Humans and horses had interacted closely for centuries, but horse serum had not been injected into humans in that way before, bypassing the human immune system.

Is it possible that this new method of exposure caused the bacterial pneumonias which ripped human lungs apart in ways never seen before?

Could pathogens relatively harmless to horse lungs make a species-jump and destroy human lungs?

In 1919, a Dutch military veterinarian named Captain Emile Bemelmans “developed an extensive theory on the relation between human and animal influenza …. In 1919, he argued that ‘the human ‘flu’ and the so-called ‘infectious disease of the breast’ of horses are exactly identical in aetiological, bacteriological and epidemiological senses’.

In her 2014 paper “‘Spanish’ flu and army horses: what historians and biologists can learn from a history of animals with flu during the 1918–1919 influenza pandemic”, Dr. Floor Haalboom describes Bemelmans’s work:

“In 1919, Bemelmans’s argument on the identical nature of human and horse influenza in the Nederlandsch Tijdschrift voor Geneeskunde (the Dutch medical journal) was reviewed in the veterinary journal,

… in 1914 he extended his theory on horse flu to several human and animal infectious diseases in an article in the Dutch medical journal.  Bemelmans listed human influenza as an example among many other animal and human diseases which he thought were accompanied by (deadly) infections of streptococci.

Although he did not yet argue that human and horse flu were exactly equal, he did explicitly note their similarities: ‘Also between the human influenza and the so-called breast disease in horses peculiar similarities exist’…

… In these papers, Bemelmans addressed the nature of influenza (although he still preferred the name ‘flu’) of both humans and horses. He opposed the ideas that Pfeiffer’s bacterium or a filterable virus caused the disease, but thought toxins made by the bacteria streptococci were responsible for its deadly secondary complications. “ (4)

Dr. Bemelmans’s contemporaneous observations have largely been lost to history, in part because of the self important attitude of the medical community.

The hubris of the medical community prevented them from listening to a lowly veterinarian.

However, Dr. Bemelmans’s observations and persistence in getting them published are extraordinarily valuable.  His awareness at the time that bateria was the killer of both humans and horses in the pandemic of 1918-19 put him decades ahead of his contemporaries.

The NIH paper describing bacteria as the predominant killer was published in 2008.(5)

See   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2599911/     https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2599911/pdf/nihms76103.pdf   

If Dr. Bemelmans was correct that horses and humans were suffering from an identical disease, are there diseases identical (or very similar) in both horses and humans?  Do any of those diseases target the lungs?

“Animal Models – A Neglected Medical Resource”, Cornelius, CE, DVM, Ph.D.N Engl J Med 1969; 281:934-944 (6)

In a 1969 paper,  Kansas State University veterinarian Dr. Charles E. Cornelius compiled a list of diseases which were very similar or identical in humans and various other species.  Among the diseases identical/very similar in humans and horses is pulmonary emphysema, which targets the lungs.

Did a pathogen which causes pulmonary emphysema “species-jump” from horses to humans in these serums and vaccines?

The vaccines were obviously manufactured in primitive, unavoidably unsafe conditions and then given to WW1 soldiers as an experiment.

What exactly was in the serums and vaccines made in the horses at the Rockefeller Institute – especially considering that the same individual horses were used to for variety of serums for multiple diseases?

Recall from Part 1 that Streptococci bacteria were commonly found in the tissue samples from the autopsies of those who died in 1918-19. (5)

Cornelius said human and horse pulmonary emphysema are identical.  Bemelmans reported that humans and horses were suffering from the same disease.

Did doctors treating soldiers suffering from “Spanish Flu” report on encountering a new killer type of pulmonary emphysema, causing  lung damage that they had ever seen before?

PULMONARY EMPHYSEMA AT CAMP HANCOCK GEORGIA

“Acute Pulmonary Emphysema Observed During the Epidemic of Influenzal Pneumonia at Camp Hancock, Georgia”Robert G. Torrey American Journal of the Medical Sciences  1919, p. 170 – 181 (7)

Captain Dr. Torrey served at Camp Hancock, just outside of Augusta, GA.  The soldiers who came through Camp Hancock were likely on their way to Charleston, SC to board ships to France, but many of them would not survive to get to the front.

Thousands died at Camp Hancock. Some who survived the illness likely made it to the ships, potentially passing the infectious bacteria to other soldiers in the unsanitary conditions which were rampant during WWI.

From Dr. Torrey’s report:

“Summary

… Certain conditions were invariably present, including an intense bronchitis and peribronchitis similar to that found in a previous epidemic of pure hemolytic streptococcus infection (Scarlet Fever).  There was also present from the first a destructive softening of the lung parenchyma.

In addition to this there was always an early and persisting generalized pulmonary emphysema which frequently was the main factor in causing death by interference with the mass movement of venous blood.

These conditions were found in every case examined at autopsy. Except for frequent otitis media (ear infection) there were almost no complications or sequelae outside of the chest.

The pulmonary emphysema, with consequent venous stasis, accounted for the cyanosis (turning blue/purple color), epistaxis (nosebleeds) and fixation of the chest in the phase of extreme inspiration (inhaling), with low stand of the diaphragm, which characterized these cases, and also accounted for the paradoxical physical signs (paradoxical breathing) in which fluid developed in the chest.”

Torrey describes what happened to these soldiers as they died.  They were coughing, becoming “cloud adults” (8) (as described in Part 1).

It looked like a bacterial infection to him.  Autopsies showed lung tissue had been damaged, which restricted blood flow, turning the dying a bluish/purple color, due to lack of oxygen.

When the patients tried to inhale, their diaphragms constricted instead of expanded, the opposite of what diaphragms are supposed to do.(9) Fluids then filled their lungs, and many did not survive, literally the fluid in their lungs strangling the soldiers to death.

FLUID IN THE LUNGS STRANGLED THE HUMAN VICTIMS OF SPANISH FLU – STRANGLES?

There is a highly contagious horse respiratory infection called Strangles (or Distemper).  If this disease can kill horses, what would it do to human lungs if introduced into humans, via injection and therefore bypassing the immune system, on a mass scale?

“Strangles is a highly contagious upper respiratory infection of horses caused by the bacteria Streptococcus equi subspecies equi (S. equi). It is transmitted by inhalation or direct contact with contaminated surfaces (for example horses sharing water buckets).“ (10)

Did streptococcus equi contaminate the serums and vaccines made in horses produced at the Rockefeller Institute and injected into soldiers in a vaccine experiment?  Was streptococcus equi in the medical serums given to the soldiers as treatments?  Was it some other pathogen which species jumped?

Did medical hubris lead to a mistake which caused a species jump which killed 50-100 million people 100 years ago?

======

REFERENCES

COMMENTS

[....]

CATRYNA WHITE January 3, 2019 at 9:56 am - Reply

One thing that is little known is that thousands of horses were shipped from Missouri, USA to Europe during WWI. Every single one of the received what is referred to as a "flu bacterium." So, not only were the soldiers and eventually the citizenry inoculated with all manner of filth, but the horses used in the war, were too.

Following an outbreak of epidemic meningitis at Camp Funston,  Kansas, in October and November, 1917, a series of antimeningitis vaccinations was undertaken on volunteer subjects from the camp. Major E. H. Schorer, Chief of the Laboratory Section at the adjacent Base Hospital at Fort Riley, offered every facility at his command and cooperated in the laboratory work connected with the vaccinations. In the camp, under the direction of the Division Surgeon, Lieutenant Colonel J. L. Shepard, a preliminary series of vaccinations on a relatively small number of volunteers served to determine the appropriate doses and the resultant local and general reactions. Following this series, the vaccine was offered by the Division Surgeon to the camp at large, and "given by the regimental surgeons to all who wished to take it.

Preliminary Series.

The preliminary series of vaccinations was carried out in the 342nd Field Artillery Regiment through the courtesy of Colonel Nugent and Major Czar C. Johnson, surgeon of the regiment. This organization volunteered en masse in response to the call issued by the Division Surgeon and offered a most promising opportunity for an extended series of observations. Moreover, only one case of meningitis had developed in the 342nd Field Artillery and the regiment had recently been covered in the search for meningococcus carriers. During the first experience the vaccination of known carriers was avoided and this regiment appeared to be free from them.

• • Choice and Preparation o' Vacc'ne.--That at least two serologically distinct disease-producing types of meningococci exist has been known since Dopter(1) in 1909 described the "parameningococcus" obtained first from the nasopharynx and then from the blood and spinal fluid of active cases of epidemic meningitis. Following Dopter's discovery Wollstein(2) confirmed the serological distinction between normal or regular meningococci and parameningococci by a comparative study of agglutination, opsonization, and complement fixation of the two types, concluding that :

  • "Because of the variations and irregularities of serum reactions existing among otherwise normal strains of meningococci it does not seem either possible or desirable to separate the parameningococci into a strictly definite class. It appears desirable to consider them as constituting a special strain among meningococci not, however, wholly consistent in itself."

