{"id":91036,"date":"2021-10-17T18:37:53","date_gmt":"2021-10-17T22:37:53","guid":{"rendered":"http:\/\/stateofthenation.co\/?p=91036"},"modified":"2021-10-18T07:21:37","modified_gmt":"2021-10-18T11:21:37","slug":"the-great-influenza-pandemic-what-really-happened-in-1918","status":"publish","type":"post","link":"https:\/\/stateofthenation.co\/?p=91036","title":{"rendered":"The Great Influenza Pandemic: What Really Happened in 1918?<\/b>"},"content":{"rendered":"

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Page 53 to 89\u00a0<\/span><\/p>\n

Volume 1 \u2022 Issue 2 \u2022 2017\u00a0<\/span><\/h5>\n

Review Article\u00a0<\/b><\/p>\n

Pulmonary Research and Respiratory Care\u00a0<\/b><\/span><\/p>\n

ISSN: 2575-9779\u00a0\u00a0<\/b><\/h4>\n

The Great Influenza Pandemic: What Really Happened in 1918?\u00a0<\/b><\/span><\/h3>\n

Dr. Lawrence Broxmeyer, MD*\u00a0<\/b><\/p>\n

\u00a0<\/b>New York Institute of Medical Research, USA\u00a0\u00a0<\/span><\/i><\/p>\n

*Corresponding Author: <\/b>Dr. Lawrence Broxmeyer MD, New York Institute of Medical Research, New York, USA.\u00a0 <\/span>Received: <\/b>October 29, 2017; <\/span>Published: <\/b>November 07, 2017\u00a0<\/span><\/p>\n

Dr. Lawrence Broxmeyer, MD\u00a0<\/span><\/p>\n

Abstract\u00a0<\/b><\/p>\n

The word Influenza comes from mid\u201318th century Italian and literally means \u2018influence\u2019. Similar to how the coronavirus\u00a0 was once best known to cause the common cold, in 1918 Influenza was felt to be so benign a disease that it was not\u00a0 reportable in the United States. And it was not until 1933 that Influenza was \u201cdiscovered\u201d. So just what was causing the\u00a0 deaths in 1918? And why did the corona \u201cvirus\u201d turn so deadly so quickly? Before we can be certain of anything, these\u00a0 questions need to be answered. But to this point, they have not been answered. In the meantime, during both events\u00a0 there was a deadly pandemic of tuberculosis going on, a pandemic which even in 2020 kills one person every 21 seconds\u00a0 for a total of at least 1.5 to 1.8 million dead in 2018 alone. Yet Robert Koch, TB\u2019s discoverer, was repeatedly forced to call\u00a0 it a virus, to assuage other authorities of his time. And, as we shall soon see, the concept that only a new and virulent\u00a0 strain of a virus can be so infectious and kill so quickly is not only fallacious, but dangerous -and completely at odds with\u00a0 what used to be called the acute form of \u201cgalloping consumption\u201d [tuberculosis] which did and still can kill in a matter\u00a0 of hours, days or weeks.\u00a0<\/span><\/p>\n

\u201cViral\u201d influenza was informally first mentioned as being behind America\u2019s 1918 influenza pandemic not by a direct\u00a0 study of the disease in humans, but rather from studies on animal diseases. In 1918, J.S. Koen, a veterinarian, observed\u00a0 a disease killing thousands of pigs which he believed to be the same disease as the now infamous influenza Pandemic\u00a0 of 1918. He felt that it was a virus. It was solely his belief. Yet new evidence and older historical findings bring up\u00a0 the possibility that influenza doesn\u2019t originate from a virus \u2013despite the indefatigable efforts, up to the present, of flu\u00a0 enthusiasts to viralize the 1918-19 pandemic. (Burnet F, Clark E. 1942) (Morens DM, Taubenberger JK. 2009). As we\u00a0 shall see, such efforts on the part of viral devotees are nothing new, and began in force with scant evidence in Great\u00a0 Britain during the 1st World War, also known as the Great War.\u00a0<\/span><\/p>\n

Volume 1 Issue 2 November 2017\u00a0<\/span><\/p>\n

\u00a9 All Copy Rights are Reserved by Dr. Lawrence Broxmeyer, MD<\/span>.\u00a0<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and Re spiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>54\u00a0<\/span><\/p>\n

Introduction<\/b><\/p>\n

\u201cViruses should be considered as viruses because viruses are viruses.\u201d\u00a0<\/b>
\n<\/b><\/p>\n

\u2013 Pioneer virologist Andr\u00e9 Lwoff in 1957\u00a0\u00a0<\/span>
\n<\/span><\/p>\n

Figure 1: <\/i><\/b>Virologist\/Molecular Biologist Dr. Stefan Lanka, PhD, University of Koblenz, Germany.\u00a0<\/span><\/i><\/p>\n

Of course, the scientific merits and existence of the Influenza virus \u201ctype A\u201d (for avian) has been established beyond\u00a0 dispute \u2013or has it? Not according to virologist Stefan Lanka and others. World-renowned German virologist\/molecular\u00a0 biologist Lanka, an expert on the documentation of viruses, who studied at the University of Koblenz, and was first to\u00a0 discover a maritime virus [1-3], simply isn\u2019t buying it. This was an old story for Lanka, who knew that scientists were\u00a0 certain that a virus was behind Lyme disease, mycoplasma pneumonia, and Legionnaires\u2019 disease before their respective\u00a0 bacteria were found. With regard to the influenza virus itself, Dr. Lanka had this to say [4]:\u00a0\u00a0<\/span><\/p>\n

\u201cDr. Jeffery Taubenberger, from whom the allegation of a reconstruction of the 1918 pandemic virus originates, works for\u00a0 the US-American army and has worked for more than 10 years on producing, on the basis of samples from different human\u00a0 corpses, short pieces of gene substance by means of the biochemical multiplication technique PCR. Out of the multitude of\u00a0 produced pieces he has selected those which came closest to the model of the genetic substance of the idea of an influenza\u00a0 virus, and has published these. In no corpse however was a virus seen or isolated or was a piece of gene substance from such\u00a0 isolated. By means of the PCR technique there were produced out of nothing pieces of gene substance whose earlier existence\u00a0 in the corpse could not be demonstrated.\u201d\u00a0<\/span><\/i><\/p>\n

\u201cIf viruses had been present, then these could have been isolated, and out of them their gene substance could have been\u00a0 isolated too; there would have been no necessity for anyone to produce laboriously, by means of PCR technique – with clearly\u00a0 a [deceptive] intention – a patchwork quilt of a model of the genetic substance of the idea of an influenza virus. … In order to\u00a0 see through this one only has to be able to add up the published length pieces, in order to ascertain that the sum of the lengths\u00a0 of the individual pieces, which supposedly makes up the entire viral gene substance of the purported influenza virus, does not\u00a0 make up the length of the idea of the genome of the influenza virus model.\u201d\u00a0<\/span><\/i><\/p>\n

\u201cEven simpler it is to ask in what publication you can find the electron microscope photo of this supposedly reconstructed\u00a0 virus. There is no such publication.\u201d\u00a0\u00a0<\/span><\/i><\/p>\n

And when questioned regarding the electron pictograph of H1N1 that the CDC came up with on their website, virologist\u00a0 Lanka attested to the fact that the H1N1 picture was bogus. He said that he had <\/span>\u201cwritten the CDC many times as to who made\u00a0 the H1N1 photos and whether they were scientifically documented as to chemical characteristics and other properties.\u201d There\u00a0 was never any reply. He concluded \u201cIf CDC refuses to cite the source of the photos, they are fake. … In conclusion, without the\u00a0 isolation of the H1N1, there is no H1N1 infecting virus. Even more bizarre is the admission by the US Government\u2019s Food and\u00a0 Drug Administration … that the \u2018test\u2019 approved for premature release to test for H1N1 is not even a proven test. More to the\u00a0 point \u2015there is no forensic evidence in any of the deaths reported to date that has been presented that proves scientifically that\u00a0 any single death being attributed to H1N1 Swine Flu virus was indeed caused by such a virus.\u201d<\/span><\/i>[4]\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER\u00a0<\/b><\/p>\n

55\u00a0<\/span><\/p>\n

Early Pandemic History\u00a0<\/b><\/p>\n

At one time, there wasn\u2019t a major research or medical center in the US that did not feel that Pfeiffer\u2019s bacillus, originally\u00a0 called <\/span>Mycobacterium Influenzae <\/span><\/i>was not behind the Great Pandemic. Even in the UK, Pfeiffer\u2019s bacillus claim to being\u00a0 behind influenza was supported by Klein, one of the founders of British bacteriology. Pfeiffer\u2019s influenza bacillus was\u00a0 indeed considered, by most, to be the cause of influenza until at least 1933. Today, the current name for Pfeiffer\u2019s bacillus is\u00a0 <\/span>Haemophilus influenzae<\/span><\/i>. Yet the National Center for Biotechnology Information of the NIH (<\/span>National Institutes of Health<\/span><\/i>),\u00a0 still lists its older designation \u201c<\/span>Mycobacterium influenzae<\/span><\/i>\u201d [5,6]. Pfeiffer\u2019s Influenza bacillus was therefore surely consid\u00a0<\/span><\/p>\n

ered a mycobacterium, just as tuberculosis is today. Pfeiffer\u2019s stained with the same \u201cacid-fast\u201d stain used to stain TB and\u00a0 many of its fungal-like and bacillary forms were quite similar to <\/span>Mycobacterium tuberculosis<\/span><\/i>. American physician Herbert\u00a0 Wade and colleague Christobal Manalang proved that Pfeiffer\u2019s had filter-passing, viral-like fungal forms, validating Pfei ffer\u2019s bacillus original name: <\/span>Mycobacterium Influenzae<\/span><\/i>. The \u201cmyco\u201d in the word mycobacterium means fungal.\u00a0<\/span><\/p>\n

Before the Great War, Harvard bacteriologist and physician S.B. Wolbach summarized filterable viruses this way:\u00a0 \u201c<\/span>By filterable viruses, we mean microorganisms which will pass through filters, the pores of which are too small to give\u00a0 passage to ordinary bacteria.<\/span><\/i>\u201d [7]\u00a0<\/span><\/p>\n

If Wolbach\u2019s choice of the words \u201cordinary bacteria\u201d seemed to differentiate these from forms of bacteria that could pass\u00a0 through a filter \u2013that was precisely his intention. Wolbach\u2019s review found four \u2018viruses\u2019 which cultivated out bacteria. He\u00a0 also mentioned that historically, the first filterable \u201cvirus\u201d discovered by Nocard in 1899, passed through a Chamberland\u00a0 filter but was subsequently cultivated back into bacterial forms, among them, one of a coccoid shape. Unfortunately, such\u00a0 bacterial forms have repeatedly muddied virologist\u2019s quests to find filter-passing \u201cviruses\u201d. Among them, said Wolbach,\u00a0 were those who sought to prove a filter passing virus for dog distemper in a field where most credible evidence pointed\u00a0 towards distemper in dogs as being a bacillary disease. Surely for Torrey and Rank it seemed \u201c<\/span>certain that if every case [<\/span><\/i>of\u00a0 dog distemper<\/span>] had been autopsied during the first week of symptoms, this bacillus might have been readily recovered from\u00a0 all<\/span><\/i>\u201d [8]. Indeed for Torrey, Carr\u00e9\u2019s theory of a filterable virus as essential to canine distemper was not confirmable, not only\u00a0 in own studies, but those of Kregenow [9], and other workers.\u00a0<\/span><\/p>\n

England\u2019s Big Push to Viralize Influenza\u00a0\u00a0<\/b><\/p>\n

But such information never stopped Walter Fletcher, head of <\/span>Britain\u2019s Medical Research Council <\/span><\/i>(MRC) from plotting,\u00a0 soon after the Great War to \u201cprove\u201d that the Great Pandemic of 1918 was caused by a filter-passing \u201cvirus\u201d. And Fletcher\u00a0 had a specific plan. He would make canine distemper in dogs, which was similar to human influenza, the experimental\u00a0 model for human influenza itself. Find a \u2018virus\u2019 and vaccine for canine distemper, predicted Fletcher, and that study would\u00a0 lead to gaining general acceptance that a virus was behind the Great Pandemic. Nor would Fletcher rest until his scheme\u00a0 was realized.\u00a0\u00a0<\/span><\/p>\n

So soon, Walter Morley Fletcher, head of the UK\u2019s MRC, which was originally founded by and for the <\/span>Royal Commission\u00a0 on Tuberculosis<\/span><\/i>, held a top secret meeting with British pathologists at England\u2019s War Department with the sole intent\u00a0 of scheming to show that the 1918 \u201cinfluenza\u201d pandemic was the work of a virus. This resulted in sending two research\u00a0 teams to France late in 1918, despite the fact that Fletcher openly admitted that any work towards proving an influenza\u00a0 virus would likely be hindered by \u201cthe difficulty of proceeding by sound experimental methods\u201d. And with no specific\u00a0 laboratory test to prove his hypothesized influenza virus, nor the means to show it, Fletcher was not far from wrong. His\u00a0 arsenal: mere symptoms and serologic tests which indirectly said, yes, this pathogen exists, it passes through a filter and it\u00a0 reacts positively in serologic assays. But unfortunately all of this certainly still did not mean it was a \u201cvirus\u201d.\u00a0\u00a0<\/span><\/p>\n

Nevertheless, Fletcher and several other zealots fully intended to pull this viral charade off, and had the influence,\u00a0 the money, the research facilities, the publicity and the publication resources to do just that, including an ongoing\u00a0 collaboration with the <\/span>Rockefeller Institute <\/span><\/i>in the US, which threw money in the form of grants towards Fletcher\u2019s project.\u00a0\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>56\u00a0<\/span><\/p>\n

And so it was that plans were carefully laid, early on, to viralize the legacy of the Great Pandemic. By the summer of 1922,\u00a0 Fletcher had already recruited virologist Patrick Playfair Laidlaw to develop a project to prove that canine distemper and\u00a0 eventually influenza in man were caused by filter-passing \u201cviral organisms\u201d. And for the better part of a decade, Laidlaw\u00a0 would work with veterinarian G.W. Dunkin on canine distemper. While it was Walter Morley Fletcher\u2019s feeling that if they\u00a0 isolated the infectious agent behind such distemper and eventually created a vaccine for it, there would be no doubt about\u00a0 their historic \u2018viral\u2019 study, in fact the filter-passing \u201cvirus\u201d that Laidlaw claimed that he had isolated, left behind many\u00a0 doubts. Yet just the fact that Laidlaw had successfully created a vaccine for dogs to prevent the deadly canine distemper\u00a0 made him somewhat of a national hero. And Walter Fletcher was not about to lose the momentum gained in this dog arena,\u00a0 making sure that Laidlaw, along with MRC virologists Smith and Andrewes, quickly pressed the case that a \u201cvirus\u201d was also\u00a0 behind influenza and the Pandemic of 1918. So less than a year after Laidlaw\u2019s group started investing their efforts into\u00a0 finding a human influenza virus, they threw together a <\/span>Lancet <\/span><\/i>paper published on July 8, 1933. What was Walter Fletcher\u2019s\u00a0 rush? It was simply that things in general where not going that well for virology in general.<\/span><\/p>\n

