Pfieffer’s influenza bacillus, a bacteria, was heavily isolated at one time or another in 1918 victims by practically all major research centers in the United States. It was therefore considered, by most, to be the cause of influenza until at least 1933. And Bradford’s, Bashford and Wilson’s 1919 influenza isolates, although easily passing through a filter, where again minute bacteria, isolated from blood and sputum in a number of cases. Their nearest competitor – a vague “filterable virus”.  

Although the term virus has existed since 1898, the infectious agent it was attempting to describe was so unclear and mysterious that for many decades scientists considered it purely theoretical. Certainly, even by 1917 “influenza” was still not felt to be serious enough to be a reportable disease and no doctor had to report it to state or local health officials. Most cases where self-limiting and gone in 10 days.  Yet the great “influenza” pandemic that swept the world in 1918–19 may have been the most virulent outbreak in history, at least in terms of the swiftness of its devastation. It killed more than 20 million persons around the world, including some 550,000 in the United States—all within two years.

By 2000 Dr. Andrew Noymer and Michel Garenne, UC Berkeley demographers, thought they knew just why this perceived discrepancy existed, reporting convincing statistics showing that undetected tuberculosis may have been the real killer in the 1918 flu epidemic. [1] Aware of recent attempts to isolate the “Influenza virus” from human cadavers and their specimens, Noymer and Garenne concluded  that: “Frustratingly, these findings have not answered the question why the 1918 virus was so virulent, nor do they offer an explanation for the unusual age profile of deaths”.

Somehow overlooked in today’s revisionist history of the flu, the influenza bacillus or Pfeiffer’s bacillus, discovered by Pfeiffer and Canon in 1892, was originally named Mycobacterium influenzae because it was thought to be related to Mycobacterium tuberculosis. Both mycobacteria stained best with carbol-fuchsin and methylene blue, bacterial stains that Koch himself used in the discovery of tuberculosis. Also Grassberger [2] observed  the same branching fungal forms in Pfeiffer’s mycobacteria  as Metchnikoff [3] had first saw in tuberculosis.

Such fungal-like forms are the hallmark of the mycobacteria (their prefix “myco” means fungal). Mycobacteria such as tuberculosis are particularly deadly precisely because they share properties of the fungi  as well as bacteria. TB was, not all that long ago, referred to as “Captain of the Men of Death”, a caption oddly used recently by a popular modern flu historian to describe “Influenza” during 1918.

Recently Tekaia of Pasteur, looking for “overall gene similarities as signatures of common ancestry” found similar genetic profiles and sequencing for Pfeiffer’s bacillus (Mycobacterium influenzae) and Mycobacterium tuberculosis, lumping them together in the same “well-defined group”. [4] Tekaia’s diagrammatic genomic tree shows the two organisms directly next to one another.

This reopened the historical argument that Pfeiffer’s and tuberculosis are related.

In the very year that Laidlaw, Andrewes and Smith claimed stake to the discovery of the human influenza “virus”, Stobie,  in The British Medical Journal,in 1933, still acknowledged the argument not for a virus, but that the real nature of “influenza” could well be a form of Mycobacterium tuberculosis.  Stobie simply reflected the active, vigorous, yet historically suppressed debate that had been raging in medical journals for decades. [5] He mentions cases of tuberculosis following influenza which together exhibited “a sinister type of disease which rarely responded to treatment.” Enter ‘galloping consumption’, the most devastating form of tuberculosis, then called consumption.

 

The Influenza Wards, Obuchow Hospital, St. Petersburg, 1890

In 1890, world-wide, a fierce “influenza” pandemic struck, killing many.  Occurring at the end of the nineteenth century, this second most severe influenza to ever hit the world, occurred at a time when there was fear that tuberculosis would destroy the civilization of Europe. 

Twenty-eight years later, those who survived that pandemic and lived to experience the Great Pandemic of 1918, tended to be less susceptible to the disease. But the lessons of 1890 were poorly understood, and therefore not carried over to 1918.

Of all the forms of “influenza” known in 1890, none was more dreaded and stuck terror into the hearts of victims and their families then that described by Wiltschur [6] as “galloping consumption”. An attending at the Obuchow Hospital, Wiltschur tells what happened when influenza punctuated previous or active cases of tuberculosis: “The (influenza) patients were, for the most part, still well nourished”. This mirrored the swine flu episode of 1918 where young healthy soldiers were suddenly decimated by disease. Wiltschur continued: “Cyanosis of the face and extremities was a frequent occurrence.” Patients exhibited severe difficulty in breathing (dyspnea), an extremely high temperature not characteristic of the flu, pulmonary hemorrhages, a rapid progression of lung disease, “with death occurring in many instances unexpectedly and suddenly.”