  • In a more recent study based on absorption of agglutinin and agglutination tests Gordon (3) has distinguished four groups of meningococci which be calls Types I. II, III, and IV. Groups I and II are distinct and correspond to the known types. They are responsible for 75 to 85 per cent of the cases of epidemic meningitis. Other meningococci he separates into Types III and IV. Tulloch (4) finds, however, that definite group relationships exist between Types I and III, and II and IV, so that a I - I I I group type and a II-IV group type can be distinguished. These and certain other strains can be classified only by the absorption of agglutinin test, since they agglutinate in two or more of the type sera. Type II also 'appears to include a complex subgroup and shows considerable variation among the cocci comprised therein." Nicolle, Debains, and Jouan, (5) employing a rapid method of agglutination or flocculation (without incubation) in low dilutions of immune horse serum, have also reported four types of the meningococcus which they designate A (Gordon I and III, regular meningococcus), B (Gordon II and IV, parameningococcus), C, and D. Types A and B are common, Types C and D relatively rare. They find that certain meningococci are related to two or more of their specific types and must therefore be classed as "indeterminates."

  • In a recent article Mathers and Herrold 6 readily distinguish the two main types by agglutination, and group around them most of their atypical strains. The strains which fail to agglutinate in type sera bave nevertheless similar antigenic properties, since "monovalent serum prepared from these strains agglutinates in a specific way meningococci belonging to one or the other of t~e large biologic groups."

It appears, therefore, that while two distinct types or groups of meningococci may be clearly differentiated, most of the other organisms that do not fall strictly within these two groups are either intermediates or irregular variants of one or the other. Meningococci of other types in as far as they can be distinguished are only occasionally responsible for a case of epidemic meningitis.

In order to cover the two pathogenic types of meningococci and variants of them, it has become the practice in this country, following the methods of Flexner and Jobling (7) and Amoss and Wollstein, (8) to prepare highly polyvalent therapeutic sera by the repeated injection of a number of representative strains with the object of producing a serum which would protect against any pathogenic strain that might be encountered. For protective inoculation high polyvalency would seem to be equally desirable, but the choice of strains for human vaccination is limited by the fact that only a few injections are practicable, whereas the production of therapeutic serum requires a long series of inoculations in which immunity is gradually built up by the repeated injection of small doses of each antigen. The inclusion of any considerable number of strains in a vaccine for human use might defeat the purpose of the vaccination by the introduction of toxic amounts of bacterial protein without a sufficient quantity of any one specific  antigen to give rise to protection against its given strain. But since 70 to 85 per cent of the cases of epidemic meningitis are caused by meningococci of the two main types, the limitation of the strains in a vaccine to representatives of these types would seem to be the rational procedure, holding out hope of protection against a large proportion of disease-producing strains.

Therefore, for the vaccine used at Camp Funston only three organisms were chosen from the stock of The Rockefeller Institute, but the vaccine may be regarded as having represented the two main types of the meningococcus. It was also anticipated that the epidemic at Camp Funston might furnish some strain or strains of meningococci not closely related to the main types and which ought therefore to be included in the vaccine, but a type study at Fort Riley showed that the sixteen strains recovered from active cases in December and January would be covered by a vaccine containing normal and para strains.

Method of Preparing Vaccine.--The vaccine used was made in the laboratory of The Rockefeller Institute. 16 hour growths on 1 percent glucose agar in Blake bottles were washed off with isotonic salt solution, like strains pooled, and the concentrated suspensions immediately heated to 65°C. for 30 minutes to kill the cocci and inactivate the autolytic ferment. Experiments have shown that this temperature does not impair the antigenic properties of the organism and the intact cocci are less toxic than their autolyzed products.

Following the usual tests for purity and sterility the suspensions were standardized, diluted in 0.85 per cent salt solution, mixed in equal proportions of the three strains in concentrations of 1,000 million, 2,000 million, 4,000 million, and 8,000 million cocci per cc. and preserved with 0.35 per cent tricresol.

All the injections in the preliminary series were made strictly subcutaneously with a fine needle (No. 25) at the insertion of the deltoid muscle, usually in the left arm unless a recent vaccina "take" had occurred. Then the right arm was used. The tincture of iodine used as antiseptic was then sponged off with alcohol.

For the determination of dosage and the study of reactions and antibody formation six groups of about 50 men each were chosen from the various companies in the regiment. Successive groups received increasing doses of vaccine in a series of three injections at 4 to 10 day intervals according to the schedule in Table I.

About 25 men of Groups I, II, III, V, and VI gave preliminary (control) blood samples for the study of immunity reactions on the day of the first injection and a later specimen was obtained from as many vaccinated men as were available on the 8th to 10th day after the third injection.

At Major Johnson's direction First Lieutenant Serge Androp, Medical Corps, obtained reports from the men at inspection the morning following the vaccirrations in regard to the resulting localand general reactions.

Dosage and Reaction.--The determination of the dosage of vaccine for subsequent groups followed from the reports of the reactions produced by the given doses. It was considered important to increase the doses gradually in order to locate closely the zone of mild reactions and to avoid unexpectedly severe results. Accordingly, the vaccinations were begun with the injection of 500 million cocci, and this initial dose was increased in successive groups by 250 or 500 million until it had reached 2,000 million. For the second and third doses in each group, the first dose was usually multiplied by two and by four. Thus it usually happened that a given dose had already been used as a second or third in one group before it was tried as the first dose in a later series.

Only two reactions of any consequence were reported from doses of less than 2,000 million cocci. An officer in Group II who explained that he had long been hypersensitive to foreign protein and had reacted severely to the typhoid and paratyphoid vaccinations developed a severe local and general reaction, with headache and malaise, after the first injection of 750 million cocci. A second officer in Group II was similarly affected after a second injection of 1,500 million cocci and was confined to bed part of the following day. The two reactions after these small doses were merely transient, but they demonstrate a factor of individual susceptibility which was found to be of considerable importance in the determination of proper doses of vaccine.

When an initial dose of 2,000 million was reached (Group V) general reactions began to appear with greater frequency. None of the men in this group felt ill enough to report at sick call the following morning, but nine men stated upon question that they had felt feverish the preceding night. Four of them had had headache also and one reported a chill. Arms were moderately sore at the site of injection, but not sore enough to interfere with routine duties.

From this time on, a small number of the men in each group reported some local or general discomfort following the vaccination. The symptom most frequently mentioned was a "feverish sensation" often accompanied by headache, which was sometimes severe enough to cause loss of sleep. Morning temperatures, when taken, were reported normal. In a few instances there was transient nausea, malaise, or aching joint pains, and three reactions were initiated with a chill. Eight men had general reactions after the first and second doses, or after the second and third, and three complained of discomfort after all three injections.

On the whole the reactions produced by' the vaccine in the preliminary series were mild as compared with those that occasionally follow injections of typhoid or paratyphoid prophylactic and there was little complaint among the men. The occurrence of an occasional reaction of greater severity even with the smaller doses, and increasing local tenderness after the injection of the larger doses of vaccine led to the choice of relatively lower doses for the general series throughout the camp rather than the attempt to push the dosage up to the limit of endurance. Later experience fully justified this decision. Doses of 2,000, 4,000, and 8,000 million had already been decided upon when Group VI was given a second injection of 5,000 or 6,000 million and a third injection of 10,000 to determine the relative security of the chosen doses. The injection ol 10,000 million cocci caused general reactions in eleven men, but none of them was confined to bed or relieved from duty following the injection.

Finally, a seventh group of 99 men received the chosen doses of vaccine at weekly intervals about a week before the corresponding injections were given in the camp at large and served as a final check on the dosage. On giving the third injections to Group VII it was noted that many of the men still had a small painless area of subcutaneous induration at the site of the former injections. This persistent induration ~has been personally experienced after injection of meningococcus vaccine. It disappears gradually, leaving no trace. A more general discussion of reactions is reserved for the report on the larger vaccination series.

Immunity Reactions.--Agglutination is the reaction of choice for the study of antibody production with the meningococcus. It is the most delicate as well as the most specific, and is most easily made on a large number of sera and in multiple dilutions. In studying agglutination, however, several factors have to be taken into account aside from the obvious requirement of a carefully standardized technique. One of the most important is the relative agglutinability of various strains of meningococci and their response to one or both of the type (normal andpara) immune bodies. Meningococci vary also in antigenic power and not always in consonance with their agglutinability, so that it is sometimes profitable to use certain type strains as antigens and other strains to test antibody production.

Most of the control sera taken in advance of vaccination from men of Groups I, II, III, V, and VI were used up in agglutination tests against the vaccine strains in a dilution of 1: 10. Except in one instance in which the para strain was partially agglutinated, the results of these tests were uniformly negative. When the first of the serum specimens, taken on the 8th and 10th days after vaccination and tested in 1:10 dilution against the vaccine strains, also gave negative results, it was decided to collect all the available sera for later study in lower dilutions and against more easily agglutinable strains. This study was subsequently made at The Rockefeller Institute. A certain number of sera from each group was examined by macroscopic agglutination with a modification of the Wright method in dilutions of 1:2 and higher against the following strains from the stock of The Rockefeller Institute:

• No. 8. A "regular" which is also agglutinated in low dilutions of para serum.