Virology as a Science Threatened\u00a0<\/b><\/p>\n

In the words of respected historian Ton van Helvoort, during the 1930s and 1940s, the concept of Laidlaw, Smith and\u00a0 Andrewes\u2019s \u201cfilterable influenza virus\u201d was subjected to such criticism that the very foundations of virology as a science\u00a0 were threatened [10]. And those threats came from many fronts.\u00a0<\/span><\/p>\n

Laidlaw\u2019s entire basis for calling dog distemper and eventually human influenza \u2018filter-passing viruses\u2019 was based on\u00a0 three roundly disputable qualities: their filterability, their resistance to culturing on ordinary bacterial culture media and\u00a0 their dependence on living tissue \u2013meaning that they could not grow outside of the animal or human body [11]. Each of\u00a0 these criteria where under constant assault, the latest of which came from Northwestern University bacteriologist Arthur\u00a0 Isaac Kendall [12]. Kendall, similar to Laidlaw in the UK had been picking up favorable press and peer-reviewed status in\u00a0 the United States \u2013but in quite the opposite direction.\u00a0<\/span><\/p>\n

Kendall knew that Laidlaw, using these three questionable criteria, was attempting to dismantle the impressive and\u00a0 plentiful evidence that showed that dog distemper was from a bacterial bacillus. Yet oddly, rather than come out and call it\u00a0 a \u2018virus\u2019, Laidlaw and Dunkin opted for the description \u201cultra-microscopic organism\u201d [11], implying a small microbe.\u00a0<\/span><\/p>\n

And so, by 1932, Dr. Arthur Kendall, director of Medical Research at Northwestern, and no fan of \u201cso-called\u201d viral\u00a0 influenza, spoke before the <\/span>Association of American Physicians <\/span><\/i>at Johns Hopkins University. Basically Kendall reminded\u00a0 virologists that his \u201cK Medium\u201d, which he used to grow \u201cviruses\u201d, contained nothing living, yet produced filterable\u00a0 bacterial forms. William Henry Welch, the dean of American Medicine, and a survivor of the Great Pandemic, rose to say\u00a0 that: \u201cKendall\u2019s observations marks a distinct advance in medicine.\u201d [13] The reasons for Welch\u2019s support was obvious.\u00a0 Kendall had executed a blistering well-written paper published in <\/span>Science <\/span><\/i>entitled <\/span>Observations upon the filterability of\u00a0 bacteria, including a filterable <\/span><\/i>[bacterial] <\/span>organism obtained from cases of influenza<\/span><\/i>.\u00a0\u00a0<\/span><\/p>\n

Therefore, in so far as Walter Morley Fletcher was concerned, one year to solidify an influenza viral study was more\u00a0 than enough. Laidlaw and team now had to publish and do so immediately: and the <\/span>Lancet <\/span><\/i>article \u201c<\/span>A virus obtained from\u00a0 influenza patients<\/span><\/i>\u201d was the result [14]. Yet, once again the best that Laidlaw and team could offer was that \u201c<\/span>The evidence\u00a0 strongly suggests that there is a viral element in epidemic influenza, and we believe that the virus is of great importance in\u00a0 the aetiology of the human disease.<\/span><\/i>\u201d However to the news hungry editors at the Lancet, heavily under the influence of the\u00a0 <\/span>Royal Medical Council<\/span><\/i>, Laidlaws carefully couched word \u201csuggests\u201d did not go quite far enough. Rather Lancet announced\u00a0 that Laidlaw\u2019s study \u201coffered almost conclusive evidence\u2026.\u201d [that a filter-passing <\/span>virus <\/span><\/i>was behind 1918] \u2013which of course\u00a0 it did not.\u00a0\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>57\u00a0<\/span><\/p>\n

Figure 2: <\/i><\/b>A poster circa 1918, this one from the Brooklyn Tuberculosis Committee. \u2018Consumption\u2019 is the older name\u00a0 for tuberculosis\u00a0<\/span><\/i><\/p>\n

Despite all of this, Pfeiffer\u2019s influenza bacillus, a bacterium, was heavily isolated at one time or another in victims of the\u00a0 1918-19 pandemic by practically all major research centers in the United States.\u00a0\u00a0<\/span><\/p>\n

A \u2018Virus\u2019 by Any Other Name\u00a0<\/b><\/p>\n

Although the term \u2018virus\u2019 has existed since 1898, the infectious agent it was attempting to describe was so unclear and\u00a0 mysterious that for many decades scientists considered it purely theoretical. Certainly, even by 1917, \u201cinfluenza\u201d was still not\u00a0 felt o be serious enough to be a reportable disease, and no doctor had to report it to state or local health officials. Most cases\u00a0 were elf-limiting and gone in 10 days. Yet the great \u201cinfluenza\u201d pandemic that swept the world in 1918\u201319 may have been the\u00a0 most irulent outbreak in history, at least in terms of the swiftness of its devastation. According to some estimates, it killed\u00a0 more than 50 million with estimates as high as 100 million persons around the world, including some 550,000 in the United\u00a0 States\u2014 and it did so swiftly, all within two years.\u00a0<\/span><\/p>\n

Figure 3: <\/i><\/b>Influenza Pandemic 1918. The dead and the dying lined up\u00a0<\/span><\/i><\/p>\n

By 2000, Dr Andrew Noymer and Michel Garenne, demographers from the University of California, Berkeley, thought\u00a0 they knew just why this discrepancy existed, reporting convincing statistics showing that undetected tuberculosis (TB)\u00a0 may have been the real killer in the 1918 flu epidemic. Aware of more recent attempts to isolate the \u201cinfluenza virus\u201d\u00a0 from human cadavers and their specimens in the US, Noymer and Garenne concluded: \u201c<\/span>Frustratingly, these findings have\u00a0 not answered the question why the 1918 virus was so virulent, nor do they offer an explanation for the unusual age profile of\u00a0 deaths<\/span><\/i>.\u201d[16] Pearl from Johns Hopkin\u2019s , who lived through the Great Pandemic, in 1919 concluded much the same, showing\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>58\u00a0<\/span><\/p>\n

that there was a definite relationship between the explosiveness and fatality of that killer pandemic in 40 American cities\u00a0 and the existing death rates of pulmonary tuberculosis and related disease [17].\u00a0\u00a0<\/span><\/p>\n

In Nishiura\u2019s study not only was TB shown to be associated with influenza death, but there was no influenza death\u00a0 among controls without tuberculosis. Nishiura concluded: \u201c<\/span>Should a highly fatal influenza pandemic occur in the future,\u00a0 testing the role of TB in characterizing the risk of death would be extremely useful in minimizing the disaster\u2026<\/span><\/i>\u201d [18].\u00a0<\/span><\/p>\n

Figure 4: <\/i><\/b>Another poster, circa 1918. New York\u2019s Shuyler Center had just loaned their tuberculosis staff to the\u00a0 American Red Cross to help organize and direct a three months emergency campaign against influenza in New York,\u00a0 New Jersey, and Connecticut at a time when they could least afford to do so. Five new tuberculosis hospitals and eight\u00a0 new TB dispensaries were scheduled to open in 1918 to meet the upsurge of that disease.\u00a0<\/span><\/i><\/p>\n

More recently, in 1999, Fredj Tekaia, of the <\/span>Institute Pasteur<\/span><\/i>, Paris, and colleagues, looking for \u201coverall gene similarities\u00a0 as signatures of common ancestry\u201d, found similar genetic profiles and sequencing for Pfeiffer\u2019s bacillus (<\/span>Mycobacterium\u00a0 influenzae<\/span><\/i>) and <\/span>Mycobacterium tuberculosis<\/span><\/i>, lumping them together in the same \u201cwell-defined group\u201d. [19] Tekaia\u2019s\u00a0 diagrammatic genomic tree shows the two organisms directly next to one another. [See figure below] This reopened the\u00a0 historical argument as to whether Pfeiffer\u2019s bacillus and tuberculosis were related.\u00a0<\/span><\/p>\n

Figure 5: <\/i><\/b>The genomic tree of Fredj Tekaia, of the Institut Pasteur, Paris,1999. Notice how close Haemophilus influenzae\u00a0 (Pfeiffer\u2019s bacillus) and M. tuberculosis are placed \u2015 directly next to one another.<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>59\u00a0<\/span><\/p>\n

In 1933, the very year that British MRC virologists Smith, Andrewes and Laidlaw claimed that they had discovered\u00a0 the virus behind human influenza \u201cvirus\u201d, Stobie, in the <\/span>British Medical Journal<\/span><\/i>, still was objecting that rather than being a\u00a0 virus, the real nature of \u201cinfluenza\u201d could well be a form of <\/span>Mycobacterium tuberculosis <\/span><\/i>[20].\u00a0\u00a0<\/span><\/p>\n

Stobie\u2019s view simply reflected the active, vigorous, yet historically suppressed debate that had been raging in medical\u00a0 journals for decades. He mentions cases of tuberculosis complicated by influenza which together exhibited \u201c<\/span>a sinister type\u00a0 of disease which rarely responded to treatment<\/span><\/i>.\u201d Enter \u201cgalloping consumption\u201d, the most devastating form of tuberculosis,\u00a0 then called \u201cconsumption\u201d \u2013 a galloping tuberculosis that could kill in hours to days, the mere memory of which brought\u00a0 terror to the faces of those who had witnessed it.\u00a0\u00a0<\/span><\/p>\n

The Reichsgesundheitsamt, Berlin, March 1882\u00a0<\/b><\/p>\n

Although it has always perplexed doctors, scientists and historians alike as to why so many microbes were involved\u00a0 during the deadly 1918 pandemic, the explanation was carefully laid out decades before by German physician\/microbiologist\u00a0 Robert Koch, the discoverer of tuberculosis. From the onset, Koch concluded [21] that other microorganisms secondarily\u00a0 infected and thus shared in the destructive work of the tubercle bacilli. Gaffky, Pansini, Cornet, Spengler, Schabad, Ortner\u00a0 and Flick, among others, verified this [22]. Various organisms, all of which reappeared to confuse scientists in 1918, were\u00a0 assigned a share in the clinical picture of tuberculosis \u2013among them the streptococcus, staphylococcus, pneumococcus\u00a0 and even the variably acid-fast influenza bacillus itself. The pyogenic, pus-forming cocci were more generally suspected\u00a0 than other bacteria of complicating tuberculosis. In the <\/span>British Medical Journal <\/span><\/i>of 28 July 1900, the following editorial\u00a0 appeared, dealing with the role of streptococci in tuberculosis: \u201c<\/span>It is a remarkable fact that\u2026the bulk of the disturbing and\u00a0 dangerous features of tuberculosis are not due to the tubercle bacillus, but to streptococci and other pyogenic organisms<\/span><\/i>.\u201d The\u00a0 pneumococci, Staphylococci and methicillin-resistant staph (MRSA) are other pyogenic pathogens that subsequently have\u00a0 been documented.\u00a0<\/span><\/p>\n

Pandemic scientist Oswald Avery of Rockefeller research explained the principle behind this phenomena six years\u00a0 before the death and destruction now known as the Great Pandemic. Secondary infection by pus forming bacteria such as\u00a0 streptococcus and pneumococcus are \u201c<\/span>particularly common in those diseases <\/span><\/i>[such as pulmonary tuberculosis] <\/span>in which\u00a0 tissue destruction and ulceration have already occurred as a result of primary infection\u201d This was because with tuberculosis,\u00a0 \u201cthe initial focus offers a ready portal of entry and a suitable nidus for secondary invaders, since local resistance is already\u00a0 diminished and the natural protective forces of the body are exhausted by the original <\/span><\/i>[tubercular] <\/span>infection<\/span><\/i>.\u201d[23] Thus did\u00a0 microorganisms normally part of the regular flora of the mouth and mucous secretions turn deadly.\u00a0<\/span><\/p>\n

The <\/span>British Medical Journal\u2019s <\/span><\/i>editorial dealing with the destructive and predominant role of streptococci in tuberculosis\u00a0 was further confirmed when Pandemic physician Edward Rosenow reported his findings that green-producing\u00a0 <\/span>Streptococcocus viridians <\/span><\/i>were more constantly found and more destructive than any other organism associated with\u00a0 influenza [24].\u00a0\u00a0<\/span><\/p>\n

Figure 6: <\/i><\/b>Researcher E.C. Rosenow, MD<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>60\u00a0<\/span><\/p>\n

Yet few were suggesting that Rosenow\u2019s green streptococci, which often normally inhabit buccal secretions, were\u00a0 behind the origin of the Pandemic of 1918.\u00a0<\/span><\/p>\n

British pathologist William Crofton chafed at the ridiculous notion that in influenza, Pfeiffer\u2019s bacillus and only Pfeiffer\u2019s\u00a0 bacillus alone should be found in pure cultures [25]. He asked whether the typhoid bacillus was ever found in pure culture.\u00a0\u00a0<\/span><\/p>\n

Obuchow Hospital, St Petersburg, Russia, 1890\u00a0\u00a0<\/b><\/p>\n

\u201cIn relation to the question of the effect of influenza upon tuberculosis, it should be pointed out that in many cases in which\u00a0 pulmonary tuberculosis has been thought to have followed an attack of influenza, it is altogether probable that the supposed\u00a0 attack of influenza was, in reality, a manifestation of an existing tuberculous infection; for tuberculoprotein, whether absorbed\u00a0 from spreading lesion or injected into the body, can cause constitutional symptoms (fever, malaise, headache, joint pains,\u00a0 anorexia, prostration) quite like those of influenza. The writer has seen attacks closely simulating influenza occur in healthy,\u00a0 tuberculin-positive laboratory workers as a result of the accidental inhalation of the vapor of boiling tuberculin.\u201d <\/span><\/i>[72]\u00a0<\/span><\/p>\n

\u2015Arnold Rich, MD, Head of Pathology, Johns Hopkins, 1946\u00a0<\/span><\/p>\n

In 1890, a fierce \u201cinfluenza\u201d struck worldwide, killing approximately a million people. Occurring at the end of the 19th\u00a0 century, this second most severe influenza ever to hit the world occurred at a time when there was fear that tuberculosis would destroy the civilization of Western Europe \u2013as it steadily moved east to ravage Eastern Europe just in time for the\u00a0 \u201cflu\u201d pandemic of 1889-1890.\u00a0<\/span><\/p>\n