Why these findings,  including the well-known rapid fatality of “galloping consumption”,  with its high fever, profuse hemorrhaging, brownish spots or splotches on the face, strawberry tongue, and typhoid-like symptoms……..  documented so clearly in and after the Pandemic of 1890, were ignored by the historians, scientists and practitioners of 1918 is beyond comprehension.

René Dubos of Rockefeller would later confirm the galloping acceleration between influenza and tuberculosis in the laboratory. [7]  Historian/researcher Dubos also assured us that galloping consumption was not an isolated, but a frequent diagnosis in the nineteenth Century. [8]

Despite persistent myths to the contrary, In the early phase of any new TB epidemic, perhaps from a new strain, tuberculosis manifests itself as an acute, generalized disease, and only much later the chronic pulmonary tuberculosis we know in today’s Western world. An example can be found in the high mortality during the 1918 ‘‘Influenza” pandemic, when African American’s were brought to fight in France during the World War I, large numbers of them dying from the accelerated tubercular ‘‘galloping consumption” of yesteryear. [ibid] But was it only this specific group that was affected circa 1918? There has been much documentation that in certain cases, depending on the virulence of the tubercular strain, that the infection can spread rapidly, causing a disease both acute and fatal, with signs and symptoms so unspecific that a proper diagnosis is impossible to make.

 

Department of Pathology and Bacteriology, University of the Philippines College of Medicine March 1918

By 1918, an important study appeared in Rockefeller Institute’s Journal of Experimental Medicine. [9] Physician Herbert Windsor Wade, an American investigator working out of the Department of Pathology and Bacteriology at the University of the Philippines’s College of Medicine and Surgery, doubted that a virus had anything to do with Influenza.

Pfeiffer continued to insist that his organism “had the best claim to serious consideration as the primary etiologic agent (cause), and its only competition is an unidentified filterable virus.” [10] Had Pfeiffer studied Wade and Manalang’s laboratory evidence, his reply  would have been quite different. Pfeiffer’s bacillus itself had a filterable virus-like form that could easily be mistaken for a “filterable” influenza “virus”.

Wade remained a voice of scientific reason throughout the 1918 Influenza pandemic, during which he personally experienced a scourge in which, depending upon the province in which he visited, from forty to ninety-five percent of Filipinos contracted the disease. At least 70,000-90,000 of them had already died. Wade knew what it was like to come into a village where there were not enough living to bury the dead. Also, being far from the United States, he was not subject to the relentless censorship of the Wilson administration, both against civilians and scientists of the Army medical corps itself. If he saw mycobacterial forms similar to those of TB in Pfeiffer’s influenza bacillus, he could and would report them without fear of being accused of fueling the flame of hysteria. And in documenting tuberculosis-like fungal forms in previously filtered Pfeiffer’s, that is exactly what Wade did.

On his deathbed, Louis Pasteur’s conscience finally overtook him, forcing him to admit that his great rival, French biochemist and M.D. Antoine Bechamp had been correct, and that he had been wrong.  Not only were microbial forms changeable, as he had documented, but they depended upon the culture media or the environment in the body’s terrain. So with his last dying breath Pasteur whispered “The terrain is everything………….”. [11] And nowhere had this become more obvious than with the mycobacteria, in which, depending upon the culture media used, either fungal or bacterial elements could be grown out. Wade’s media grew out fungal forms, after its spores went through a filter. They were therefore “filterable”, but they were not ‘viruses’.

In the words of microbiologist Milton Wainwright, Wade and Manalang had now committed “the ultimate pleomorphist heresy”, [12] documenting that a bacteria or mycobacteria could have more than one form in its life cycle.

Pfeiffer himself, when he discovered his bacillus, had seen these same forms, but described them as “pseudo” influenza. Pfeiffer simply failed to see both forms of his discovery as one and the same, central to the nature of his influenza bacillus.