• No. 10. An intermediate which agglutinates in both "regular" and para serum.

• No. 60. One of Dopter's paras which is relatively easily agglutinable and was represented in the vaccine.

On account of the limited amounts of serum available and the low dilutions required, the following method of agglutination was employed:

• Capillary glass tubing of an internal diameter of 2 mm. is drawn out into capsules 8 to 10 cm. long (Fig. 1). For use the ends are snapped off and a nipple is slipped on one end and folded double, giving accurate control of the aspirated fluids. A file mark measures equal volumes of serum and salt solution for successive dilutions, which are made in the capsule and deposited in a row on a plate of solid paraffin in a Petri dish. The paraffin plate is conveniently cleaned by melting off a thin layer in hot water. Equal amounts of a serum dilution and a meningococcus suspension are measured in the capsule, mixed on the paraffin plate, and drawn up to form a column about 1 to 1.5 cm. long. Four or five such specimens, separated by air bubbles, are sealed in a capsule for incubation. Only one dilution of a serum shouldbe used in a single capsule, but several meningococcus suspensions (4 billion per cc.) may be tested against it, as the admixture of specimens in the capsule is inappreciable. The capsules are woven through holes in a card which designates their contents, and incubated in a horizontal position for 24 hours at 55°C. Complete agglutination is indicated by a widespread flocculated sediment of organisms (Fig. 2). The flocculi are distributed through the clear fluid on rolling the tube briskly between the palms (Fig. 3). Absence of agglutination corresponds to a smooth line of sediment, which goes into even suspension on whirling. Partial agglutination is easily recognized in a combination of the two types of sediment. Results are read with the unaided eye or under a small hand lens.

As stated above, most of the control sera had been exhausted before this more comprehensive series of tests was undertaken. There remained fourteen normal control sera frorh Group VI, and it happened that the practically negative results obtained with the sera of Groups I, II, and III admit these specimens as controls, since the small doses of vaccine used in these groups did not give rise to demonstrable antibody formation. To these may be added twelve sera from supposed non-contacts obtained in New York City.

Table II shows the absence of agglutination in Groups I, II, and III with few exceptions. In three cases only was more than a partial agglutination of one strain in the 1 : 2 dilution observed. The titers in these cases ran as follows:

It may be assumed, therefore, that the number of unvaccinated men whose sera would a g g l u t i n a t e any of these chosen strains of meningococci is small, and on the basis of this assumption the observation that twelve of fifteen sera from Group IV agglutinate Strain 10 partially or completely is unmistakable evidence of antibody formation through the agency of the vaccine. Group V, in which the dosage reached that chosen for the camp at large, confirms this evidence of reaction, for all the twenty-two sera studied contained antibodies for the meningococcus. In some instances the more easily agglutinable strains were agglutinated in a dilution of 1 : 32 or 1 : 64  (Table III).

The final evidence of antibody production is furnished by a direct comparison of sera from Group VI taken before the first vaccination with sera taken 9 days after the third injection of vaccine, in which the appearance or increase in agglutinins is observable in all but two instances. The presence of agglutinins in the sera from Group VII merely confirms the previous findings. It may, therefore, be stated that the injection of well tolerated doses of meningococcus vaccine is followed by specific antibody formation in the human body.

The preliminary series of vaccinations, therefore, served to establish the method of injection, the proper dosage for extended vaccination, the reactions which might be expected to follow the chosen doses, and the production of immune bodies in the serum of vaccinated men. On the basis of these findings the vaccine was offered to the camp at large.

General Series.

The vaccine used in the general series of inoculations in the camp was made by Lieutenant Peter K. Olitsky at The Rockefeller Institute by the methods already described. It was shipped to Fort Riley in bulk and was diluted in isotonic salt solution to standard concentration, preserved with 0.3 per cent cresol and distributed in 50cc. bottles to the regimental surgeons under Major Schorer's direction. The use of two suspensions, one of 4,000 million cocci per cc. (Vaccine A and B) , and the other of 8,000 million (Vaccine C), adjusted the injection volumes to 0.5 and 1 cc. of Vaccine A and B and then 1 cc. of Vaccine C, volumes similar to those for the typhoid prophylactic, with doses of 2,000 million, 4,000 million, and 8,000 million cocci to be given at weekly intervals.

At the direction of the Division Surgeon, the. Division Training Officer, Captain Albert Bower, to whom especial thanks is due for his mediation between the regimental surgeons and the laboratory, called a meeting of the surgeons at which the method of giving the vaccine and the results to be expected and observed were fully described and discussed. The surgeons were thus informed of the procedure and object of the vaccination and their cooperation was enlisted, without which little could have been accomplished. The response of the men when the vaccine was offered to them was due in large measure to the interest and example of the regimental surgeons.

According to the statistics of the division headquarters, the total strength of the 89th Division at this time was approximately 25,000 officers and men. Of the~e, 4,792 (19per cent) took the first injection, 4,257 (17 per cent) the second also, and 3,702 (15 per cent) completed the series.

Part of the men received the full dosage as planned. About half of those vaccinated, whose third injection was due after February 4, 1918, were given a final injection of 4,000 million, on account of the occurrence of several fairly severe reactions from the larger dose among medical officers at Fort Riley. In some regiments the vaccinations had been completed before February 5.

Reactions.--After the first injections had been given, the opinion was almost universal in the camp that the vaccine caused less general and local reaction than the typhoid prophylactic. In very few regiments was a man excused from duty the following day on account of the reaction from the vaccination. The general feeling was that the second dose caused less reaction than the first, but there were a few men in almost every organization who had reactions of moderate severity, sometimes being confined to bed for the day with headache, joint pains, and nausea. Several cases of looseness of the bowels or transient diarrhea were noted. This symptom had not been encountered before. Careful inquiry in individual cases often elicited the information that men who complained of the effects of vaccination were suffering from mild coryza, bronchitis, etc., at the time of injection.

Among the units who took the third injections before the dosage was reduced, and so received a third dose of 8,000 million meningococci, there were several instances of fairly severe reactions, general and local, which necessitated relief from duty the following day. The reactions were not more severe than those that occasionally follow paratyphoid prophylactic and no untoward results were reported. The large majority of the men seem to have suffered no appreciable reaction whatever. The smaller doses of 4,000 million cocci caused even fewer reactions.

As in the preliminary series, the factor of individual susceptibility was prominent, a few officers and men suffering severely from doses which caused no general discomfort in the great majority o'f the men. In general, the more severe reactions occurred among the commissioned officers, and especially among the medical officers at the Base Hospital and in the Medical Officers' Training Camp at Fort Riley, due in part perhaps to more confining occupations, higher nervous tension, and more introspection than was common among the enlisted men. In one regiment, through a misunderstanding, four men were given an initial dose of 8,000 million cocci, which was well tolerated. The surgeon reported:

• • • "One had chill for 30 minutes, headache for 1 hour, slight local reaction.

    • One had slight headache, slight local reaction.

    • One had severe local reaction and headache for 24 hours.

    • One had slight local reaction, headache for 12 hours."

A survey of the reports of the regimental surgeons and of the observations in the preliminary series shows that headache was the most frequent symptom following injection, and accompanied most of the other symptoms encountered. Sometimes the reaction was initiated by a chill or chilly sensation, and a number of men complained of fever or feverish sensations during the following night. Next in frequency came nausea (occasionally vomiting), dizziness, and general "aches and pains" in the joints and muscles, which in a few instances were especially localized in the neck or lumbar region, causing stiff neck or stiff back. A few injections were followed by diarrhea. The reactions, therefore, occasionally simulated the onset of epidemic meningitis and several vaccinated men were sent as suspects to the Base Hospital for diagnosis.

Such transient reactions are illustrated by the following brief protocols:

• • • Individual 1.--C. D., Private, Battery D, 342nd Field Artillery.

    • Jan. 15, 1918. 1st injection 2,000 million. "Sore arm."

    • Jan. 22. 2nd injection 4,000 million. "Sore arm, headache."

    • Jan. 29. 3rd injection 8,000 million. "Began to feel badly about 15 minutes later and had a chill. 3 hours later was sent to the Base Hospital complaining of headache, lumbar pain, stiff neck, and fever, 103°F. No nausea. Went to sleep about 2 hours later and slept well. Had entirely recovered the next morning."

    • Individual 2.--L. N., Private, Field Hospital Company 354, 314th Sanitary Train.

    • Jan. 21, 1918. 1st injection 2,000 million. "Slight local soreness."

    • Jan. 28. 2nd injection 4,000 million. "Slight local soreness."