Of all the forms of \u201cinfluenza\u201d known in 1890, none was more dreaded nor struck more terror into the hearts of victims\u00a0 and their families than that described by Wiltschur as \u201cgalloping consumption\u201d [26]. An attending physician at the Obuchow\u00a0 Hospital, St. Petersburg, Wiltschur, astounded by the number of TB patients coming down with influenza, documented\u00a0 what happened when influenza punctuated previous dormant or active cases of tuberculosis: \u201c<\/span>The <\/span><\/i>[influenza] <\/span>patients were,\u00a0 for the most part, still well nourished<\/span><\/i>\u201d, chronicled Wiltschur in Obuchow. This mirrored the flu pandemic of 1918, where\u00a0 healthy young soldiers were suddenly decimated by disease. Wiltschur continued: \u201c<\/span>Cyanosis of the face and extremities\u00a0 was a frequent occurrence<\/span><\/i>.\u201d Patients exhibited severe difficulty in breathing (dyspnea), an extremely high temperature not\u00a0 characteristic of the flu, pulmonary hemorrhages and a rapid progression of lung disease, \u201c<\/span>with death occurring in many\u00a0 instances unexpectedly and suddenly.<\/span><\/i>\u201d Wiltschur was witnessing the acute blood-borne (miliary) form of virulent galloping\u00a0 tuberculosis, a disease which according to McCall Anderson [27], then Professor of Clinical Medicine at the University of\u00a0 Glascow, could kill within a few days even without influenza. It began with high fever and pneumonia in one or both lungs.\u00a0 And even when this was not the case, acute \u201cgalloping\u201d tuberculosis was usually rapidly fatal. To San Francisco pathologist\u00a0 Albert Abrams, a physician originally from Heidelberg, in galloping consumption \u201c<\/span>usually the entire lung becomes affected\u00a0 and the condition is not unlike that of an acute pneumonia.<\/span><\/i>\u201d [28] Why these findings, including the well-known high fatality\u00a0 of \u201cgalloping consumption\u201d with its high fever, profuse hemorrhaging, brownish spots or splotches on the face, strawberry\u00a0 tongue and typhoid-like symptoms, all documented so clearly in and after the pandemic of 1890, were ignored by the\u00a0 historians, scientists and practitioners of 1918 and beyond, defies comprehension.\u00a0<\/span><\/p>\n

Historian\/researcher Ren\u00e9 Dubos, of the <\/span>Rockefeller Institute for Medical Research<\/span><\/i>, assured his readers that \u201cgalloping\u00a0 consumption\u201d was not an isolated, but a frequent diagnosis in the 19th century [29]. Despite persistent myths to the\u00a0 contrary, in the early phase of any new TB epidemic from a new and virulent strain, tuberculosis manifests itself as an acute\u00a0 disease and only much later as the chronic pulmonary tuberculosis that we know in today\u2019s Western world. An example of\u00a0 this was found in the high mortality during the 1918 \u201cinfluenza\u201d pandemic, when African Americans were brought to fight\u00a0 in France during World War I, large numbers of them dying from the accelerated tubercular \u201cgalloping consumption\u201d of\u00a0 yesteryear. But was it only this specific group that was affected circa 1918? Thomas Mays\u2019 study of galloping consumptive\u00a0 cases in America were Caucasian. Mays [30], an infectious disease specialist at Philadelphia polyclinic, during the Pandemic<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>61\u00a0<\/span><\/p>\n

of 1890, spoke of such \u201cacute\u201d tuberculosis formerly called \u201cgalloping consumption\u201d which not only \u201cinvariably\u201d resulted\u00a0 in death but depending upon its intensity, could kill young people in their prime within two or three days \u2013although the\u00a0 majority of cases lived 11 days to five weeks, and could even endure for three or four months.\u00a0<\/span><\/p>\n

Just listening to and percussing the chest, which the US Army\u2019s medical department would heavily rely upon in\u00a0 assessing new recruits during the upcoming Great War, would not be satisfactory, said Mays. The sounds heard simply\u00a0 presented as a bronchitis. Furthermore, in an acute tubercular involvement, pleurisy, an inflammation of the lining of the\u00a0 lung, was frequent and extensive. To Thomas Mays, it was the degree of fever that was a reliable index of the degree and\u00a0 intensity of galloping tubercular consumption, similar to the extremely high fevers often recorded during both of the large\u00a0 \u2018flu\u201d pandemics. Such sprinting tuberculosis was usually blood borne (or miliary), seeding the blood, and could cause the\u00a0 symptoms such as a splitting headache \u2013if it had time to reach the serous coverings of the brain before death. Also nose\u00a0 bleeds (epistaxis) could occur, and sometimes hemoptysis (the spitting up of blood tinged sputum), as the ceaseless cough\u00a0 took its toll and marked difficulty of breathing arose. Indeed acute tuberculosis could have many hemorrhagic\u00a0 manifestations. And cyanosis, the blue to dark blue discoloration of the skin and mucous membranes was never far\u00a0 away. All told, Mays\u2019 description of the signs and symptoms of \u201cgalloping\u201d tubercular consumption remain a version in\u00a0 miniature of the 1918 Great Pandemic \u2013a disease both acute and fatal, with signs and symptoms so non-specific that a\u00a0 proper diagnosis was near impossible to make.\u00a0<\/span><\/p>\n

College of Medicine and Surgery, Philippines, 1919<\/b><\/p>\n

Figure 7: <\/i><\/b>Influenza. University of the Philippines pre WW II, where\u00a0\u00a0<\/span><\/i><\/p>\n

Wade and Manalang conducted their landmark study\u00a0<\/span><\/i><\/p>\n

Pivotal to an understanding of how and why what was once called <\/span>Mycobacterium Influenzae <\/span><\/i>or Pfeiffer\u2019s bacillus was\u00a0 both mistaken for a filterable virus, misclassified, and at the same time often elusive to bacteriologists is found in Wade and\u00a0 Manalang\u2019s work, which revealed mycobacterial-like fungal forms in Pfeiffer\u2019s bacillus.\u00a0\u00a0<\/span><\/p>\n

In the beginning of 1920, an important study [31] appeared in The Rockefeller Institute\u2019s <\/span>Journal of Experimental\u00a0 Medicine<\/span><\/i>. Physician Herbert Windsor Wade, an American investigator working out of the Department of Pathology and\u00a0 Bacteriology at the <\/span>University of the Philippines College of Medicine and Surgery<\/span><\/i>, doubted that a filter-passing virus had\u00a0 anything to do with the then current influenza pandemic. And Wade, with Filipino national Dr. Christobal Manalang, proved\u00a0 this in 1919 in their university laboratory.\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>62\u00a0<\/span><\/p>\n

Figure 8: <\/i><\/b>Dr. Richard Pfeiffer\u00a0<\/span><\/i><\/p>\n

When history\u2019s deadliest influenza pandemic began, researchers around the world began to search for Pfeiffer\u2019s\u00a0 bacillus in patients, hoping to develop antisera and vaccines that would protect against infection. In many patients, but not\u00a0 all, Pfeiffer\u2019s was found. Failures to isolate Pfeiffer\u2019s bacillus, at one time also known as <\/span>Bacillus influenzae <\/span><\/i>(now known\u00a0 as <\/span>Haemophilus influenzae<\/span><\/i>) were largely chalked up to inadequate technique, as this bacteria was notoriously difficult to\u00a0 culture. Wade and Manalang\u2019s study not only verified such difficulty in isolating Pfeiffer\u2019s bacillary forms, but exposed\u00a0 fungal forms, some of them filterable, and that were not being counted as pathogenic, even by Pfeiffer himself. Pfeiffer\u00a0 would eventually correct his thoughts: true Pfeiffer\u2019s influenza bacillus was not just a bacillus. It also had pathogenic\u00a0 mycobacterial fungus-like forms. But such an admission came only later.\u00a0<\/span><\/p>\n

Yet through it all, Pfeiffer still insisted that his organism \u201c<\/span>had the best claim to serious consideration as the primary\u00a0 etiologic agent [cause] for influenza, and that its only competition was a \u201cvague, unidentified filterable virus<\/span><\/i>\u201d. [32] Had\u00a0 Pfeiffer studied and understood Wade and Manalang\u2019s laboratory evidence, his comment would have been quite different.\u00a0 Pfeiffer\u2019s bacillus itself could have easily been mistaken for that \u201cunidentified filterable influenza virus\u201d.\u00a0<\/span><\/p>\n

Figure 9: <\/i><\/b>Wade and Manalang. Growth from Pfeiffer\u2019s bacilli. Fungal branching was witnessed in all 3 strains of\u00a0 rigorously purified Pfeiffer\u2019s bacilli used in their experiment. Clusters of mycobacterial-like fungal growth are\u00a0 shown in their Figs. 19 thru 21. The long, more or less frequently branching filaments and the numbers of\u00a0 laterally formed fungal conidial bodies (spores) are particularly striking.<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>63\u00a0<\/span><\/p>\n

Wade remained a voice of scientific reason throughout the 1918 influenza pandemic, during which he personally\u00a0 experienced a scourge in which, depending upon which province he visited, from 40 to 95 per cent of Filipinos had\u00a0 contracted the disease. In a country ravaged by TB, at least 70,000\u201390,000 Filipinos had already died, as had 20 million\u00a0 in TB-ridden India. Wade knew what it was like to come into a Philippine village where there were not enough living\u00a0 to bury the dead. Also, being far from the United States, he was not subject to the relentless censorship of the Wilson\u00a0 administration, both against civilians and scientists of the US Army Medical Corps itself. If he saw tubercular mycobacterial\u00a0 forms similar to those of TB in Pfeiffer\u2019s influenza bacillus, he could and would report them without fear of being accused of\u00a0 fueling the flames of hysteria. And in documenting such viral appearing, tuberculosis-like fungal forms in Pfeiffer\u2019s bacillus,\u00a0 that is exactly what Wade did.\u00a0<\/span><\/p>\n

Wade\u2019s media grew out fungal forms and its fungal spores went through a filter. They were therefore \u201cfilterable\u201d, but\u00a0 they were not \u201cviruses\u201d.\u00a0\u00a0<\/span><\/p>\n

In the words of UK microbiologist Milton Wainwright, Wade and Manalang had now committed \u201cthe ultimate\u00a0 pleomorphist heresy\u201d[33], documenting that a bacterium or mycobacterium could have more than one form in its life cycle.\u00a0<\/span><\/p>\n

Back in the UK\u00a0\u00a0<\/b><\/p>\n

Meanwhile in the UK, a special panel on the \u2018<\/span>Bacteriology of Influenza<\/span><\/i>\u2019, was chaired by pathologist Major W. B. Leishman,\u00a0 MB, RAMC. Walter Morley Fletcher had worked closely with William Boog Leishman, who became an Advisor on Pathology\u00a0 to Britain\u2019s War Office. Leishman of all people realized the implication of Wade\u2019s study in the Philippines. In 1902 Leishman\u00a0 had published a review on microbes similar to Wade\u2019s acid-fast TB-like organism [34]. And when William Boog Leishman\u00a0 edited the Medical Services Pathology for the <\/span>History of the Great War <\/span><\/i>based on official documents [35], the work of Majors\u00a0 Rhea and Malloch in that book stuck with him in which Pfeiffer\u2019s was \u201c<\/span>found to be by far and away the predominating\u00a0 organism of the sputum<\/span><\/i>\u201d, and how the cut surfaces of autopsied pandemic pneumonias resembled \u201c<\/span>the cut surface of\u00a0 the lung in many cases to what is seen in acute miliary tuberculosis<\/span><\/i>.\u201d Leishman wondered how many in the meeting had\u00a0 considered the acid-fast properties of Pfeiffer\u2019s cell-wall-deficient forms during the pandemic: how they stained like TB,\u00a0 and how they looked like viruses.\u00a0<\/span><\/p>\n

Figure 10: <\/i><\/b>Dr. Simon Flexner, then head of the Rockefeller Institute of Research\u00a0<\/span><\/i><\/p>\n

Meanwhile, in the US, it was no accident that Wade and Manalang\u2019s paper was published by <\/span>The Rockefeller Institute<\/span><\/i>.\u00a0 Simon Flexner, then director at the Institute, once followed similar acid-fast fungal forms, associating them with\u00a0 tuberculosis. And he found this similar correlation with the influenza bacillus fascinating. Ironically, Flexner called his\u00a0 filterable fungal forms inside TB \u201cpseudotuberculosis\u201d, just as Pfeiffer had labeled them \u201cpseudoinfluenza\u201d [36].\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>64\u00a0<\/span><\/p>\n

Simon Flexner was a key figure in the 1918 pandemic, heavily influencing Rockefeller research. He also had full status\u00a0 in the close-knit band of major US research operatives during the Pandemic. Why had he not taken the cue, following his\u00a0 own editorial instincts and run with Wade\u2019s study further? Wade had found that Pfeiffer\u2019s mycobacterial fungal forms could\u00a0 appear as filterable viruses. Even a 1918 <\/span>British Medical Journal <\/span><\/i>editorial (1918:2:665) had supported this as a key factor\u00a0 in the mystery of the Great Pandemic.\u00a0<\/span><\/p>\n

Actually, one researcher had carefully listened to Wade. But since that researcher wasn\u2019t a member of the US scientific\u00a0 hierarchy, he would be ignored. His name: Dr. Victor Conrad von Unruh.\u00a0<\/span><\/p>\n

Medical Reserve Corps, NYC, 1917\u00a0<\/b><\/p>\n

Physician\/researcher Victor Conrad von Unruh was born in 1868 in Dolowitz, Germany, at a time when German\u00a0 medical research and science were unrivalled. He immigrated to the US, and by 1917 he had received the commission\u00a0 of Captain in the Medical Reserve Corps, New York City. The pandemic of 1918 was about to hit hard. Von Unruh\u2019s \u201c<\/span>A\u00a0 Comparative Study of the Acid Fast Bacilli<\/span><\/i>\u201d had appeared in 1916, two years prior to the killing fields of 1918 [37].\u00a0\u00a0<\/span><\/p>\n

Because Pfeiffer\u2019s bacillus could stain acid-fast, von Unruh, like others, had been evaluating what medical texts such\u00a0 as Stengel\u2019s [38] referred to as <\/span>Mycobacterium influenzae<\/span><\/i>, also known as <\/span>Bacillus influenzae<\/span><\/i>. There, the entire influenza\u00a0 group was thought to be caused by this acid-fast mycobacterial bacillus, which was similar to the tubercle bacillus. Both\u00a0 microbes had fowl, swine and human forms. Von Unruh never saw the need to look for a \u201cfilterable virus\u201d or \u201cinfluenza\u201d in\u00a0 the thousands of hogs that died abruptly with flu-like symptoms just before the pandemic, as did virologist Richard Shope.\u00a0 Why should he?\u00a0\u00a0<\/span><\/p>\n