    • Feb. 4. 3rd injection 8,000 million. "About an hour and a half after injection, was taken with a severe chill and a subnormal temperature. About 20 minutes later his temperature rose to 103.6°F. and then fell within the next 2 hours to 101°F. Temperature normal the following morning. He complained of no other symptoms."

The most severe illness immediately following vaccination is described by the officer himself as follows:

• • • Individual 3.--J. M. K., First Lieutenant, 314th Sanitary Train.

    • Jan. 21, 1918. 1st injection 2,000 million. 4.30 p.m. Soreness at site of injection in evening. Slept well.

    • Jan. 22. Awakened feeling drowsy and listless. Local soreness worse. Pains in back of neck, calves of legs, thighs, lumbar region, and both arms. No appetite. Symptoms grew worse after holding sick call at the Infirmary. Perspired on slight exertion. Felt chilly and warm by turn. Went to quarters and lay in bunk. Soon felt feverish. Developed diarrhea about i1 a.m. Eight movements in 5 hours. Cup of hot chocolate at 1 p.m. Felt nauseated. Vomited six times in next 3 hours. Took sodium bicarbonate, 2 gm. in glass of warm water, promptly vomited. Retained 15 minutes later, and then began to feel better. Felt well next morning but had no appetite. Bowels still loose. Returned to duty. Appetite returned the evening of Jan. 24. Local soreness persisted 3 days.

      • • Jan. 22, 9.45 a. m . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Temperature (F) = 98.4  , Pulse = 86

        • 1.15 p. m . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Temperature (F) = 99.8 , Pulse = 82

        • 3.45 p. m . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Temperature (F) = 101.0 , Pulse = 92

        • 7.30 p. m . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Temperature (F) = 101.8 , Pulse = 108

        • 10.00 p. m . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Temperature (F) = 100.0 , Pulse = 98

        • Jan. 2.3, 7.25 a. m . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Temperature (F) = 97.8 , Pulse = 98

    • Jan. 28. 2nd injection 4,000 million. Local reaction severe. Duration 3 days. General reaction, malaise of 24 hours duration.

    • Feb. 4. 3rd injection 8,000 million. Local reaction severe. Duration 4 days. General reaction, nausea, looseness of bowels (not diarrhea), chilliness, but no fever. Muscle soreness severe and general. Appetite absent for 2 days.

The occurrence of such reactions as those described above was rare but they illustrate the importance of the factor of individual susceptibility. The great majority of the men vaccinated were reported to have had no general symptoms, and very few men were confined to quarters after any dose of the vaccine.

Occurrence of Meningitis after Vaccination.--The records of cases of epidemic meningitis in Camp Funston have been followed up to June 4, 1918, thus covering the period that the 89th Division remained in camp. In the interval between January 21 when the vaccination was started in the camp and June 4, 46 cases of meningitis are reported to have entered the Base Hospital at Fort Riley. Of these patients, three had received one, two, or three injections of antimeningitis vaccine. The following data have been collected in regard to these cases.

• • • Case 1.--L. T., Second Lieutenant, 314th Engineers.

    • Jan. 21, 1918. 1st injection 2,000 million. Next day neck was rather stiff. slight headache. Well for next 2 days, but working very hard on double duty.

    • Jan. 25. Fainted at Officers' Call. Felt "under the weather" with indefinite symptoms the next 2 days but remained on duty.

    • Jan. 28. 2nd injection 4,000 million. This made him feel so much better that he remarked to his friends that he "was getting to,be a dope fiend in the stuff and couldn't get along without it."

    • Jan. 29. Felt worse again, headache, "no ambition.': Following days he remained on duty, but tired easily and often felt chilly and feverish, had stiff neck and joint pains.

    • Feb. 2. Remained in bed. Throbbing headache, became nauseated and vomited twice. Sent to Base Hospital. Lumbar puncture on arrival showed a turbid fluid with many leukocytes and moderate numbers of intracellular Gram-negative diploeocci.

    • Lieutenant T. had a very mild case of meningitis which yielded promptly to serum treatment.

    • Case 2.--E. H., Corporal, Company C, 354th Infantry.

    • Jan. 21, 1918. 1st injection 2,000 million. "Never felt anything. Arm not very sore."

    • Jan. 26. Went on 5 days leave, returning Jan. 31, and so missed second injection.

    • Feb. 1. "Felt sore all over." Had chills. Frontal headache.

    • Feb. 2. Headache continued, stiff joints and aching pains. Sent to Base Hospital. Diagnosis, epidemic meningitis.

    • Corporal H. had a severe case of meningitis but recovered.

    • Case 3.--J. C. N., Private, Company B, 340th Machine Gun Battalion.

    • Jan. 24, 1918. 1st injection 2,000 million.

    • Jan. 31. 2nd injection 4,000 million.

    • Feb. 8. 3rd injection 4,000 million. Reactions not reported.

    • Mar. 31. Acute otitis media and right frontal sinusitis.

    • Apr. 16. Epidemic cerebrospinal meningitis.

    • Apr. 24. Cerebrospinal fluid found positive for meningococcus for the last time.

    • Apr. 27. Ulcer of right cornea followed by slight opacity with slight impairment of vision.

    • May 5. Right facial paralysis which has since improved considerably.

    • Private N. will be ready for assignment to domestic military service about July 1, 1918.

The examples of Lieutenant T and Corporal H are instructive, since they may well be, and probably are, instances of meningococcus inoculation in individuals in the incubation period of a meningococcus meningitis, Assuming this to be the fact, the indication is tha~ ne harm was done by the procedure. But whether this is the precise fact or not, the cases have no real bearing on the value of antimeningitis vaccination, because the interval between the first inoculation and the diagnosis of the meningitis was too brief to permit immunization to be effected.

It is clear that Private N developed meningitis at a period at which protection following vaccination should have been present. In his case the vaccination must be considered as having failed to afford protection. A study of the type of the infecting meningococcus would conceivably have thrown light on the incident, or the incident may merely indicate that occasional individuals fail to be adequately immunized, just as in the ahalogous procedure of antityphoid inoculation.

Immunity Reactions, General Series.--In addition to the blood samples taken for study in the preliminary series of vaccinations, similar samples were obtained from a group of men in each of three regiments who had completed the vaccination series. The serum specimens were taken at an interval of from 10 to 18 days after the third injections had been given, and were examined for agglutinins by the method already described. The results of these tests are shown in Table IV. The sera of 50 men showed some content of agglutinins; the sera of 16 others failed to do so.

Examination for Agglutinins of the Blood Serum of Chronic Carriers.

While every case of epidemic meningitis is presumed to develop from the carrier state, many observers have noted the rarity of the disease among chronic carriers. The presence of the meningococcus in the nasopharynx is but one of the factors in the accident which results in the bacterial invasion of the body, and the relatively low infectivity of the meningococcus is to be credited to causes of resistance on the part of the carrier host among which may well be the appearance of immune bodies in the blood as the result of the multiplication of meningococci in the nasopharynx.

If the presence of agglutinins for the meningococcus could be demonstrated in the blood of chronic carriers, light would thereby be thrown on the mechanism of this resistance. With the object of detecting the possible existence of meningococcus agglutinins in the blood serum of carriers, a number of such sera have been studied in low dilutions by the capsule method described in an earlier section of this report.

Through the courtesy of Passed Assistant Surgeon J. L. Waterman, United States Naval Hospital, Brooklyn NavyYard, and Dr. F. S.Westmoreland, Riverside Hospital, New York, opportunity was given to obtain blood samples from a number of chronic carriers of the meningococcus, and the corresponding carrier strains were kindly furnished by Dr. A. W. Williams of the Department of Health, of the City of New York, or obtained directly from the men themselves. The men studied were known to have harbored meningococci for from 4 to 16 weeks.

20 carrier strains of the meningococcus have been subjected to the agglutination tests in low dilutions with the sera of the hosts from whom they were obtained and the carrier sera were tested against the stock strains of spinal origin that had been studied in the sera of vaccinated men from Camp Funston. 18 of the carrier strains were also  tested with 12 normal sera from supposed non-contacts as controls. The results of these tests are recorded in Tables V to IX. The trials with non-contact sera (Table V) show that with two exceptions the carrier strains are not usually agglutinated in normal sera in a 1 : 2 dilution. One of the exceptional strains was partially or completely agglutinated by 9 and the other by 8 of the 12 sera. The other cultures were only occasionally agglutinated in this low dilution of normal serum. One supposedly normal serum agglutinated 11 of the 18 carrier strains. In the presence of sera from their hosts, however,  all but 4 of these carrier strains were agglutinated (Table VI) and the sera in most instances showed agglutinins for stock spinal strains of the meningococcus. Subsequently the sera were reexamined in multiple dilutions, and at this time 2 of those previously found negative agglutinated their strains up to 1:4 and 1:8 (Table VII). The titers of the other sera ran from 1 : 4 to 1 : 64.

Appearance of Agglutinins in Sera after Storage.--On numerous occasions we have observed an increase in agglutinating power in sera which have stood at ice box temperature for some time. The fact was reported in a recent paper (9) as having occurred with typhoid agglufinins in guinea pig sera, and Tulloch (4) records an instance in  rabbit serum during immunization to the meningococcus. This he explains as due to the presence of constituents of the serum or of the organisms which do not take part in the mechanism of agglutination, but which may be present "in such quantity or in such a physical state that they protect the united antibody-antigen complex from the flocculating action of the electrolytes."

Table VIII shows the appearance of agglutinins in some of the sera under discussion after they had stood, sealed, at 4°C. for some time. The other sera were not examined so early after bleeding. The inconstancy of the phenomenon has already been described ° and is implied by Tulloch in his reference to "this particular serum."

A variation of a different order was encountered when ten of the sera studied on May 29 or June 12 were examined on June 24 in multiple dilutions with the stock spinal strains (Table IX). Six of the ten had agglutinated Strain 8 in the 1:2 dilution. Now all but one serum failed to do so. Strains 10 and 60, however, were agglutinated in various serum dilutions by practically all the specimens examined, including No. 43, which had failed to agglutinate its homologous strain. Agglutinins for these spinal strains are only rarely found in normal sera (Table II).

DISCUSSION.

• • Heretofore meningococcus vaccines have not been extensively employed for prophylactic immunization, and only a few references are to be found in the literature that relate vaccination experiences. Davis, TM in 1907, describing animal experiments and the therapeutic use of an autogenous vaccine reported a personal experience in which he suffered a very severe reaction following the subcutaneous injection of a 24 hour slant culture of a meningococcus heated to 65°C. for 30 minutes. Shortly after inoculation, nausea and vomiting were followed by a severe chill, lasting half an hour, and then intense headache, muscular pain, purging, and vomiting of bile. His temperature rose to 103°F., and during the remainder of the day, and in the night following, nausea and vomiting continued, with headache, thirst, and marked prostration. Later symptoms included a diffuse rash, herpes, and in the urine granular, hyaline, and epithelial casts. The reaction subsided gradually. The leukocytes rose to 44,050 on the 3rd day, and the opsonic index reached 2.3 on the 2nd day, returning to normal by the 5th day. 

  • Sophian and Black n studied agglutination and complement fixation in serum specimens from ten students who had been vaccinated with two or three doses of a monovalent vaccine. The doses given were 500 or 1,000 million, 1,000 or 2,000 million, and 2,000 million cocci, at 7 day intervals. Their vaccine had been heated to 50°C. for 1 hour. Following the vaccinations they noted malaise, frontal headache, and slight fever with occasionally more severe symptoms; intense frontal or vertical headache, general bodily pain, nausea, vomiting, and a rise of temperature to 102-104°F. Labial herpes was seen. Using a readily agglutinable organism, they found the agglutinin titers of the sera of their vaccinated subjects to range from 1 : 200 to 1: 1,500. Complement was fixed in serum dilutions up to 1 : 250.12 Complement-fixing antibodies were found in low dilutions of the serum of seven of these men after an interval of 2 years.

  • Sophian and Black refer to Hall's experience in Kansas City in the vaccination of about 280 persons in families in which meningitis had occurred. A number of doctors and nurses were likewise inoculated, and in no instance did the disease occur subsequent to vaccination. About 100 persons in Dallas were vaccinated, but most of them did not complete the vaccination series. Two nurses developed epidemic meningitis some weeks after a series of two inoculations; both recovered.

  • Recently Whitmore, Fennel, and Petersen TM have reported an experience with a polyvalent lipovaccine in which total doses of 40,000 million or 80,000 million cocci were given subcutaneously in one or two injections. 55 men in all were vaccinated. 40,000 million cocci in one dose did not cause any general reaction. Two doses of 40,000 million cocci each at a 3 day interval were followed by two instances of constitutional reaction among 25 men. 5 men received 80,000 million cocci in a single injection which was followed after 24 hours by a moderate general reaction. In the first days after vaccination with the larger doses agglutinin formation was observed against three of the vaccine strains, especially those that respond to antibodies of both the normal and the para type.

These reports from the literature coincide with the present experience with meningococcus vaccine in their descriptions of the reactions that may be expected, and of the appearance of specific antibodies in the blood after vaccination. As Sophian and Black pointed out, the general symptoms indicate some degree of meningeal irritation and occasionally they may simulate the onset of meningitis. The symptoms are not progressive, however, and even though severe, they clear up in a few hours. In one instance in which a lumbar puncture was done on a suspect 3 days after a secdnd dose of vaccine the spinal fluid was found normal. The illness described by Davis is instructive to show the severity of the symptoms which may follow an injection of meningococcus substance many times the proper dose. Whitmore, Fennel, and Petersen, by protecting their vaccine in oil, were able to give much larger doses in a single injection with only moderate constitutional effects.

Whatever may be the relation of agglutinins to specific protection against invasion the agglutination test is recognized as the most reliable indication of antibody formation due to the meningococcus, and is used generally in the standardization of therapeutic sera as an index of potency. With equal reason the presence of agglutinins may be taken as an index of active immunization after vaccination. We do not know the ratio of agglutinin formation to protective power, and can only discover by wide experience what agglutinin titers correspond to relatively complete immunity to meningococcus invasion. It is perhaps significant, however, that the agglutinin titers  of the sera of vaccinated men are of the same order of serum dilutions, namely 1 : 4 to 1 : 64+, as those of chronic carriers of the meningococcus, who are usually refractory to the strains carried. A study of the blood of cases of meningitis which have recovered without serum treatment might be instructive in this connection.

Meningococcus agglutinins appear not to have been found previously in the blood of chronic carriers. Cathoire, (14) in a brief communication, reported that the agglutinin study of carrier sera led to no positive result, but with the Wright technique he was able to show a constant increase in opsonic power compared with sera from normal persons, and he therefore concluded that the relative immunity of carriers is to be explained by a specific change in the serum.

Herrick (15) thinks that the occurrence of relapses in some cases of epidemic meningitis "lends discouragement to vaccine prophylaxis and other measures for the production of immunity." It should be pointed out that relapses are probably caused by reinfection from small pockets in the meninges in which the meningococcus has been walled off, and so permitted to survive therapeutic measures otherwise effective. It may be mentioned in passing that the occurrence of relapses in typhoid fever has been no contraindication to the employment of typhoid prophylaxis. The object of prophylactic vaccination is to oppose the meningococcus at the threshold, and if a systemic invasion precedes the spinal infection, as recent observations tend to show, the building up of antibodies in the blood stream is the means by which a hematogenous incursion is to be combated.

SUMMARY.

• 1. A meningococcus vaccine suspended in salt solution has been given subcutaneously as a prophylactic to about 3,700 volunteers in three injections of 2,000 million, 4,000 million, and 4,000 or 8,000 million cocci at weekly intervals.

  2. These doses rarely caused more than the mildest local and general reactions. Exceptionally a more severe reaction emphasized the presence of an unusual individual susceptibility to the vaccine. In such instances the symptoms were in part those of meningeal irritation and sometimes simulated the onset of meningitis.

  3. Specific meningococcus agglutinins have been demonstrated in the blood serum of vaccinated men as compared with normal controls.

  4. Moreover, agglutinins have been demonstrated in the blood serum of chronic carriers of the meningococcus. Evidence is thus brought forward that the relative immunity of chronic carriers to epidemic meningitis may be due to the presence of specific antibodies in the blood stream.

https://www.archives.gov/publications/prologue/2017/fall/tonys-lab

2017-09-usa-national-archives-prologue-magazine-tonys-lab-ww1-germ-warfare.pdf

“Tony’s Lab” 

Germ Warfare in WWI Used on Horses in the U.S.

Fall 2017, Vol. 49, No. 3

By David Pfeiffer

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A shipment of horses at a New York City rail yard, 1918. (165-WW-280A-050)

On a chilly November night in 1915, a dockhand crept silently through the darkness near the Newport News, Virginia, shipyard as he approached dockside corrals filled with horses destined to board British or French transport ships headed for Europe to aid in the Allied war effort.

As he neared the Breeze Point wharf, he carried a brown paper package and rubber gloves. He snapped on the gloves and removed from the package two glass syringes containing a yellow liquid.

The dockhand, a stevedore named John Grant, checked out the hundreds of horses and mules in the British remount depot. Taking care to avoid the night watchmen, he went to the first mule corral. Then he jabbed the needles into the hides of as many mules that he could reach. After jabbing many horses in two pens, he dumped the rest of the liquid in the animal’s water basins and food troughs and threw the gloves and syringes into the river.

During 1915–1916, thousands of horses and mules were killed in these horse pens. The yellow liquid, which carried the glanders bacteria, had been cooked up in what was known as “Tony’s Lab” by an American-born German agent named Anton Dilger.

German espionage and sabotage in the United States was going on long before the United States formally entered the war in April 1917. Dilger’s work was just one of many ways the Germans sought to undermine America’s ability to aid its allies. Fewer horses and mules would make moving artillery and other war materiel much more difficult; it had become a strategic priority for Germany.