Figure 11: <\/i><\/b>Virologist Dr. Richard Shope\u00a0<\/span><\/i><\/p>\n

Shope, the American virologist credited with the first isolation of the influenza \u201cvirus\u201d, seemed oblivious to the fact\u00a0 that more than 60 per cent of hogs circa 1918 were tubercular from fowl TB (<\/span>Mycobacterium avium<\/span><\/i>), a fact that gave hog\u00a0 breeders such concern that large-scale efforts were under way to rid farms and chicken flocks of avian tuberculosis. The\u00a0 situation had become so grave in hogs and cattle that by 1917, one year before the most destructive pandemic ever, <\/span>The\u00a0 Cooperative State\u2013Federal Tuberculosis Eradication Program<\/span><\/i>, administered by the US Department of Agriculture and the\u00a0 Animal and Plant Health Inspection Service (<\/span>APHIS<\/span><\/i>), had to be instituted. For in 1917, it was estimated that 25 per cent\u00a0 of deaths from tuberculosis in adult humans were caused by animal tuberculosis. [39] Nor did the fact that swine freely\u00a0 infected humans and vice versa faze von Unruh. Swine were a mycobacterial laboratory; although they held primarily fowl\u00a0 tuberculosis, they could also acquire bovine and human forms and freely infect people with whatever combined virulent\u00a0 mycobacterial strains resulted.\u00a0<\/span><\/p>\n

In \u201c<\/span>A Comparative Study of the Acid Fast Bacilli<\/span><\/i>\u201d, von Unruh stressed that the many cases of influenza he had investigated\u00a0 contained both the resting (dormant) form of TB and the influenza bacillus. Although Pfeiffer had likewise documented<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>65\u00a0<\/span><\/p>\n

chronic colonization with his bacillus in TB patients, von Unruh saw this, and the fact that they were both mycobacteria as\u00a0 more suggestive of \u201ca common ancestry or origin\u201d. Von Unruh wrote: \u201c<\/span>We have in influenza the fever, malaise, loss of weight,\u00a0 invasion by the organism of the same anatomical structures as in tuberculosis; we have chronic cases of bronchitis in which\u00a0 the influenza bacillus is constantly present; and lastly, we know that typical tuberculosis often follows an attack, however mild,\u00a0 of influenza<\/span><\/i>.\u201d [37]\u00a0<\/span><\/p>\n

Figure 12: <\/i><\/b>Retentions and Condemnations On Account of Tuberculosis, per 1,000 Head of Swine Slaughtered Between\u00a0 1907 and 1922. (Proceedings of the Twenty-Eighth Annual meeting of the United States Live Stock Sanitary Association.\u00a0 Chicago, December 3-5, 1924 p.102)\u00a0<\/span><\/i><\/p>\n

Such tubercular infection could in turn lead to other secondary bacterial infections. Noymer and Garenne\u2019s statement\u00a0 that tuberculosis was behind the many deaths in the 1918 pandemic was specifically based upon the well-known concept\u00a0 that the secondary bacterial infections that cropped up in 1918 were common in TB-infected lungs. Noymer and Garenne:\u00a0 \u201c<\/span>It is highly plausible that TB infection laid the ground for the massive secondary bacterial pneumonias that killed the victims\u00a0 of the flu in 1918<\/span><\/i>.\u201d [16]\u00a0\u00a0<\/span><\/p>\n

Medical Reserve Corps, New York City, July 1918<\/b><\/p>\n

Victor von Unruh continued to see many reasons to pin a common ancestry onto the two organisms. Both the\u00a0 influenza bacillus and the quiescent TB formed Much\u2019s granules. Much\u2019s granules, named after their discoverer, Hans Much,\u00a0 passed through filters \u2013then a major criterion for diagnosing a virus. Furthermore, both the influenza bacillus and TB were\u00a0 mycobacteria, with the branched fungal forms characteristic of the mycobacteria. And both could stain with \u201cacid-fast\u201d\u00a0 mycobacterial stains. Von Unruh wrote: \u201c<\/span>Therefore my conclusion is that the influenza bacillus is merely a weaker or dwarfed\u00a0 form of the real tubercle bacillus, a strain that in this case failed of better development because of a higher degree of resistance\u00a0 in the host. In both tuberculosis and influenza we deal with the self-same organism that in tuberculosis is fully developed, while\u00a0 in influenza it lacks development. In other words, we are dealing with a difference in degree only, but not in kind<\/span><\/i>.\u201d [37]\u00a0\u00a0<\/span><\/p>\n

Von Unruh\u2019s distinction is suggestive of a similar, well-acknowledged comparison between the damaging effects\u00a0 that <\/span>Mycobacterium tuberculosis <\/span><\/i>has inflicted on man for centuries and the better resistance that humans with a healthy\u00a0 immune system have had against bird or fowl tuberculosis (<\/span>Mycobacterium avium<\/span><\/i>), found in swine as well. Did types of\u00a0 fowl tuberculosis in the form of Mycobacterium (Haemophilus) <\/span>influenzae suis <\/span><\/i>from pigs combine additively with latent\u00a0 human tuberculosis to cause the deadly galloping consumption of 1918\u201319?\u00a0<\/span><\/p>\n

Victor von Unruh\u2019s findings could have been taken lightly, were it not for similar thoughts published in the more\u00a0 prestigious medical journals of his time.\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>66\u00a0<\/span><\/p>\n

US Department of Agriculture, Washington, DC, 1917:\u00a0<\/b><\/p>\n

\u00a0<\/b>Figure 13: <\/i><\/b>USDA Administrative Building, 1917\u00a0<\/span><\/i><\/p>\n

It had to be more than a coincidence that by the autumn of 1918 thousands of Midwest pigs died, seemingly from the\u00a0 same flu-like illness and in the same Haskell County location in which the worst human pandemic in history, which would\u00a0 kill between 20 and 100 million people was about to begin. The small towns that peppered Haskell County lay west of\u00a0 Dodge City in rich farmland dense with hogs and chickens.\u00a0<\/span><\/p>\n

US Inspector and veterinarian J.S. Koen, much to the chagrin of the pork industry, insisted that not only was he seeing\u00a0 pigs get the same \u2018\u2018flu-like\u2019\u2019 illness as human victims, but that he had actually seen the two species transfect one another.\u00a0 Koen, for lack of another term, and with no evidence other than a hunch, quickly called this unknown disease in pigs \u201cswine\u00a0 influenza\u2019\u2019, even as it killed pig after pig.\u00a0\u00a0<\/span><\/p>\n

Koen knew better.<\/span><\/p>\n

That thousands of pigs died in the Autumn of 1918 was problematical in that bird or fowl TB also called <\/span>Avian\u00a0 tuberculosis <\/span><\/i>or <\/span>Mycobacterium avium <\/span><\/i>routinely infects birds as well as hogs and sometimes cattle \u2013but could, under the\u00a0 right conditions also infect man. And to complete this picture, <\/span>Mycobacterium tuberculosis<\/span><\/i>, although primarily\u00a0 affecting humans, could also be transmitted to hogs and cattle. So tuberculosis struck at will and affected all warm blooded\u00a0 vertebrates, its \u201catypical strains\u201d other than human tuberculosis apparently getting into humans through the respiratory\u00a0 tract [40]. Also, unknown at this time, but pertinent, since Kansas sits squarely in America\u2019s \u2018\u2018dustbowl\u2019\u2019, were the results\u00a0 of a European experiment wherein guinea pigs exposed to organisms like <\/span>Avian tuberculosis <\/span><\/i>got little or no lung disease.\u00a0 However, when these mycobacteria were placed in dust aerosols, guinea pigs came down with progressive, fatal lung\u00a0 disease, not unlike what was occurring at the inception of the pandemic of 1918 [41].\u00a0\u00a0<\/span><\/p>\n

Furthermore, although many blindly insist that infection with fowl tuberculosis (<\/span>M. avium<\/span><\/i>) requires some \u2018\u2018defect\u2019\u2019\u00a0 in the human immune system, that defect could be as simple as dust tying up the body\u2019s defenses. Certainly a previous\u00a0 tubercular infection, common in 1918, with or without accompanying \u2018\u2018chronic bronchitis\u2019\u2019 would be, in many cases, more\u00a0 than enough to qualify a person as a \u2018\u2018compromised host\u2019\u2019, unleashing an animal or soil non-tubercular superimposed\u00a0 mycobacterial infection. Expert Rosenzweig found a surprising number of such cases in younger adults free of coexisting\u00a0 disease [42]. Rosenzweig isolated a case of Fowl tuberculosis (<\/span>M. avium-intercellulare<\/span><\/i>) in human lungs [43], commenting,\u00a0 that, although the average case of fowl TB in humans was thought to involve host compromise, that otherwise healthy hosts\u00a0 could also be affected in which severe and progressive disease would and did occur. <\/span>Mycobacterium kansasii <\/span><\/i>and certain\u00a0 forms of <\/span>M. avium <\/span><\/i>are the commonest forms of Non-Tubercular Mycobacteria (NTM) in human lungs. And hemoptysis, the\u00a0 coughing up of blood so common in 1918 pandemic victims, is more common in <\/span>Mycobacterium kansasii <\/span><\/i>induced disease\u00a0 [44]. But why, besides the fact that <\/span>M. avium <\/span><\/i>and <\/span>M. kansasii <\/span><\/i>were in abundance, should everything have begun in Kansas?\u00a0\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>67\u00a0<\/span><\/p>\n

Epidemiologically, although the present pandemic of human TB began in 16th century England, it reached its peak in\u00a0 1780 as a result of industrial revolution and the spread of cities, which allowed person-to-person spread. It then traveled\u00a0 rapidly to other large western European cities reaching a second peak in the early 1800s. It was only by the mid and later\u00a0 1800s that North and South American waves spiked. Likewise, peak mortality rates for New England in the US came first\u00a0 and it was only with industrial development that the US epidemic traveled to the Midwest years later and finally the West\u00a0 [40].\u00a0<\/span><\/p>\n

So by 1918, it could be said, in so far as tuberculosis was concerned, that the world was a super-saturated sponge ready\u00a0 to ignite and that among its most vulnerable parts was the very Midwest where the 1918 unknown pandemic hit, in rural\u00a0 Haskell country, Kansas, in the midst of a natural pig slaughter, a few hundred miles from Camp Funston, today Fort Riley.\u00a0\u00a0<\/span><\/p>\n

As the situation worsened, in 1917, the US Bureau of Animal Industry sent out inspectors to conduct an educational\u00a0 campaign on the dangers of bovine and hog tuberculosis. By 1918, the increase in hog tuberculosis had become all too\u00a0 noticeable.\u00a0<\/span><\/p>\n

Although Influenza virus type A was subsequently baptized \u201cthe avian influenza\u201d or \u201cthe bird flu virus\u201d, it had been\u00a0 known for 20 years previous to the Great Pandemic of 1918 that swine were susceptible to poultry tuberculosis just as\u00a0 it was general knowledge that since 1907 there had been an enormous increase in tuberculous farmyard poultry in large\u00a0 sections of the country, Kansas and Nebraska included. Comparative pathologist Herbert Fox, maintained that not only\u00a0 were primates like man the most susceptible to TB, but it was these same primates, including man, that were the most\u00a0 susceptible of all mammals, and perhaps all animals to tuberculosis [45] \u2013a disease which could present as a rapid,\u00a0 progressive tubercular inflammation. Speaking at the Twenty-Eighth Annual Meeting of the <\/span>US Livestock Sanitary\u00a0 Association<\/span><\/i>, Fox maintained that infection from one species to another was already well known in 1918, including human\u00a0 tuberculosis found in certain birds, and that there was both bovine \u201cand human TB in species no one thought they would\u00a0 be found in.\u201d\u00a0\u00a0<\/span><\/p>\n

Pigs had involuntarily become the living laboratory thru which three of the main types of tuberculosis (human, cow and\u00a0 fowl) could mutate through the genetic exchange by their viral mycobacteriophages, much in the same fashion as has been\u00a0 attributed to the \u2018\u2018influenza virus\u2019\u2019. The stage was set for disaster.\u00a0<\/span><\/p>\n

Ground Zero: Haskell Country, Kansas: Autumn of 1918:<\/b><\/p>\n

Figure 14: <\/i><\/b>Haskell County, Kansas\u00a0<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>68\u00a0<\/span><\/p>\n

America had already entered World War 1. And though consensus has it that the lethal epidemic of 1918 began in\u00a0 Camp Funston, Kansas as early as January, physician Dr. Loring Miner of Haskell Country, situated 300 miles southwest of\u00a0 Funston\u2019s perimeter, was already knee-deep in the medical struggle of his life. Miner, an alumni of Ohio University\u2019s School\u00a0 of Medicine, had decided to become a county doctor in rural America. Loring liked to drink. Yet In the first thirty years of\u00a0 his life in Haskell, Miner\u2019s excellent clinical skills had solidified his reputation as a physician to the point where most of his\u00a0 patients agreed that they would rather have a Loring Miner, occasionally drunk, than another doctor fully sober. But soon,\u00a0 a string of deadly events was about to happen that would sober-up even Loring Miner. Suddenly frantic townspeople were\u00a0 hunting him down at all hours of the day and night, reporting that members of their family would wake up one day feeling\u00a0 fine, have a severe headache by noon, be bedridden by late afternoon, with many of them lying dead by the following\u00a0 morning. The situation was bizarre. A febrile disease of unknown origin, progressing to fulminant pneumonia, was cutting\u00a0 down dozens of Haskell\u2019s strongest and most robust men and women, directly in front of Dr. Loring Miner.\u00a0\u00a0<\/span><\/p>\n

By 1918, Haskell County was one of the poorest areas in America. The spirit of invention and change that had\u00a0 swept America for decades, bringing with it the railroad, the telegraph, and now electricity, had mostly passed Haskell\u00a0 by. Its inhabitants, mostly farmers, grew grain, and raised poultry, hogs, and cattle. Its dominant building material was\u00a0 sod \u2013topsoil held together by the roots of foliage. Even the Haskell post office, built in 1918, was sod.\u00a0<\/span><\/p>\n

So you might just say that Haskell was just a place where people, hogs, poultry, earthen sod houses, cattle, and manure\u00a0 melded into one.\u00a0<\/span><\/p>\n

Figure 15: <\/i><\/b>The sod hut-house of a Haskell Kansas farmer\u00a0<\/span><\/i><\/p>\n

Miner would try to see to it that this small rural epidemic got national attention, through the April 1918 issue of what\u00a0 today is called <\/span>The Morbidity and Mortality Weekly Report <\/span><\/i>[46]. He noted that the disease appeared to be associated with\u00a0 farms. If it was influenza, which at that time wasn\u2019t considered lethal enough to be a reportable disease, it wasn\u2019t acting like\u00a0 any influenza Miner had ever seen, killing the strong indiscriminately.\u00a0\u00a0<\/span><\/p>\n