Anton Dilger’s Early Life Spent Around Horses, Riding

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Anton Dilger’s passport photo, attached to his 1916 application. (National Archives, RG 76)

Dilger was born on a horse farm, named Greenfield, near Front Royal, Virginia, on February 13, 1884. He was the son of Hubert Dilger, a German immigrant and a U.S. Army captain who had received the Medal of Honor for his service as a horse artillery officer at the Battle of Chancellorsville in the spring of 1863.

Hubert Dilger, an expert horseman, was instrumental in saving Union forces in the fighting retreat of General Hooker’s troops during Confederate General Stonewall Jackson’s flank attack at the end of the battle. The Confederates won the battle but did not destroy Hooker’s army, due partly to the efforts of Captain Dilger.

At Greenfield, Anton was taught to ride and to hunt and fish. He was also well acquainted with German culture. Four of his sisters married Germans and moved back to Germany. As a boy, Anton idolized his famous great grandfather on his mother’s side, Dr. Freidrich Tiedemann, known as the “great physiologist of Heidelberg.”

Anton’s grandfather was also a German medical doctor, so, unsurprisingly, Anton was sent, at the age of nine, to study in Germany. He stayed at his sister Edna’s house in Mannheim and enjoyed a comfortable life in Germany.

He passed the medical exam at the University of Heidelberg in 1908 and by 1909 was an assistant at the university surgical clinic while researching his doctoral dissertation. While studying microbiology and germ culture, he learned how to set up a tissue-culture lab. Ironically one of his challenges was how to prevent bacterial infections in animal tissue cultures. Later, in Washington, D.C., he applied his expertise for the opposite purpose.

German Government Shows Interest in Dilger as Agent

Dilger received his doctoral degree in 1912, a year after Hubert Dilger died.  Greenfield farm was in decline, and the family sold off part of the farm to the U.S. government. During the years before World War I, it became part of a U.S. Army Remount Depot, where the Army gathered, evaluated, and trained warhorses.

The young and handsome Doctor Dilger cemented his reputation back in Germany as a superb surgeon and a ladies man. Once war arrived, Dilger served in military hospitals performing battlefield surgery in Serbia and Bulgaria in 1914 and in Rastatt, Germany, in 1915. Seeing family members wounded and killed in the conflict hastened his conversion to a pro-German and anti-Allied outlook.

As a German patriot in possession of a U.S. passport, he was a prime candidate for recruitment by German intelligence to work in America.

According to German records, Dilger left Germany on September 29, 1915, working with the Imperial Prussian War Ministry in America.

Officially neutral, the United States provided loans and other goods and supplies to the Allies. Because America supplied hundreds of thousands of horses and mules to the war effort, the Prussian Imperial War Ministry was very interested in cutting off this supply.

Dilger, Brother, and Sister Leave Farm for Chevy Chase

Anton boarded the Dutch passenger liner Noordam in Amsterdam, bound for New York City and heading toward his final destination of Washington, D.C. Among the items he carried was a small briefcase filled with fragile glass test tubes that contained the basis for manufacturing the glanders germ. The glanders bacteria was a primary killer of horses and mules.

With the help of his sister Jo, who lived with her family in northwest Washington, D.C., he searched for a rental house where he could establish a physician’s office and set up a small laboratory for his experiments. He hung up his shingle but never saw any patients.

During a visit to Greenfield in December 1915, Anton persuaded his sister Em and his brother Carl to join him in Washington. He asked Em to be the housekeeper and Carl, a former beer brewer, to help in the lab. More importantly to Anton, she could be hostess and consequently discourage any possible gossip. Em had no idea that her brother was a German agent.

Carl had had his own brewery in Montana and knew how to propagate yeast and ferment vats of beer, a useful skill when it came to cooking up cultures. After Anton confided in him the nature of his mission, Carl was eager to help.

Anton settled in a two-story white brick house in the 5500 block of 33rd Street, NW, near Connecticut Avenue, not far from Chevy Chase Circle. Even in those days, Chevy Chase was a fast-growing and fashionable neighborhood, only six miles from the White House.

There was even a tramline connecting Chevy Chase with downtown. Because Chevy Chase was a new neighborhood with lots of strangers, Anton could easily blend in. Most important, the house had a spacious basement with a separate entrance that Anton could turn into a secret lab. It was a case of hiding in plain sight. 

Anton Sets Up “Tony’s Lab”

Anton and Carl bought lab equipment and wire cages for the guinea pigs they would use to test the effectiveness of the poison they were to manufacture. They had an incubation oven, sterilizing machine, petri dishes and rows of glass vials. Later, Anton’s associates would call the basement “Tony’s Lab.”

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A poisoned horse at Covington, Kentucky. (111-SC-6991)

For several months, the brothers incubated vials of anthrax and glanders. They were careful not to touch the cultures, since the bacteria in the cultures could also kill men. At room temperature, the cultures would be effective for about a month.

When the cultures were ready to go, German agents (Abeteilung IIB) from Baltimore stopped by the house each week to pick them up. These German agents then delivered the cultures to ports on the East Coast, including Newport News, Norfolk, Baltimore and New York, where hired stevedores would secretly inject the animals or contaminate their food supplies with the deadly germs.

The German agent who picked up the cultures at the little house on 33rd Street was Capt. Frederick Hinsch, one of the leaders of the Baltimore group of German agents. To demonstrate the effectiveness of the cultures, Anton showed him the guinea pigs; they were listless and dying. Hinsch was satisfied. In exchange for the cultures, Hinsch handed over a few thousand dollars to cover expenses, such as equipment, glassware purchases, house rental, and salaries for both Anton and Carl. The money came from Paul Hilken, the Baltimore paymaster.

The Baltimore group worked out of the offices of the North German Lloyd steamship line. Hinsch was charged with organizing dockhands, German sailors, and others for sabotage operations such as planting cigar bombs in U.S. ships carrying munitions, distributing flyers to get dockworkers to strike, and poisoning horses and mules being shipped to the Allies.

This was not the first German attempt at killing American horses. Agents earlier attempted to bomb or derail trains packed with horses or mules headed for British remount depots such as Newport News. In January 1915, the Germans planned to bomb transport trains in Canada that carried ammunition as well as warhorses. As it turned out, the cold Canadian winter made it difficult to lay the explosives.

New York City Police Increase Guards on Horses

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Anton Dilger applied for a U.S. passport for his return to Germany in 1916. (National Archives, RG 76)

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A letter recommendating that Anton Dilger be granted a passport. (National Archives, RG 76)

After another plan to bomb trains heading out of the Chicago stockyards went awry, the Germans turned to germ warfare as a more efficient method to stem the supply of horses and mules heading to the Allies.

An attempt at germ warfare in May 1915 did not work because the saboteur, Erik von Steinmetz, did not know enough microbiology to keep the cultures alive. It became evident to the German General Staff that they had to have an agent who knew bacteriology and knew what he was doing. That agent was Dr. Anton Dilger.

The Dilgers continued to operate their lab until January 29, 1916, when Anton suddenly returned to Germany using a new U.S. passport he had obtained so he could, as he told the Department of State, work as a doctor in Heidelberg. He had also gotten a letter of recommendation from an acquaintance in the U.S. Army Medical Corps.

What had happened?

Capt. Tom Tunney was a New York City police detective and head of the department’s bomb squad assigned to investigate and apprehend the culprits in the bombing of buildings and ships in New York harbor. In the winter of 1915–1916, he gathered information concerning Steinmetz’s attempted germ attack and wondered if the Germans were going to make another attempt. He had no suspects and no clues—nothing but the fear of another attack.

Captain Tunney ordered doubling the guards at the New York horse corrals and spread the word along the waterfront to be on the lookout for enemy agents who might attempt to poison the animals. He later found out that his vigilance succeeded in preventing a large-scale biological attack.

At a secret meeting in late January 1916, Hilken, being somewhat cautious, told Hinsch and Dilger that “They’re on to us.” He had learned from Paul Koenig, a German agent in the New York area, that New York police were asking questions around the harbor about plots to poison horses awaiting shipment to the Allies. There were also more guards around the horse corrals. At the meeting, Dilger was handed a cable that ordered him back to Berlin “for discussions.” Anton had gotten his wish to get back to Germany, and Dilger’s lab had succeeded in remaining undetected. 

U.S. Agents Interview Anton, Deem Him Not a Traitor

After Anton left, Carl Dilger continued the work of the lab with Fred Herrmann, a good friend of Anton’s, who had been living at the house. They added the manufacture of incendiary pencils and other explosives to their repertoire. Some of these incendiaries ended up being used in the Black Tom explosion in New Jersey, a munitions factory that supplied ammunition to the Allies

Because Carl tended to brag about his mission after having more than a couple of beers at the local taverns, Hilken and Hinsch pushed him out of the operation in May 1916. They sent him to Berlin with an important sealed message to the Political Section of the General Staff. The message was to keep Carl in Germany so that he could not undermine the sabotage operation in America, but the message was lost, and Carl continued in service delivering incendiary tubes. Herrman stayed on at the lab.