Miner\u2019s report was the warning, but went unheeded. So while the Haskell epidemic ended as abruptly as it had begun,\u00a0 soon disease spread to Army barracks in nearby Funston. Many of Haskell counties young farmers had been incorporated\u00a0 into Camp Funston. Lt. Colonel Warren T. Vaughan, a physician of the <\/span>Department of Preventive Medicine and Hygiene at\u00a0 Harvard Medical School <\/span><\/i>and now on the Army\u2019s Medical Board, indicated that the epidemic at Funston began on March\u00a0 5th 1918, offering: \u201c<\/span>The Board decided that the disease should be called influenza, but our only basis for such decision were\u00a0 the clinical symptoms and the contagious character.\u201d <\/span><\/i>Ibid p.16<\/span><\/i> And that \u201cThe difficulty in making a decision in the presence of an\u00a0 epidemic is very similar to that of deciding whether the epidemics of former times were in each case influenza<\/span><\/i>.\u201d [47]<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER\u00a0<\/b><\/p>\n

69\u00a0<\/span><\/p>\n

Camp Funston, Kansas, Spring of 1918:<\/b><\/p>\n

Figure 16: <\/i><\/b>Camp Funston, Kansas, 1918. Because the country was at war, farm boys from isolated communities such as\u00a0 Haskell County were on the move. During the spring, a soldier from Haskell County probably brought this new\u00a0 and virulent form of influenza to Camp Funston, a military camp in Kansas.\u00a0<\/span><\/i><\/p>\n

\u201cDuring the 1918 epidemic we saw men in the army camps who passed through an attack of influenza-pneumonia and died\u00a0 within a few weeks from tuberculous pneumonia or miliary <\/span><\/i>[blood-borne] <\/span>tuberculosis. These men had previously been so free\u00a0 from signs of their tuberculosis, as to be accepted for military service as healthy individuals.\u201d <\/span><\/i>Ibid p. 220<\/span><\/i>\u00a0<\/span><\/i><\/p>\n

-Lt. Colonel Warren T. Vaughan, MD\u00a0<\/span><\/p>\n

Whatever the agent responsible for influenza, concluded Vaughan, whether viral or bacterial, many individuals with\u00a0 pulmonary tuberculosis did get influenza, and that this disease, having been contracted, in many cases hastened fatal\u00a0 termination of both the tuberculous process and the patient.\u00a0<\/span><\/p>\n

Fort Riley, Kansas was a sprawling establishment housing 26,000 men and encompassing an entire camp, Camp\u00a0 Funston. Soldiers there often complained about the inhospitable weather: bone-chilling winters and sweltering summers.\u00a0 Squeezed between these extremes were the blinding dust storms. Within the camp, thousands of horses, hogs, mules and\u00a0 chickens produced in excess of a stifling nine tons of manure each month. And the accepted method for its disposal was\u00a0 to burn it, even against driving wind. State Veterinarian W.J. Butler would report at the 28<\/span>th<\/span> Meeting of the <\/span>United States\u00a0 Live Stock Sanitary Association<\/span><\/i>: \u201cI consider contaminated manure and stagnant water the most important factors in the\u00a0 spread and propagation of tuberculosis\u201d [48]. And so on Saturday, the 9<\/span>th<\/span> of March, 1918, a threatening black sky forecast\u00a0 the coming of a major dust storm. When this storm combined with the ashes of over 9 tons of burning manure, a stinking,\u00a0 stinging yellow haze resulted. The sun was said to have gone black in Kansas that day. Two days later, on March 11<\/span>th<\/span>,\u00a0 company cook Albert Gitchell reported to the Funston infirmary saying he had \u201ca bad cold\u201d. Among his symptoms were a\u00a0 headache, a sore throat, muscle aches, chills and fever. He also reported cleaning pig pens on March 4th, one week before\u00a0 feeling sick. Gitchell would never recover from this, his last illness. And by noon of March 14<\/span>th<\/span>, a hundred men joined him\u00a0 at the Army infirmary he had walked into. Within a month 1,000 men were sick and approximately 50 dead [49]. Camp\u00a0 Funston was having a deadly epidemic.\u00a0<\/span><\/p>\n

These deaths were highly unusual, but nothing like what would return in the fall, when the disease would come back\u00a0 with a vengeance, seeming to gain strength through human passage. Camp Funston in March, Camp Devens in September,\u00a0 then across the country and the world, leaving an estimated 20-100 million dead globally, at least 600,000 to a million of\u00a0 them American, in the span of less than two years \u2013the most destructive plague that man had ever witnessed.\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>70\u00a0<\/span><\/p>\n

Figure 17: <\/i><\/b>Army training camps in the U.S. in 1918, Camp Funston sitting in the middle of the Country. Source: War\u00a0 Department (US). Annual report, 1919. Washington: Government Printing Office; 1920. p. 1519\u00a0<\/span><\/i><\/p>\n

Kansas might have been situated in the middle of the United States, but it also found itself a state with a fairly high inci dence of TB, sandwiched between states with some of the highest incidence of tuberculosis in the United States [Figure 19]:<\/span><\/p>\n

Figure 18: <\/i><\/b>Kansas on a US Map\u00a0<\/span><\/i><\/p>\n

Figure 19: <\/i><\/b>Map of the United States, circa 1918, showing by States the varying incidence of pulmonary\u00a0 tuberculosis as found at mobilization camps in the first million men drafted. The highest incidence\u00a0 is in the blacked-out and darkened-grid designated States, most of them Southern. Note that Kansas,\u00a0 were Fort Funston was located and the Influenza epidemic initially broke out, is squarely sandwiched\u00a0 between some of the States, marked in solid black, with the highest incidence of tuberculosis in the US.\u00a0<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>71\u00a0<\/span><\/p>\n

And if one took into account the states from which Funston drew its personnel [See Figure 21] \u2013its catchment area, then\u00a0 the highest incidence of TB found in US army mobilization camps for the first million men in WWI was far and away within\u00a0 the circumference from which Camp Funston\u2019s recruits were drawn.\u00a0<\/span><\/p>\n

In his post-mortem of the Great Pandemic, in <\/span>The Medical Department of the United States Army in the World War<\/span><\/i>,\u00a0 Major Milton W. Hall, M.D spoke of inflammatory diseases of the respiratory tract [50] freely using the word \u201cinfluenza\u201d to\u00a0 explain what happened in 1918 while at the same time admitting that the cause of such influenza was entirely unknown.\u00a0 Pneumonia is what killed in 1918. But pneumonia from what?\u00a0<\/span><\/p>\n

Hall addresses these deadly \u201catypical\u201d pneumonias, saying this:\u00a0\u00a0<\/span><\/p>\n

\u201c<\/span>The high incidence of pneumonia was largely confined to camps which were made up of men from the states of the south\u00a0 and southeastern part of the country, States whose men had been shown by Civil War figures to be far more susceptible to the\u00a0 respiratory diseases in serious form than those in the north and west<\/span><\/i>.\u201d [50]\u00a0\u00a0<\/span><\/p>\n

Clearly, in 1918 at the time of the mobilization of the first one million men, there existed a specific disease\u00a0 predominantly in the \u201csouth and southeastern\u201d parts of the United States \u2013and that disease was pulmonary tuberculosis.\u00a0 [See Map Figure 19, above] Furthermore, in the US in 1918, death through tuberculosis was, in the age group under 45,\u00a0 at an all-time high, targeting the very same age range that would suffer the most deaths in the Great Pandemic [51,52].\u00a0 Similarly, by 1918, tubercular deaths had spiked around the world, including such places as Japan and Australia.\u00a0<\/span><\/p>\n

In 1905, Flick had already concluded that one-fifth of all tubercular patients gave previous histories of pneumonia\u00a0 [53], something which Baum and Amberson pursued in their discussion of how non-tuberculous pneumonias could\u00a0 and did often complicate the pneumonia of pulmonary tuberculosis [54]. Within a year of Major Milton Hall\u2019s pandemic\u00a0 monograph for Surgeon General Ireland, Rist pointed to how lobar and other pneumonias, so frequently calculated\u00a0 statistically as being aside and apart from tuberculosis, were frequently being mistaken for the sudden onset of lung\u00a0 tuberculosis with its lobar or lobular localization [55]. In almost 50 per cent of 300 consecutive admissions,\u00a0 Rist mentioned, there was an acute onset of an \u201catypical\u201d tubercular pneumonia, for which Rist provided the following\u00a0 description:\u00a0\u00a0<\/span><\/p>\n

\u201c. . . <\/span>it has the appearance of an acute pulmonary or pleuropulmonary episode. Chills and fever initiate it, the fever being\u00a0 generally high. Pain in the sides, coughing, and expectoration are always present. The sputum may be rusty as in ordinary\u00a0 lobar pneumonia; dullness or flatness, tubular breathing, and crepitant rales.<\/span><\/i>\u201d [55]\u00a0<\/span><\/p>\n

Rist\u2019s \u2018atypical\u2019 tubercular pneumonia was the same term used by Major Milton W. Hall, M.D for his atypical \u2018influenza\u2019\u00a0 pneumonia.\u00a0\u00a0<\/span><\/p>\n

While Rist pointed out the many cases of pulmonary tuberculosis mistaken for lobar and other pneumonias,\u00a0 Harvard\u2019s physician and epidemiologist Lt Colonel WT Vaughan spoke of the two clinical scenarios he found most prevalent\u00a0 during 1918: First, \u201c<\/span>a clinical picture which closely simulates ordinary lobar pneumonia<\/span><\/i>\u201d. Second, an illness which \u201c<\/span>is most\u00a0 suggestive of acute tubercular infection, and it is only by repeated examination of the expectoration that the clinician can\u00a0 satisfy himself he is not really over-looking a case of acute pulmonary tuberculosis<\/span><\/i>.\u201d [47]. The problem was, that quick-killing\u00a0 acute galloping tubercular consumption often did not yield any positive sputum or \u201cexpectoration\u201d evidence.\u00a0<\/span><\/p>\n

Farber and Clarke reported 100 cases which were admitted to a general hospital for non-tuberculous pneumonia,\u00a0 which were found to be of a tubercular cause [56].\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER\u00a0<\/b><\/p>\n

72\u00a0<\/span><\/p>\n

Office of the Surgeon General of the United States, Washington DC, October, 1918 <\/b><\/p>\n

Figure 20: <\/i><\/b>Surgeon General Merritte Weber Ireland\u00a0<\/span><\/i><\/p>\n

\u201c<\/span>In the differential diagnosis influenza, acute miliary tuberculosis, sepsis, and malarial fevers must be differentiated<\/span><\/i>.\u201d [57]\u00a0 \u2013Maj. Gen. Merritte Weber Ireland, US Army, <\/span>Surgeon General <\/span><\/i>during the later stage of the Great Pandemic of 1918.\u00a0\u00a0<\/span><\/p>\n

Thus did physician and pandemic of 1918 Surgeon General Merritte Weber Ireland, come to admit, seven years after\u00a0 the censor-ridden Woodrow Wilson administration, that during the Pandemic of 1918 it was difficult, if not impossible, to\u00a0 differentiate \u201cinfluenza\u201d from acute miliary tuberculosis, both of which often began with similar flu-like symptoms.\u00a0\u00a0<\/span><\/p>\n

Ireland directed physician and Colonel George Bushnell to elaborate further in Chapter Three of <\/span>The Medical\u00a0 Department of the United States Army in the World War<\/span><\/i>, regarding how to \u201celiminate\u201d tuberculosis from the army. Colonel\u00a0 Bushnell, constantly referring to a \u201ctuberculosis virus\u201d, long after Koch had discovered his tubercle bacilli, was realistic, if\u00a0 not brutally frank. Bushnell:\u00a0<\/span><\/p>\n

\u201cWhat may be called the modern view is based upon the well-established fact that practically every civilized adult has\u00a0 come into contact with the tubercle bacillus and has thereby acquired what in a sense is a tuberculous infection. Evidence of\u00a0 chronic tuberculous changes is found in some cases of pulmonary tuberculosis with acutely fatal termination. That they are\u00a0 not found in all such cases which occur in civilized man is largely accounted for by the difficulties of the search. Even Nigeli in\u00a0 his classical investigations which finally resulted in finding tuberculous changes present in 97 to 98 per cent of autopsies, at\u00a0 the beginning found only 40 per cent.\u201d <\/span><\/i>Ibid<\/span><\/i> [57], <\/span><\/i>pp.173,188<\/span><\/i>\u00a0<\/span><\/i><\/p>\n

American Surgeon General from October 4<\/span>th<\/span> 1918 to May 31<\/span>st<\/span> 1931, Merritte Weber Ireland knew what baptism by fire\u00a0 was all about. And his didn\u2019t begin in October, 1918. Having obtained his M.D. degree Ireland immediately joined the Army\u2019s\u00a0 medical service and was commissioned Assistant Surgeon from Indiana on May 4<\/span>th<\/span> 1891. He was in the Philippines during\u00a0 the Filipino-American war, where some of the greatest atrocities, on both sides, were committed in the history of warfare.\u00a0 And while there, Ireland saw direct field action, participating in a dozen engagements in the provinces of Cavite, Camarines,\u00a0 and Albay in southern Luzon.\u00a0\u00a0<\/span><\/p>\n

Once back in the US, Ireland made the rounds through the Army\u2019s fortifications, including a stint at Fort Funston,\u00a0 Kansas under Major John Von R. Hoff. While at Funston, Ireland took direct charge of the first company for instruction\u00a0 of the Hospital Corps organized by Captain Hoff. During WW 1, Funston\u2019s main purpose was to train soldiers drafted in\u00a0 Midwestern states to fight overseas.\u00a0<\/span><\/p>\n

Surgeon General Ireland, as Gorgas before him, both knew that the army had a tubercular problem on its hands. They\u00a0 also knew that it could only get worse. War and tuberculosis simply fed off of one another. As early as 1915, the tubercular\u00a0 death rate had not only increased in all countries at war, but even in some, like the United States, that had not yet taken\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>73\u00a0<\/span><\/p>\n

direct action in the conflict. And as the global conflict mushroomed, it became more and more obvious that war was\u00a0 increasingly and commonly spawning deadly forms of tuberculosis with a rapid course and without any tendency towards\u00a0 healing. Such acute, \u201cgalloping\u201d forms would be extremely difficult to diagnose, with little time to evolve into the chest x-ray\u00a0 and other evidence that doctors relied upon.\u00a0\u00a0<\/span><\/p>\n

At the time S. Adolphus Knopf estimated that 176,091 in the US army of 1918 were either already tubercular or were\u00a0 strongly predisposed to developing or contracting the disease [58]. And so as soon as war was declared Surgeon General\u00a0 Gorgas, and then Ireland after him , moved to expand a single 500 bed TB facility at Fort Bayard, New Mexico into a 10,000\u00a0 bed chain of tubercular hospitals around the country. Never had any nation, in so short a time, constructed, equipped and\u00a0 made operational such an efficient chain of TB hospitals for its military personnel. Nor was there a wasted bed.\u00a0\u00a0<\/span><\/p>\n