After the Black Tom explosion in July 1916 and the increased law enforcement scrutiny that followed, Herrmann decided to close up the lab and move to St. Louis. The St. Louis operation failed since Herrmann did not have Anton’s medical and scientific knowledge, and the germ cultures died.

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The Black Tom munitions depot in New Jersey was a prime target for saboteurs. Germany was eventually held accountable for the devastating explosion there. (111-SC-95793)

Amazingly, it was the local police, like Captain Tunney in New York, not the national law enforcement entities such as the Bureau of Investigation, the Secret Service, and Military Intelligence, that were most effective against German sabotage operations. Bureaucratic inefficiencies, lack of law enforcement authority, and lack of staff contributed to their failure.

For example, an agent of the Bureau of Investigation interviewed Anton Dilger in July 1917 while he was visiting one of his brothers at Greenfield. He had come to America to deliver secret coded messages from Berlin to German agents and diplomats. Later in July, he was interviewed again by another bureau agent while he was staying at his sister Jo’s house in Washington. Again, this interview did not raise any red flags, the agent saying in his report that “Dr. Dilger is not a man who would be guilty of any traitorous acts towards this country.” Anton Dilger had slipped through the bureau’s fingers.

Anton Receives Iron Cross for His Service to Germany

Anton then went to Mexico to join with the other Baltimore-based agents, specifically Hinsch and Hilken, who had escaped the United States after the declaration of war in April 1917. Taking on the alias “Dr. Delmar,” Anton’s main mission from Berlin was to promote a Mexican invasion of the United States, and he raised money to finance the proposed campaign. Feuding among Anton, the German agents, and Berlin caused the campaign to fizzle, but Anton was still awarded the Iron Cross in January 1918 in recognition of his sabotage and espionage work.

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Carl Dilger applied for a passport in 1916 to allow him to travel to Germany. (National Archives, RG 76)

Even so, Anton had made enemies both in Mexico and Berlin. Now in Spain, he feared that Allied investigators were finally catching up to him. Then came the Spanish influenza epidemic of 1918–1919, which killed possibly as many as 50 million people worldwide. On October 17, 1918, Anton Dilger died of influenza in Madrid at the age of 34. That was the official story. Ironically, he was a germ saboteur killed by an infectious disease.

There were problems with this version of events. Carl Dilger and Fred Herrmann later claimed that they suspected German agents had murdered Anton—that he had been poisoned “because he knew too much.” In testimony years later to the Mixed Claims Commission, they alleged that Anton’s cover had been blown and Allied agents were closing in. There is still some doubt whether Anton even died in Madrid in 1918. The details of his death remain murky to this day.

The Mixed Claims Commission, U.S. and Germany, was established in 1922 for the purpose of satisfying claims of the United States and its citizens against Germany since 1914. By 1933, most of the claims had been settled. The largest group of unsettled claims were the sabotage claims, which consisted of the 153 claims of U.S. citizens who suffered losses as a result of German sabotage in 1916–1917. The sabotage claims remained before the commission for more than 12 years, and due to German intransigence, it was not until 1939 that a decision was rendered in favor of the U.S. claimants.

According to later estimates, the German germ sabotage campaign in America killed thousands of horses during World War I. Even so, that number was not a significant factor in the war effort since more than over 750,000 horses were shipped to the Allies from America. This was the first modern germ warfare campaign in history. But it was not the last.

The story of Anton Dilger and “Tony’s Lab” are filled with ironies. But the most notable one is that an American-born son of a Civil War hero, who loved horses and was an expert horseman, became a German agent whose germ cultures were responsible for the deaths of thousands of horses in the United States during World War I.

David A. Pfeiffer retired earlier this year after 40 years as an archivist at the National Archives, specializing in transportation and diplomatic records. Over the years, he has written a number of articles for Prologue, including the award-winning “Bridging the Mississippi: The Railroads and Steamboats Clash at the Rock Island Bridge” in Summer 2004. He holds a bachelor’s degree from Ithaca College and a master’s degree from George Mason University, both in history.

Note on Sources

The main primary source that I consulted was the records of the Mixed Claims Commission, United States and Germany, 1922–1941. The records are part of Record Group 76: Records of Boundary and Claims Commissions and Arbitrations housed at the National Archives at College Park in Maryland. The MCC records include a tremendous amount of information on the sabotage claims cases and their eventual settlement. The record series consulted for this article were the Records Relating to German Saboteurs and Their Activities, Chronological List of German Sabotage Activities, 1893–1927 (Entry 73), which has a great chronology of the surveillance of German agents, and the Records Relating to German Saboteurs (Entry 76). There are files on Anton and Carl Dilger, Frederick Herrmann, Paul Hilken, and Frederick Hinsch, and others. I also briefly checked the Testimony of Frederick L Herrmann and Theodore J. Wozniak, 1930 (Entry 79) and Testimony in Sabotage Cases, 1930 (Entry 82).

There are two agent reports on interviews with Anton Dilger during July 1917 in the Records of the Federal Bureau of Investigation (Record Group 65), Investigative Cases Files of the Bureau, 1908–1922 (Microfilm Publication M1085), Old German Files #33415 and #26601. These records are also at the National Archives at College Park.

My main secondary source was The Fourth Horseman: One Man’s Mission to Wage the Great War in America, by Robert Koenig. This is the definitive work on Anton Dilger, and the author pieced together a great story of Dilger and World War I German sabotage. As he mentioned in his note to sources, there are many gaps in the records and his personal letters. And espionage is not usually well documented.

Other books consulted include the classic on German espionage, particularly Black Tom and Kingsland, by Jules Witcover titled Sabotage at Black Tom: Imperial Germany’s Secret War in America, 1914–1917. See also The Secret War on the United States in 1915: A Tale of Sabotage, Labor Unrest and Border Troubles, by Heribert von Feilistzsch; The Detonators: The Secret Plot to Destroy America and an Epic Hunt for Justice, by Chad Millman; and the Dark Invasion, 1915, Germany’s Secret War and the Hunt for the First Terrorist Cell in America, by Howard Blum. There is also a very good post in the WETA Boundary Stones blog, by Mark Jones titled “‘Tony’s Lab’ and World War I Germ Sabotage in Washington.”

I also consulted a book review on the Fourth Horseman by Jack Woodall titled “Bioterror Is Nothing New.” And finally, I looked at a piece by Sarah McCammon of NPR on April 6, 2017, called “The Unsung Equestrian Heroes of World War I and the Plot to Poison Them” (www.npr.org/2017/04/06/522594344/the-unsung-equestrian-heroes-of-world-war-i-and-the-plot-to-poison-them)

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THE ROCKEFELLER INSTITUTE FOR MEDICAL RESEARCH

BUILDINGS AND EQUIPMENT -  NEW YORK CITY

THE principal laboratory buildings of the Institute are situated on the cliff overlooking the East River, at the end of East 66th Street, New York City. The situation insures excellent light and air, and greater quiet than would be enjoyed in the more accessible and crowded central parts of the city. The central structure, the first erected (in 1905-06) (see frontispiece) is a laboratory and administration building with five floors and a light basement, and has a series of accessory rooms on the roof. It covers a ground area of 136 feet by 60 feet. Another laboratory building, containing six floors. and two basements and covering 150 feet by 62 feet of ground, shown at the left of the frontispiece, was opened in 1916. In both buildings each floor is arranged with laboratories and offices about a central corridor. The construction of both buildings is fire-proof and such ,  that all interior partitions can be altered or removed as occasion requires. Hot and cold water, steam, compressed air, suction, gas, and electric current are supplied to the laboratories. Refrigeration by means of a brine circulation is carried to central positions in the buildings and several large thermostats are a part of the construction. Pipes and drains, vents, and conduits, are exposed or carried through accessible ducts wherever possible, to facilitate inspection and alteration.

In addition to the laboratories these buildings provide administrative offices, an assembly room, library, publication division, a central supply room, illustration division, x-ray division, and facilities for section making, sterilization, and the making of culture media.

The animal house is an eastward extension of the new laboratory building. In it are kept small animals, such as rabbits, guinea pigs, monkeys, etc. There is also provision for ten horses and a smaller number of goats and sheep. Two cold rooms are arranged for aquaria. The building includes arrangements for the storage and preparation of foods, the repair and sterilization of cages, and the incineration of refuse. Walls and floors are finished so that they can be washed down with a hose. The cages are suspended on metal racks instead of being placed on the floor.