Fort Funston was in Kansas, a state named after the Kansa Native American tribe, Kansa often said to mean \u201cpeople\u00a0 of the wind\u201d or \u201cpeople of the south wind\u201d \u2013originally was a Dakota Sioux word. Pandemic physician Fishberg seemed\u00a0 aware that the inhalation of dust is a strong predisposing factor in the instigation of tubercular lung disease, lowering the\u00a0 resisting powers of the invaded lung, and preparing the soil for the deposit of tubercular bacilli to thrive on inflamed, dust\u00a0 damaged tissue [59].\u00a0\u00a0<\/span><\/p>\n

Figure 21: <\/i><\/b>Map of the United States showing the catchment areas of each of the 16 National Army Cantonments, 1917.\u00a0 Camp Funston\u2019s area included many from the American Plains Indians.\u00a0<\/span><\/i><\/p>\n

Merritte Weber Ireland knew that the War Department looked at American Indians as its secret weapon \u2013a group with\u00a0 little fear of the enemy and an almost inborn ability when it came to scouting, reconnaissance, the ability to plan accurate\u00a0 and unexpected attacks \u2013and an uncanny marksmanship.\u00a0<\/span><\/p>\n

Thousands of American Indian from various tribes had been moved to the area that is now Kansas from the eastern\u00a0 United States and Great Lakes area. <\/span>The Indian Removal Act of 1830 <\/span><\/i>resulted in the settlement of more than 10,000\u00a0 American Indians to what is now Kansas. And by the time of the Great Pandemic, four American Indian tribes still retained\u00a0 reservations there.\u00a0\u00a0<\/span><\/p>\n

Camp Funston sat just off of Fort Riley on the banks of the Republican River. When war became imminent, Congress\u00a0 quickly established a draft, and more than 4,600 Selective Service draft boards screened 10 million men to find the\u00a0 strongest and most fit among them, including 12,500 American Indians, some from the Lakota Sioux [60]. What is known\u00a0 is that at least one multi-tribal group of Indians enlisted at Lawrence, Kansas, from the Haskell Indian School and trained\u00a0 at Funston.<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>74\u00a0<\/span><\/p>\n

The American Indians, once removed from their native habitat and shoved onto reservations, where no strangers to\u00a0 killer epidemics. Ireland had witnessed some of these himself. Just five years before the Great Pandemic of 1918, almost\u00a0 three thousand Sioux where made prisoners of war and forced to move into barracks, where a people to whom tuberculosis\u00a0 had been rare in their native habitat turned, inside their barracks and reservations, into a tubercular inferno of death in\u00a0 its most acute, \u201cgalloping\u201d form, reaching a mortality by 1913 ten times higher than anything that Europe had seen in the\u00a0 worst of its nineteenth-century epidemics.\u00a0<\/span><\/p>\n

Nor was it just the Sioux or just those in barracks. What happened to the Sioux was being seen in Indian reservations\u00a0 across the country, including those of the Navaho. In fact it was on such reservations that Indian tubercular mortality\u00a0 rate reached the highest rate anywhere at any time [61]. The problem was that some of the children from these Indian\u00a0 reservations where in Fort Funston now, where unlike the treatment given to other minorities, they were purposely being\u00a0 integrated into regular white military units in a strategy to assimilate them into American culture, and many of these Indian\u00a0 inductees were now at Fort Funston.\u00a0<\/span><\/p>\n

Figure 22: <\/i><\/b>American Indian Student battalion at Haskell Institute in Kansas, 1920s. Many from Haskell served\u00a0 with great distinction during the Great War after being trained at Fort Funston, Kansas\u00a0<\/span><\/i><\/p>\n

As recruits entered Camp Funston through the post\u2019s main gates they had to display their identification and were then\u00a0 directed towards a long line to be examined by camp doctors.\u00a0\u00a0<\/span><\/p>\n

Figure 23. <\/i><\/b>Draftees entering Fort Funston at the War\u2019s beginning<\/span><\/i><\/p>\n

Because of their sheer number and the burden placed on the Medical Corps, the process was of necessity so fast that\u00a0 some men took their mandatory oath of loyalty before the physician had completed his examination, leaving half-dressed\u00a0 young soldiers to pledge their allegiance to the country [62]. There was much emphasis in the Medical Corp towards simply\u00a0 detecting TB through auscultation of the chest with a stethoscope. And as is the case today, the tuberculin skin test could\u00a0 and often was negative even with active tuberculosis.\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER\u00a0<\/b><\/p>\n

75\u00a0<\/span><\/p>\n

Bureau of Laboratories, 1918<\/b><\/p>\n

Figure 24: <\/i><\/b>Dr. William Hallock Park\u00a0<\/span><\/i><\/p>\n

Something was eating at physician\/researcher\/editor William Park during the carnage of 1918. Park, heading the\u00a0 state-of-the-art <\/span>Bureau of Laboratories <\/span><\/i>in New York City, was relied upon by both the US Government Health Corps and\u00a0 other major research centers across the country. Along with collaborators, including bacteriologist Anna Williams, Park\u00a0 co-authored the important teaching text, <\/span>Pathogenic Microorganisms <\/span><\/i>[63].\u00a0<\/span><\/p>\n

At first, Park blamed Pfeiffer\u2019s bacillus for the 1918 pandemic and reported it to the US Army Health Corps. But\u00a0 flustered by the secondary infections and lack of consistency in other labs in isolating Pfeiffer\u2019s, Park flip-flopped,\u00a0 cautioning against attributing the pandemic solely to Pfeiffer\u2019s. By the same token, Park felt uncomfortable with the\u00a0 muzzling of the media and medical corps by the Wilson administration regarding the ferocity of the 1918 American\u00a0 epidemic in general \u2013that is, until it was too late to deny its viciousness. So although Pfeiffer\u2019s influenza bacillus, also\u00a0 known as <\/span>Mycobacterium influenzae<\/span><\/i>, was no longer at the top of his choices for the causal agent of the 1918 pandemic, it\u00a0 was its association with another mycobacterium, tuberculosis, which bothered Park the most. He had just re-read Flick\u2019s\u00a0 account of what preceded both Great Pandemics.\u00a0<\/span><\/p>\n

By 1888, physician Lawrence Flick, citing US census reports leading into the two greatest world \u201cinfluenza\u201d pandemics\u00a0 in history, reported that out of every 1,000,000 deaths, 242,842 males and 302,046 females died of tuberculosis. This\u00a0 as for all nationalities and colors. Specific subsets within these statistics revealed that among African Americans, every\u00a0 million deaths represented 248,179 males and 326,973 females having died of tuberculosis. Among people of Irish\u00a0 parentage, 309,507 males and 375,636 females died of TB for every million deaths. And among people of German\u00a0 parentage, its victims numbered 249,498 males and 254,958 females for every one million deaths [64].\u00a0<\/span><\/p>\n

Although Park had seen these statistics before, their effect was not lost on him: \u201c<\/span>Consumptives <\/span><\/i>[people with\u00a0 tuberculosis] <\/span>frequently carry influenza bacilli <\/span><\/i>[Pfeiffer\u2019s bacilli] <\/span>for years and are particularly susceptible to attacks of\u00a0 influenza<\/span><\/i>\u201d [63].\u00a0\u00a0<\/span><\/p>\n

In 1918, with \u201cflu\u201d victims dropping all around them, John B. Hawes, MD, of the Massachusetts General Hospital, and\u00a0 Richard Cabot, MD, of Harvard, wrote: \u201c<\/span>One of the diseases most frequently mistaken for pulmonary tuberculosis is influenza,\u00a0 chronic or acute.<\/span><\/i>\u201d According to Hawes and Cabot, the symptoms of both diseases were often identical [65]. <\/span><\/p>\n

\u00a0<\/span><\/i>Figure 25: <\/i><\/b>Influenza. Death was all around in 1918\u00a0<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>76\u00a0<\/span><\/p>\n

Tufts pulmonologist Edward O. Otis also caught Park\u2019s attention. Otis not only mirrored Hawes and Cabot\u2019s view,\u00a0 he went a step further: \u201c<\/span>Often a patient gives the history of a previous attack of influenza which may have been an active\u00a0 outbreak of a latent tuberculous focus, which later again became inactive<\/span><\/i>.\u201d [66]\u00a0<\/span><\/p>\n

Back in 1901, an editorial in the <\/span>Journal of the American Medical Association <\/span><\/i>specifically cited Liverpool physician R.\u00a0 Buchanan: \u201c<\/span>Dr. R.J.M. Buchanan makes the not improbable suggestion that many of the so-called sporadic cases of influenza\u00a0 are really symptomatic of the initial infection of tuberculosis, or possibly an exacerbation of a latent tuberculosis previously\u00a0 unsuspected or undetected.<\/span><\/i>\u201d [67] In saying this, Buchanan had fired the shot heard around the world, and physician Walter\u00a0 Lindley, editor of the <\/span>Southern California Practitioner<\/span><\/i>, was quick to respond. Lindley on Buchanan: \u201c<\/span>The author, impressed\u00a0 by the large number of instances in which patients have referred the commencement of their ill-health to an attack of so-called\u00a0 influenza, conceives that many of the so-called sporadic cases of influenza are really symptomatic of the initial infection of\u00a0 tuberculosis or possibly an exacerbation of a latent tuberculosis<\/span><\/i>.\u201d [68]\u00a0<\/span><\/p>\n

A complaint by Wakley and Wakley in the Lancet in 1899 regarding an epidemic of infectious fever raging in New York\u00a0 is also appropriate in that it portrayed how the public at large cherished and demanded their own right to self-diagnose\u00a0 their \u2018flu\u2019: \u201c<\/span>The name \u2018influenza\u2019 seems to have a strong attraction for some people. Every ache and pain, no matter where\u00a0 located and whether accompanied by fever or not, is at once put down as \u2018influenza\u2019; every headache, every coryza [nasal\u00a0 congestion, common cold], every sore-throat, every attack of gastroenteritis, from whatever cause, is promptly self-diagnosed\u00a0 as \u2018influenza\u2019, and when the practitioner arrives upon the scene he will be expected to fall in with this view, and there is a great\u00a0 temptation to do so<\/span><\/i>.\u201d [69] The authors go on to suggest that the rise in temperature and general malaise frequently met with\u00a0 in this New York epidemic wasn\u2019t influenza at all.\u00a0<\/span><\/p>\n

Hendrickson, who practiced during the Great Pandemic of 1918\u201319, spoke even more bluntly: \u201c<\/span>No doubt there were many cases of tuberculosis whose death certificates were labeled influenza during the pandemic owing\u00a0 to lack of time to make a diagnosis by the overworked physician<\/span><\/i>.\u201d [70]\u00a0\u00a0<\/span><\/p>\n

Figure 26: <\/i><\/b>Two nurses watching as a 1918 pandemic patient dies<\/span><\/i><\/p>\n

And so, as the greatest influenza pandemic of all time continued to rage, other doctors were speaking out. In 1920,\u00a0 with the killing fields of 1918\u201319 laid out clearly before him, British physician Marcus Paterson took yet another jab at\u00a0 the \u201cflu\u201d epidemic. He wrote: \u201c<\/span>During the time I was Resident Medical Officer at Brompton, it was <\/span><\/i>usual <\/span>to classify a rise\u00a0 of temperature in an ordinary case of \u2018chronic\u2019 pulmonary tuberculosis as influenza, even when there was no epidemic<\/span><\/i>.\u201d As\u00a0 for the well-known sick feeling (malaise) and preliminary symptoms of reactivated tuberculosis, Paterson asked: \u201c<\/span>Are\u00a0 these symptoms any different from those of the ordinary onset of influenza? They are not, simply because they denote not a\u00a0 particular disease, but a toxemia due to bacterial action<\/span><\/i>.\u201d [71]\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>77\u00a0<\/span><\/p>\n

Paterson\u2019s reference to clinicians confusion of sorting out influenza from TB was pointed: \u201c<\/span>Surely there is no more\u00a0 emphatic testimony to the clinical difficulties of a differentiation between the two diseases when one group of clinicians\u00a0 describes a rise of temperature in a proven case of tuberculosis to be influenza, and another section terms an arrested case of\u00a0 tuberculosis with pyrexia [fever] an active case of tuberculosis<\/span><\/i>.\u201d\u00a0<\/span><\/p>\n

Writing in 1920, after the greatest pound-for-pound health catastrophe ever, Paterson said what every physician still\u00a0 learns as a resident: \u201c<\/span>Before the war, it was usual to classify a sudden onset of acute symptoms as influenza, and it is very easy\u00a0 to appreciate the reason. When a person is taken ill, the patient\u2019s friends demand to know at once what the ailment is: hence\u00a0 it must be given a name, and \u2018influenza\u2019 is a good enough term for the moment<\/span><\/i>.\u201d\u00a0<\/span><\/p>\n

What Paterson left out, as a given, was the hysteria in the family and immediate community that would ensue were\u00a0 a diagnosis of tuberculosis rendered. Instead, he went on to say that he knew of no physician who could differentiate\u00a0 clinically between tuberculosis and influenza \u0336 quickly adding that he \u201c<\/span>shudders to think<\/span><\/i>\u201d of the number of times that\u00a0 \u201c<\/span>tubercle bacillus have been classified as influenza without further investigation<\/span><\/i>\u201d. To Paterson, this represented countless\u00a0 opportunities to cure the real cause, masked under the designation \u201cinfluenza\u201d. His conclusion: \u201c<\/span>There is no research\u00a0 required here. It is a known fact that what is at present called influenza is often tuberculosis. But the knowledge is not\u00a0 practically applied. It is information of inappreciable value lying idle. It is no new discovery, or its import would ring\u00a0 throughout the world<\/span><\/i>.\u201d In fact, for Paterson, much like it was for von Unruh, \u201cinfluenza\u201d was simply the first indication of\u00a0 tuberculosis.\u00a0<\/span><\/p>\n

Rockefeller Institute for Medical Research, NYC, 1931<\/b><\/p>\n

American virologist Richard E. Shope, based in the Department of Animal Pathology at the <\/span>Rockefeller Institute<\/span><\/i>, was in\u00a0 direct communication with British investigators Smith, Andrewes and Laidlaw at Mill Hill, England, and sent samples of his\u00a0 flu virus and Pfeiffer\u2019s bacillus. But the British group, in return, wasn\u2019t being 100 per cent supportive.\u00a0<\/span><\/p>\n