The hospital (see frontispiece) is a seven-story building, with two additional basement floors in the wall of the East River cliff, and a roof-house. It is connected by a covered bridge at the level of the third floor with a  two-story and basement isolation pavilion, and with the laboratory building beyond. The first floor of the hospital provides for the administration and reception rooms, and for the quarters of the resident staff. The second floor is entirely occupied by the nurses' quarters. The third floor contains a number of small rooms for the accommodation of one or two patients each. The fourth, fifth, and half of the sixth floors are arranged for ward patients. The hospital is planned with the idea of enabling the staff and nurses to give an unusual amount of attention to each of a small number of patients. The general wards are for only six or eight beds each. The balconies at each end of the building are large enough to permit all the beds t0 be rolled out in pleasant weather. The seventh floor of the hospital and. half of the sixth are devoted to laboratories.

It is the policy of the hospital to engage each member of the staff in both clinical and laboratory work, and to provide ample laboratory facilities as near the wards as possible. On the roof is a small operating suite. On this floor also is a sun room for patients.

A power house built and operated by the Institute provides the buildings with heat, light, electric power, pressure, refrigeration, vacuum, and filtered water. It has reserve capacity for future buildings.

BUILDINGS NEAR PRINCETON, NEW JERSEY

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WAR ACTIVITIES OF THE INSTITUTE

THE Institute was created to conduct, assist, and encourage research. It has left largely to other agencies the task of carrying into effect, on an extensive scale, discoveries and methods of immediate practical utility made and developed by its staff. But for the period of the belligerency of the United States the activities of the Institute were chiefly diverted to the service of our own nation and the other allied nations in their common struggle against the Central Powers.

Fortunately the Institute had made contributions looking toward the prevention and the curative treatment of disease which offered immediate application to the medical problems likely to arise in connection with the greatly enlarged personnel of the United States Army and Navy. For example, curative serums for epidemic meningitis and for one of the forms of pneumonia had been worked out here. Moreover, under the support of the Rockefeller Foundation, one of its members, Dr. Alexis Carrel, in conjunction with Dr. H. D. Dakin, had perfected at Compiegne, France, in the early period of the war, a method of treating infected surgical wounds, which had come to have wide applicability in practice. That important medical and allied problems would arise and call for investigation was also patent. The several laboratories of the Institute were so equipped in men and materials as to enable it to supplement the various research and otlJ.er laboratories at the command of the Government. All these resources were placed at the disposal of the Surgeon General and other governmental agencies, and were freely used by them during the war.

The war activities of the_ Institute may be divided into three classes: first, the establishment of teaching courses in the surgical treatment of wounds, in bacteriology, specific treatment of pneumonia, cardiography,. clinical chemistry, and the .technical side of bacteriology and histology; second, special research work in various aspects of bacteriology, immunology, biochemistry of antiseptics, chemotherapy, effects of poison gas, acetone formation, and the methods of preparing certain drugs of German origin employed as therapeutic agents; and third, the production of serum on a large scale for the treatment of meningitis, pneumonia, and dysentery.

TEACHING COURSES

1. The Surgical Treatment of Wounds.-The War Demonstration

   1. Hospital of the Institute was planned as a school in which to teach military surgeons the art of applying the Carrel-Dakin treatment. Moreover, it was considered desirable to erect in the United States a unit hospital which might serve in construction and equipment as a model for such structures to be established on the western front.

   2. The hospital was composed of double-walled and double-roofed wooden buildings of paneled and take-down construction. In order to make it useful not only for the practical aims of war instruction in surgery, but as a model of a small hospital unit which might be copied, as in fact it was repeatedly, the details of structure· and equipment were carefully attended to. Thus grouped conveniently about two central ward buildings (see frontispiece) each providing twenty-five beds, with necessary attendance and service facilities, were research and operating pavilions, kitchen, and mess-rooms for nurses and employees, laundry, laboratories, lecture rooms, executive_ offices, and storage, with separate dormitories for physicians, nurses, maids, and orderlies. These were all connected by covered corridors,_ the more essential of which were completely enclosed. Heat, light, and power were furnished from the Power House of the Institute. The wards were ventilated by ceiling louvres with fan sashes in the windows, which by a turn of the hand could be substituted by muslin screens. By the lowering of large panels in the sides of the wards these could be thrown open at will for air in hot weather, or as. 􀁮re escapes in an emergency.

   3. The patients in the hospital at first were drawn from the civilian community, and finally, as the wounded were returned from France to the United States, from the Army and Navy.

   4. The teaching staff of the hospital consisted of surgeons, bacteriologists, and chemists assigned by the Surgeon General of the Army for instruction purposes, and of French military surgeons commissioned by the French Ministry of War. The course of instruction for medical officers covered a period of two weeks. The number of army and navy officers and enlisted personnel of _various grades given instruction from the opening of the hospital in August, 1917, to its close in April, 1919, was about 1,100. Twenty􀁰seven nurses and eighty-three civilians also received instruction.

2. Courses in Bacteriology, Immunology, and Clinical Chemistry.

   1. The fact was early recognized by the Directors of the Institute that the Surgeon General would make heavy demands upon the personnel of the bacteriological and clinical chemical laboratories of the I country. It was thought probable that the existing highly trained personnel would prove inadequate to meet the needs. On the other hand, the number of partially trained bacteriologists and clinical chemists in the United States among practitioners of medicine who had ·entered the United States service as commissioned medical officers and others was obviously much larger. Hence it was proposed to establish teaching courses in bacteriology, serology, and medical chemistry for the latter class of students.

   2. The Surgeon Generals of the Army and Navy gladly availed themselves of this suggestion and nearly 600 medical officers and others attended the courses. The classes were conducted largely by members of the scientific staff of the Institute, many of whom were commissioned officers in the army and assigned to this duty.

3. Treatment of Pneumonia.

   1. One of the most serious menaces to the health of our troops has been pneumonia. The serum developed at the Hospital of the Institute for the treatment of so called Type I pneumonia having been demonstrated to be efficacious, it was imperative that military surgeons of the United States should be familiar with the best methods of its application. Hence arrangements were perfected by which medical officers were sent as internes to the Hospital of the Institute, remaining there from six weeks to several months, during which period they learned the modern technique of diagnosis and specific treatment of the disease. The officers so trained were later assigned to base hospitals in this country and abroad.

4. Cardiography.

   1. A small number of specially qualified medical officers were given instructions in modern methods of studying the heart by means of graphic methods: electrocardiograph, polygraph, and x-ray. This course was interrupted by the assignment of its head (Dr. Cohn) to overseas service.

   2. The Institute Hospital and the War Demonstration Hospital were officially designated as United States Army Auxiliary Hospital No. 1, and the laboratories as United States Army Auxiliary Laboratory No. 1.

SPECIAL RESEARCH WORK

IN ADDITION to new questions which were investigated as they arose in connection with therapeutic serum manufacture on a large scale, to meet the emergency of war-time requirements, a number of special problems were taken up.

The special chemotherapeutic studies in progress at the Institute on the treatment of syphilis, the requirements of the Army and Navy in this respect, and the possibility of devising a more effective and less costly drug than the German preparation salvarsan led to a promising series of laboratory and clinical studies not yet completed.

Among the other activities carried forward by members of the staff of the Institute were: important contributions to the methods of preparing a protective and curative serum for gaseous gangrene,- whose control became so serious a problem early in 'the war; the making of acetone in aircraft production, by a new process involving bacterial action; studies on the synthesis of drugs, leading to contributions on the manufacture of certain drugs having important uses in the medical service; studies on poison gases. When hostilities ceased, Dr. Carrel and his assistants brought to a close in France studies in hemorrhage and shock, well under way in his temporary hospital at St. Cloud to which they were driven by the German aggressions at Compiegne. A series of studies was undertaken on the occurrence and characters of hemolytic and other streptococci which had been found to be of _ serious import in certain pneumonias, complicating measles, and influenza, especially in military establishments.

Researches on pneumococcic and meningococcic vaccine and on meningitis carriers were carried on in the Institute in New York or in field studies in various military camps and cantonments.

SERUM PRODUCTION

In order to help meet the suddenly increased demand for the curative serums worked out at the Institute, a special stable for horses was quickly erected and a special and suitable laboratory staff assembled at the Department of Animal Pathology. In undertaking serum manufacture on a large scale, the officers of the Institute had another object in view; namely, the standardization of the product. This latter consideration became of high importance in establishing standards for the commercial produ􀁊ers. Three kinds of curative serums were manufactured in quantity; namely, antimeningococcic,, antipneumococcic Type I, and antidysenteric (polyvalent). Other serums intended for diagnostic purposes, such as Types I, II, III, and IV antimeningococcic, and Types II and III antipneumococcic serums were produced in smaller amounts. The quantities of the several kinds of serums distributed are as follows: 939.40 liters, or 46,970 bottles (20 cc.) of antimeningococcic serum; 344.79 liters, or 3,447 bottles (100 cc.) of antipneumococcic serum; 78 .36 liters, or 3,918 bottles (20 cc.) of antidysenteric serum. The amounts partially include the various diagnostic serums issued.

Reference should be made to the fact that before the United States entered the war, the In􀁌titute had resumed the preparation of antimeningococcic serum, in order to meet the requests from England, France, Belgium, Italy, and other countries.