Figure 27: <\/i><\/b>Dr. Patrick Playfair Laidlaw\u00a0<\/span><\/i><\/p>\n

Virologists like Shope and Laidlaw saw a great opportunity for virology provided by the 1918\u201319 pandemic. Shope\u00a0 began the first salvo on swine \u201cinfluenza\u201d, again falling back on the stale conception that the mild disease and flu-like\u00a0 symptoms were created in pigs by what he believed to be a \u201cfilterable virus\u201d[73]. Shope had the singular advantage of\u00a0 realizing that since 1918, pigs had been coming down with the same \u201cinfluenza\u201d each year. Having lived in Iowa, he had\u00a0 grown up with the knowledge. But beginning his investigations in earnest, Shope became perplexed. Not a virus but a\u00a0 bacterium kept cropping up in swine mucous secretions, and it resembled Pfeiffer\u2019s bacillus or <\/span>Haemophilus influenzae <\/span><\/i>(H.\u00a0 flu) more than anything else. The problem was that he couldn\u2019t infect most of his subjects with the bacterium alone. So he\u00a0 took the mucous secretions of sick pigs and put them through a filter which he thought would only yield a virus. However,\u00a0 incredibly, even the filtrate from the discharge just gave low-grade symptoms. So if it wasn\u2019t a \u201cvirus\u201d that had caused the\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>78\u00a0<\/span><\/p>\n

deadly strains of flu, and if it wasn\u2019t a bacterium present in most malignant \u201cflu\u201d, what could it be? To Shope\u2019s mind, possibly\u00a0 both, working in conjunction with one another. In 1931, he introduced both the \u201cvirus\u201d and Pfeiffer\u2019s bacillus into animals\u00a0 [74], which subsequently came down with just the deadly \u201cflu\u201d complicated with pneumonia that killed between 20 and\u00a0 100 million people in 1918\u201319.\u00a0<\/span><\/p>\n

Figure 28<\/i><\/b>: <\/span>Dr. Richard Shope. Originally Shope was looking for simply a bacterial cause such as Pfeiffer\u2019s bacillus for\u00a0 \u201cswine influenza\u201d, as the medical orthodoxy of his day dictated. There is no evidence in the literature that Shope even knew about the filterable forms of H. influenza (Pfeiffer\u2019s bacillus) which also appeared \u201cviral\u201d.\u00a0<\/span><\/i><\/p>\n

As late as 1944, Shope still was insisting that the pandemic influenza was this meld of \u201cvirus\u201d plus Pfeiffer\u2019s bacillus\u00a0 [75]. But as opposed to what\u2019s written in today\u2019s revisionist history, the idea wasn\u2019t really his. When Shope was a teenager,\u00a0 the announcement that hog cholera (swine flu) was due to the combined action of a bacterium and a virus stimulated\u00a0 French-Canadian microbiologist F\u00e9lix d\u2019H\u00e9relle in 1917 to publish his discovery of bacteriophages \u2013viruses which live in\u00a0 and can destroy or alter the shape of bacteria \u2013followed by d\u2019H\u00e9relle\u2019s 1921 classic book on such bacterial viruses [76].\u00a0 Not only could such viral bacteriophages alter the shape of a bacteria [or mycobacteria in the case of mycobacteriophages],\u00a0 causing virus-like, cell-wall-deficient forms, but such phages could also change a microbe\u2019s staining characteristics and\u00a0 moreover, its virulence. Therefore an individual with a latent case of TB could potentially be at risk for the reactivation\u00a0 of previously quiescent infection when another mycobacterial infection [<\/span>M. avium, M. Influenzae<\/span><\/i>] occurred \u2013through the\u00a0 injection of phage DNA into previously latent TB.\u00a0<\/span><\/p>\n

Actually, it was only sometime after joining Rockefeller in 1928, that Richard Shope switched his interest from\u00a0 tuberculosis to virology. There is no evidence in the literature that Shope even knew about the filterable forms of\u00a0 <\/span>H. influenza <\/span><\/i>(Pfeiffer\u2019s bacillus) which also appeared \u201cviral\u201d. To accept Shope\u2019s conclusion, an exception had to be made.\u00a0 There wasn\u2019t a single cause behind the 1918\u201319 pandemic, but two: a virus and a bacterium.\u00a0<\/span><\/p>\n

UK Medical Research Council, Mill Hill Farm, 1932<\/b><\/p>\n

Figure 29<\/i><\/b>: <\/b>Mill Hill \u2018Farm\u2019 Laboratories, at the UK MRC\u2019s National Institute for Medical Research facilities in\u00a0 north London. As far back as 1921, the MRC purchased this 40 acre agricultural site, then part of Rhodes Farm,\u00a0 to breed experimental animals at and do studies in.\u00a0<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>79\u00a0<\/span><\/p>\n

British virologists Smith, Andrewes and Laidlaw, as was the case for head of the UK\u2019s MRC (<\/span>Medical Research Council<\/span><\/i>)\u00a0 Walter Fletcher, all saw the study and cure of canine distemper in dogs as the soft underbelly to promote finding the virus\u00a0 that caused the Influenza Pandemic of 1918. The only problem was, that the vast weight of evidence was pointed in an\u00a0 entirely different direction, towards the fact that canine distemper was caused by a filterable bacterial bacillus, and not a\u00a0 virus. In fact Laidlaw\u2019s entire set of criteria for calling a pathogen a virus: such as that it could pass through a filter, and that\u00a0 it could not grow on artificial media was on shaky grounds, and he knew it.\u00a0\u00a0<\/span><\/p>\n

Nor was the fact lost on many that Patrick Playfair Laidlaw\u2019s team seemed to fly directly in the face of Shope\u2019s\u00a0 multifactorial conclusion, which said that both a virus and Pfeiffer\u2019s bacillus from swine were necessary to acquire the flu.\u00a0 Just the \u201cvirus\u201d itself was necessary, claimed the British trio [77].\u00a0<\/span><\/p>\n

Figure 30<\/i><\/b>: <\/b>Sir Christopher Howard Andrewes\u00a0<\/span><\/i><\/p>\n

Christopher Howard Andrewes, who would subsequently receive the lion\u2019s share of credit for discovering the human\u00a0 influenza virus, thought that he had discovered the viral cause of rheumatic fever at the Rockefeller Institute as far back\u00a0 as 1923 [78]. When that didn\u2019t pan out, and back in England, he, similar to Shope in America, put his efforts into the futile\u00a0 attempt to find a virus behind all cancers.\u00a0\u00a0<\/span><\/p>\n

Figure 31<\/i><\/b>: <\/b>Sir Howard Christopher Andrewes\u2019s Cancer Book\u00a0<\/span><\/i><\/p>\n

But when virus-admirer Walter Fletcher, first secretary of Britain\u2019s MRC, started his new scheme to once and for all\u00a0 viralize Influenza, Andrewes soon found himself at the Mill Hill farm under virologist Patrick P. Laidlaw and his colleague\u00a0 Wilson Smith. The MRC was originally founded as a consequence of the recommendations of the <\/span>Royal Commission on\u00a0 Tuberculosis<\/span><\/i>, but if Walter Fletcher had anything to say about it, it would now go viral.<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER\u00a0<\/b><\/p>\n

80\u00a0<\/span><\/p>\n

Figure 32<\/i><\/b>: <\/b>Sir Walter Fletcher of England\u2019s MRC. Fletcher seemed to have a great affection for viral research:\u00a0 \u201cThere are many reasons for suspecting that cancer may prove to be a virus disease, in which case all the elaborate\u00a0 work done in studying viruses will in due time find its use here.\u201d\u00a0<\/span><\/i><\/p>\n

So when influenza re-appeared in epidemic proportions during the autumn of 1932, Andrewes and Smith executed\u00a0 an experimental outline planned long in advance by Laidlaw and designed to reveal their hypothetical virus. In the midst\u00a0 of this, Andrewes began to feel unwell with flu-like symptoms. Immediately, Smith, having passed Andrewes\u2019 respiratory\u00a0 secretions through a filter, began to inject his colleague\u2019s mucus intra-cerebrally and intra-testicularly into mice, rabbits\u00a0 and guinea pigs. Nothing happened immediately, but just afterwards Laidlaw was informed by the director of Wellcome\u00a0 laboratory, their reference lab, that some of their ferrets appeared to be suffering from influenza at the same time as the\u00a0 epidemic of influenza was raging among Wellcome\u2019s staff. Ferrets, traditionally used for rabbit hunting and in rat control,\u00a0 had never been used in medical research until Laidlaw and Dunkin used them in their dog distemper studies. And it turned\u00a0 out that these Wellcome ferrets didn\u2019t have influenza but were suffering from distemper. In addition ferrets are extremely\u00a0 sensitive to tubercular mycobacteria as well, and <\/span>Mycobacterium avium, M. bovis <\/span><\/i>and human <\/span>M. tuberculosis <\/span><\/i>have all been\u00a0 isolated from ferrets [79]. In fact the very same techniques used by Andrews Smith and Laidlaw could easily have\u00a0 transmitted tubercular infection to their ferrets [80].\u00a0\u00a0<\/span><\/p>\n

But never mind, Smith had another idea and then inoculated several other ferrets through their nose with filtrates from\u00a0 Andrewes nasal secretions. Shortly thereafter \u201cinfluenza\u201d appeared. Subsequently, Wilson Smith himself came down with\u00a0 a flu that the rest of the group suspected was from a ferret. From the filtrate of this strain, the infectious agent WS (Wilson\u00a0 Smith) was isolated.\u00a0<\/span><\/p>\n

Figure 33<\/i><\/b>: <\/b>Nasal injection of the ferret. Andrewes is the one holding the pipette, and his assistant holds the ferret,\u00a0 demonstrating the standard technique of instilling \u2018virus\u2019 material into the nose of a ferret. The ferret was\u00a0 anaesthetized with ether, to ease injection of the virus material. Source: Picture Post,\u00a0\u00a0<\/span><\/i><\/p>\n

\u2018Can We Beat Influenza?\u2019 2nd of February 1946, p. 10.<\/span><\/i><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>81\u00a0<\/span><\/p>\n

But as head of a government lab at that time, Dr. William Crofton actually examined the famed WS strain that had\u00a0 afflicted Wilson Smith, and that today is still being used in research; bearing the alphanumeric notation A\/WS\/1933, for\u00a0 Influenza A\/Wilson Smith\/1933. Crofton, of all people, knew that there was nothing \u201cviral\u201d about strain WS, which he had\u00a0 personally investigated. Nor did it have anything to do with \u201cinfluenza\u201d. Smith, Andrewes and Laidlaw where in pathologist\u00a0 William Crofton\u2019s mind clearly perpetrating a deceptive fraud, and Crofton fully intended to stop them.\u00a0\u00a0<\/span><\/p>\n

During the summer and winter of 1918, Crofton was isolating Pfeiffer\u2019s bacillus from 100 per cent of influenza\u00a0 cases. But to do so, he was using improved special-growth agents and a sufficiently high-powered microscope. Crofton\u2019s\u00a0 \u201cmoist-chamber method\u201d kept his culture medium warm and moist. If the microbe wasn\u2019t kept warm, Crofton found, then it\u00a0 couldn\u2019t be isolated in every case. Pfeiffer\u2019s bacillus was clearly pleomorphic (many forms) with viral-like forms that could\u00a0 easily pass through a filter.\u00a0<\/span><\/p>\n

So, in 1938, when Crofton was final able to corner Andrewes, who was presenting a paper before the Epidemiology\u00a0 Section of the Royal Society of Medicine, Crofton said this:\u00a0\u00a0<\/span><\/p>\n

\u201c<\/span>I asked him how then he knew that his colleague Wilson Smith, from whom was first isolated the virus, had, in fact\u00a0 influenza, and how he and his fellows dared to advertise to the four corners of the earth that at long last the [viral] cause of\u00a0 influenza had been discovered. I told him that I had ascertained that Wilson Smith had, in fact, influenza, because he was\u00a0 swarming with [bacterial or mycobacterial] influenza bacilli. I asked him why no cultures on proper medium were made from\u00a0 the infected ferret to ascertain if the Pfeiffer bacillus could be grown, as it would have been inevitably if, in fact, influenza had\u00a0 been transmitted. Andrewes replied not one word, and the authorities of the section would not publish my criticism.<\/span><\/i>\u201d [25]\u00a0\u00a0<\/span><\/p>\n

Apparently the fix was already in through powerful monied UK governmental forces at Mill Hill\u2019s MRC led by Sir Walter\u00a0 Fletcher. Crofton didn\u2019t stand a chance. Neither did the rest of the world, which was forced to accept influenza as a virus.\u00a0<\/span><\/p>\n

Christopher Andrewes, now flushed with victory, suggested with the help of Burnet and Bang that the term\u00a0 \u201cmyxovirus\u201d, meaning \u201cmucous virus\u201d, be incorporated into a family name for the influenzas [81]. This, one imagines, was\u00a0 because the organism came from mucous secretions. By May 1935, another from this group, Patrick Playfair Laidlaw, who\u00a0 in his deceptive viral studies did anything but play fair, wrote \u201c<\/span>Epidemic Influenza: A Virus Disease<\/span><\/i>\u201d\u2013an article seemingly\u00a0 titled to assure himself that this was the case. In this document, Laidlaw would give the only credence he saw fit to Crofton\u00a0 and the many scientists like Crofton who did not believe him, saying that although he thought that it was \u201cgradually\u201d being\u00a0 proven that a \u201cfilterable virus\u201d was primarily responsible for epidemic influenza, \u201cPfeiffer\u2019s bacillus or <\/span>Haemophilus\u00a0 influenzae <\/span><\/i>is still regarded by many observers as the prime cause of the disease and many of its complications\u201d [82].\u00a0 Actually, it was the MRC and its influence not only in the UK but abroad that would make sure that this \u201cgradually\u201d became\u00a0 much more accelerated \u2013much, much more accelerated.\u00a0<\/span><\/p>\n

Crofton was convinced by the confirmation of scientists like Calmette at Pasteur regarding how certain forms of\u00a0 tuberculosis, appearing both minuscule and viral, could pass through the smallest of filters. Crofton himself then established\u00a0 that tuberculosis could disappear into tissues as viruses did, and then go through filters which stopped cold even most of\u00a0 those \u201cnow invariably called viral disease\u201d. \u201c<\/span>Surely, then<\/span><\/i>\u201d, Crofton concluded, \u201c<\/span>Tuberculosis has more right to be considered a\u00a0 true virus than these <\/span><\/i>(25).\u201d So, at a time when viral forms of TB where scarcely being documented, Crofton struggled to link\u00a0 H. Flu with the TB it so often infected in coordination with, as historical and political momentum carried Laidlaw\u2019s study\u00a0 through for posterity. Pfeiffer\u2019s strongly resembled TB; it was just smaller. A great opportunity was missed to correct the\u00a0 record.\u00a0<\/span><\/p>\n

The Name Game<\/b><\/p>\n

After the pandemic of 1918\u201319, the name of Pfeiffer\u2019s bacillus, <\/span>Mycobacterium influenzae<\/span><\/i>, was officially changed to\u00a0 <\/span>Haemophilus influenzae<\/span><\/i>. American bacteriologist Margaret Pittman [83], pinpointed the influenza bacillus\u2019s name change\u00a0\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>82\u00a0<\/span><\/p>\n

to a 1920 report by Charles-Edward A. Winslow and colleagues for the <\/span>Society of American Bacteriologists<\/span><\/i>\u2019 nomenclature\u00a0 committee.\u00a0\u00a0<\/span><\/p>\n

\u00a0<\/span>Figure 34<\/i><\/b>: <\/b>Dr. C.-E. A. Winslow<\/span><\/i><\/p>\n

By any stretch, C.-E. A. Winslow was far from the ideal choice to head a panel to rename <\/span>Mycobacterium influenzae <\/span><\/i>to <\/span>Haemophilus influenzae<\/span><\/i>. Not only was he an avid one-form-only bacteriologist [84], leaving very little room for a\u00a0 microbe which could appear in both fungal and bacterial forms, but his unique thought processes became obvious when, as\u00a0 Professor of Public Health at Yale, he said he believed that posture was a neglected cause of tuberculosis, a disease known\u00a0 since antiquity for its spine-bending changes.\u00a0<\/span><\/p>\n

Yet Winslow and his colleagues decided to ignore Pfeiffer\u2019s bacillus\u2019s previously documented fungal forms, concluding\u00a0 that, unlike the mycobacteria, it stained Gram-negative and liked hemoglobin. But neither was conclusive enough to\u00a0 warrant the name change that Winslow had in mind. Tuberculosis researcher Stephen J Maher of the <\/span>Connecticut State Tuberculosis Commission <\/span><\/i>wrote in 1913: \u201cAll non-acid coccal and bacillary derivatives of the tubercle bacillus are, strange\u00a0 to say, Gram-negative.\u201d [85] Krylow confirmed Maher\u2019s observation that TB could stain Gram-negative, [86] \u2013just like\u00a0 Pfeiffer\u2019s bacillus.\u00a0<\/span><\/p>\n

The Gram stain, developed by Hans Christian Gram, separates bacteria based on their cell walls. The thick layers in\u00a0 \u201cGram-positive\u201d cell walls stain purple, while the thin \u201cGram-negative\u201d cell walls appear pink. Like other bacilli, cultures of\u00a0 TB, on the other hand, could be Gram-positive when young but might become Gram-negative as they aged. Hans Much saw\u00a0 this in 1907 [87], and Chandrasekhar reported it again in 1983 [88]. Therefore, the fact that Pfeiffer\u2019s influenza bacillus\u00a0 was Gram-negative still didn\u2019t rule it out as a bacillary derivative of the tubercle bacillus. Furthermore, the organism was\u00a0 arbitrarily named <\/span>Haemophilus influenzae <\/span><\/i>(from the Greek <\/span>haemophilus<\/span><\/i>, meaning blood-loving), but it grew on the same\u00a0 blood-based cultures on which <\/span>Mycobacterium tuberculosis <\/span><\/i>had long been known to thrive [89].\u00a0\u00a0<\/span><\/p>\n

To many in the lay and scientific communities, bacterial names and classifications are hallowed ground. But Sneath and\u00a0 Brenner\u2019s 1992 paper [90] for the <\/span>American Society for Microbiology <\/span><\/i>clarified that there was no such thing as an official\u00a0 classification of bacteria or \u201capproved lists\u201d and that even Bergey\u2019s Manual was not \u201cofficial\u201d, but merely the best consensus\u00a0 at the time. Therefore, Sneath and Brenner said, bacterial lists and classifications (called \u201ctaxonomy\u201d) are partly a matter\u00a0 of judgment and opinion, as is all science, and, until new information is available, different bacteriologists may legitimately\u00a0 hold different views. In the same vein, George Fox and colleagues remind us that even with regard to today\u2019s sacred 16S\u00a0 rRNA sequence identity as a criterion for species identification, 16S rRNA may not be sufficient alone to guarantee species\u00a0 identity[91]. Today, we are carefully taught that Pfeiffer\u2019s bacillus, historically <\/span>Mycobacterium influenzae<\/span><\/i>, was erroneously\u00a0 thought to have caused and been behind the Great Pandemic of 1918\u201319. We are not taught that Pfeiffer\u2019s bacillus itself\u00a0 has a virus-like cell-wall-deficient phase which goes right through a filter. Nor are we taught that its original difficulty in\u00a0 cultivation on normal media alone, without blood\u2019s hemoglobin, almost classified Pfeiffer\u2019s bacillus, <\/span>a priori<\/span><\/i>, as a \u201cvirus\u201d in\u00a0 the minds of those who relentlessly track a virus as being behind influenza.\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER\u00a0<\/b><\/p>\n

83\u00a0<\/span><\/p>\n

Virology on the Ropes<\/b><\/p>\n

It was in 1952 that Cornelius P. Rhoads, Director of the <\/span>Sloan Kettering Institute for Cancer Research <\/span><\/i>in New York City,\u00a0 remarked in the introduction to a conference on viruses and cancer that the term \u201cvirus\u201d had achieved \u201c<\/span>a high professional\u00a0 status with doubtful credentials<\/span><\/i>\u201d [92]. Rhoads wasn\u2019t alone.\u00a0<\/span><\/p>\n

Papers such as that of Peter Palese [93], of the Mount Sinai School of Medicine in Manhattan, remind us that, even in\u00a0 1992, millions in China already had antibodies to H5N1, meaning that they had contracted it and that their immune system\u00a0 had little trouble fending it off.\u00a0<\/span><\/p>\n

And as Dutch science historian Ton van Helvoort accurately pointed out, by the 1950s the word \u201cvirus\u201d had become so\u00a0 moldable a concept that one could speak of viruses without the existence of any consensus whatsoever of what viruses\u00a0 were [94]. Extremely supportive of this moldability among virologists was biophysicist Max Delbr\u00fcck\u2019s subtitle for\u00a0 \u201cViruses 1950\u201d, a conference held at the California Institute of Technology: \u201c<\/span>Proceedings of a conference on the similarities\u00a0 and dissimilarities between viruses attacking animals, plants, and bacteria, respectively<\/span><\/i>\u201d [95]. Indeed, in the 1930s and\u00a0 1940s, the concept of \u201cfilterable virus\u201d was subjected to such criticism that its very foundations were threatened.\u00a0<\/span><\/p>\n

But in truth, until the late 1940s influenza viruses were studied as infections, which, although filterable, were conceived\u00a0 of as analogous to bacteria, a kind of ultra-bacteria. Not to be deterred, and still seeing Influenza as a great opportunity\u00a0 for virology, in 1941 virologist Hirst [96] claimed that influenza \u2018\u2018virus\u2019\u2019 could agglutinate red blood cells of fowl and other\u00a0 animal species. Hirst showed that \u2018\u2018virus\u2019\u2019 particles first adsorbed to the red cells and, after a certain time, eluted again as\u00a0 a result of what could be interpreted as an enzymatic reaction. But six years later, Middlebrook and Dubos (1948) made\u00a0 this seem nothing more than a cheap hat trick by showing that similarly red blood cell agglutination could be produced by\u00a0 sera from patients with tuberculosis [97]. Takahashi and Ono then reviewed similar red cell agglutination occurring in the\u00a0 presence of tubercular serums [98,99].\u00a0<\/span><\/p>\n

The \u201cH\u201d and \u201cN\u201d of influenza sub-typing, revolves around two glycoproteins called hemagglutinin (HA) and\u00a0 neuraminidase (NA), both of which can be, and are, associated with infectious diseases such as the minuscule, viral forms\u00a0 of tuberculosis, a disease which ought to be high on the differential diagnosis for \u2018flu-like illness\u2019 . Since August, 2008, a\u00a0 Medline study in the <\/span>Journal of Clinical Biochemistry <\/span><\/i>showed that sputum neuraminidase levels over 1.0 mU per mL were\u00a0 proven associated with having tuberculosis in 92% of cases, previous to which bacteria closely related to TB were shown,\u00a0 through crystallization, to produce the same protein neuraminidase used to subtype \u2018Influenza\u2019 [100]. Furthermore, as\u00a0 of 2006, it has become obvious in Menozzi\u2019s study that similar to Influenza, tuberculosis not only uses hemagglutinin to\u00a0 attach to the lung\u2019s epithelial cells it invades, but requires hemagglutinin for dissemination of the disease to the rest of the\u00a0 body [101].\u00a0\u00a0<\/span><\/p>\n

There was much the same \u201cInfluenza\u201d talk when in 1990, a new multi-drug-resistant (MDR) tuberculosis outbreak took\u00a0 place in a large Miami municipal hospital. Soon thereafter, similar outbreaks in three New York City hospitals left many\u00a0 sufferers dying within weeks. By 1992, approximately two years later, drug-resistant tuberculosis had spread to seventeen\u00a0 US states, with mini-epidemics in Florida, Michigan, New York, California, Texas, Massachusetts, and Pennsylvania and\u00a0 was reported, not by the American, but the international media, as out of control. By 1993 the <\/span>World Health Organization\u00a0<\/span><\/i><\/p>\n

(WHO), proclaimed tuberculosis a global health emergency, an emergency which since then it has never lifted.\u00a0<\/span><\/p>\n

To say that the history of the theoretical underpinning of virology has been a tortuous one is probably an\u00a0 understatement, and, incredibly, many virologists even to this day persist in using the flawed reasoning that that which\u00a0 passes through a microfilter is a virus. Certainly, one exception to these is virologist\/molecular biologist Stefan Lanka,\u00a0 who questions the very existence of H1N1 and its allied forms as a swine flu virus altogether. Lanka, after reviewing the\u00a0 data, came to the conclusion that studies, micropictographs and even the data have been manipulated. Through personal\u00a0 communication, he has assured this author that his repeated investigative letters to the <\/span>National Institutes of Health <\/span><\/i>(NIH)\u00a0\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>84\u00a0<\/span><\/p>\n

regarding supportive material for the \u201cinfluenza virus\u201d have gone unaddressed and unanswered [102]. Virologist Lanka\u00a0 therefore concludes that the pictures the CDC is showing are liposomes from dead cell cultures that have been reduced,\u00a0 and then centrifuged with a solvent. In addition he feels that US attempts that supposedly wrested a virus from cadaver\u00a0 specimens were contrived and deceptive.\u00a0<\/span><\/p>\n

\u00a0<\/span>Figure 35<\/i><\/b>: <\/b>Influenza from CDC showing these as the H1N1 virus.\u00a0<\/span><\/i><\/p>\n

\u00a0<\/span><\/i>Figure 36<\/i><\/b>: <\/b>A Liposomal Delivery System<\/span><\/i><\/p>\n

Shannon Brownlee and Jeanne Lenzer are not new to writing sharp warnings regarding public health. Among their\u00a0 writings listed on Medline is a <\/span>British Medical Journal <\/span><\/i>treatment entitled \u201c<\/span>Doctor takes \u2018march of shame\u2019 to atone for drug\u00a0 company payments<\/span><\/i>\u201d [103]. That influenza vaccination and oral antiviral studies have been consistently pushed and paid\u00a0 for by pharmaceutical companies themselves is no secret. But once in a while, unsponsored papers such as Brownlee and\u00a0 Lenzer\u2019s 2009 article in The Atlantic clear the misinformation:\u00a0<\/span><\/p>\n

\u201c<\/span>Whether this season\u2019s swine flu turns out to be deadly or mild, most experts agree that it\u2019s only a matter of time before\u00a0 we\u2019re hit by a truly devastating flu <\/span><\/i>[or coronavirus] <\/span>pandemic \u2014 one that might kill more people worldwide than have died of\u00a0 the plague and AIDS combined. In the US, the main lines of defense are pharmaceutical\u2014vaccines and antiviral drugs to limit\u00a0 the spread of flu and prevent people from dying from it. Yet now some flu experts are challenging the medical orthodoxy and\u00a0 arguing that for those most in need of protection, flu shots and antiviral drugs may provide little to none. So where does that\u00a0 leave us if a bad pandemic strikes?\u2026<\/span><\/i>\u201d [104]\u00a0<\/span><\/p>\n

Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>85\u00a0<\/span><\/p>\n

The authors added: \u201c<\/span>But what if everything we think we know about fighting influenza <\/span><\/i>[or coronavirus] <\/span>is wrong? What\u00a0 if flu vaccines do not protect people from dying \u2013particularly the elderly, who account for 90 percent of deaths from seasonal\u00a0 flu? And what if the expensive antiviral drugs that the government has stockpiled over the past few years also have little, if\u00a0 any power to reduce the number of people who die or are hospitalized? The US government\u2014with the support of leaders in\u00a0 the public-health and medical communities\u2014has put its faith in the power of vaccines and antiviral drugs to limit the spread\u00a0 and lethality of swine flu. Other plans to contain the pandemic seem anemic by comparison. Yet some top flu researchers are\u00a0 deeply skeptical of both flu vaccines and antivirals. Like the engineers who warned for years about the levees of New Orleans,\u00a0 these experts caution that our defenses may be flawed, and quite possibly useless against a truly lethal flu. And that unless we\u00a0 are willing to ask fundamental questions about the science behind flu vaccines and antiviral drugs, we could find ourselves, in\u00a0 a bad epidemic, as helpless as the citizens of New Orleans during Hurricane Katrina<\/span><\/i>.\u201d\u00a0<\/span><\/p>\n

This paper has intentionally questioned perhaps the most fundamental question about the science behind influenza\u00a0 and its vaccine and antiviral cures: is it really a virus at all? For if it is indeed a form of viral, cell-wall-deficient mycobacteria\u00a0 such as <\/span>Mycobacterium influenzae <\/span><\/i>or <\/span>Mycobacterium tuberculosis<\/span><\/i>, or <\/span>Mycobacterium avium<\/span><\/i>, as many physicians and scientists\u00a0 in the past have suggested, we could indeed find ourselves in the midst of another devastating, infectious Hurricane\u00a0 Katrina, worldwide.\u00a0\u00a0<\/span><\/p>\n

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    Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

    The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>86\u00a0<\/span><\/p>\n

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      Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

      The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>87\u00a0<\/span><\/p>\n

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        Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

        The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>88\u00a0<\/span><\/p>\n

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          Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

          The Great Influenza Pandemic: What Really Happened in 1918? BROXMEYER <\/b>89\u00a0<\/span><\/p>\n

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            Citation: <\/i><\/b>Dr. Lawrence Broxmeyer MD. \u201cThe Great Influenza Pandemic: What Really Happened in 1918?\u201d <\/span>Pulmonology Research and\u00a0 Respiratory Care <\/span><\/i>1.2 (2017): 53-89. DOI: 10.5281 ZENODO. 1044179\u00a0<\/span><\/p>\n

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