It was no mistake that Wade and Manalang’s paper was published at Rockefeller in 1919. Simon Flexner, then director at Rockefeller Research, once followed similar acid-fast fungal forms associated with tuberculosis and found this similar association with the influenza bacillus fascinating. Flexner had called his filterable fungal forms inside TB “pseudotuberculosis”. [13]

Flexner was a key figure in the 1918 Pandemic, heavily influencing both Rockefeller research and America’s struggle with devastating disease. Why had not he, or any of the other close-knit band of major scientific researchers in the pandemic-stricken U.S., taken the cue of Wade’s study and run with it. The possible link between mycobacteria and their filterable forms could have quelled the controversy that swirled around whether influenza was bacterial or viral.  Even the British Medical Journal had suggested this.

The answer is that one researcher had. But since he wasn’t a member of the US scientific hierarchy, he would be ignored. His name: Dr. Victor Conrad von Unruh.

 

New York Medical Reserve Corp; Office of Captain Victor Conrad von Unruh, MD; September 1917

Physician-researcher Victor Conrad von Unruh was born in 1868 Dahlewitz Germany at a time when German medical research and science were unrivaled. Immigrating to the U.S., by 1917 Von Unruh received the commission of Captain in the New York Medical Reserve Corps. The Pandemic of 1918 was about to hit, hard. Von Unruh’s “A comparative Study of the Acid Fast Bacilli” appeared two years prior to the killing fields of 1918. [14] To this day, his study appears in the Catalogue of the Library of The Surgeon General’s Office – United States Army, 1920, a reminder for posterity.

Because Pfeiffer’s bacillus stained acid-fast, von Unruh, like others, had been evaluating what medical texts such as Stengel’s [15] referred to as Mycobacteria Influenzae, also known as Bacillus Influenzae. The entire influenza group was felt to be caused by this acid-fast mycobacterial bacilli, which was similar to the tubercle bacillus. Both microbes had fowl, swine and human forms. 

Von Unruh never saw the need to look for a “filterable virus” or “influenza” in the thousands of hogs that died abruptly with flu-like symptoms just before the pandemic as did virologist Richard Shope. Why should he? Shope, the American virologist credited with the first isolation of the influenza “virus”, seemed oblivious to the fact that more than 60% of hogs circa 1918 were tubercular from fowl TB, a fact that gave breeders of hogs such concern that large scale efforts where underway to rid farms and chicken flocks of avian tuberculosis. The situation had become so grave in hogs and cattle that by 1917, one year before the most destructive pandemic ever, the Cooperative State-Federal Tuberculosis Eradication Program, administered by the US Department of Agriculture (USDA) and Animal and Plant Health Inspection Service (APHIS),  had to be instituted. For in 1917 it was estimated that 25% of deaths from tuberculosis in adult humans were caused by animal tuberculosis. [16] Nor did the fact that swine freely infected humans and vice versa faze von Unruh. Swine where a mycobacterial laboratory, and although they held primarily fowl tuberculosis they could also acquire bovine and human forms, and freely infect people.

In A Comparative Study of the Acid Fast Bacilli, Von Unruh, brought things a step further. The many cases of influenza he had investigated contained both the resting (dormant) form of TB and the influenza bacillus. Although Pfeiffer had likewise documented chronic colonization with his bacillus in TB patients, von Unruh saw this, and the fact that they were both mycobacteria as more suggestive of “a  common ancestry or origin”.

Von Unruh: “We have in influenza the fever, malaise, loss of weight, invasion by the organism of the same anatomical structures as in tuberculosis; we have chronic cases of bronchitis in which the influenza bacillus is constantly present; and lastly, we know that typical tuberculosis often follows an attack, however mild, of influenza.”

Such tubercular infection could in turn lead to other secondary bacterial infections. Noymer and Garenne’s [Ibid] statement that tuberculosis was behind the many deaths in the  pandemic of 1918, was specifically based upon the well known concept that the secondary bacterial infections that cropped up in 1918 are common in TB-infected lungs. Noymer: “It is highly plausible that TB infection laid the ground for the massive secondary bacterial pneumonias that killed the victims of the flu in 1918.” [Ibid]

 

The Reichsgesundheitsamt, Berlin March,1882

Although it has always perplexed doctors, scientists and historians alike as to why so many microbes where involved during the deadly 1918 epidemic, the explanation was laid out clearly by Robert Koch, discoverer of tuberculosis, decades before.

From the onset Koch concluded [17] that other microorganisms shared in the destructive work of the tubercle bacilli. Gaffky, Pansini, Cornet, Spendgler, Schabad, Sata, Ortner, and Flick, among others, agreed. [18]

Various organisms, all of which reappeared to confuse scientists in 1918 were assigned a share in the clinical picture of tuberculosis – among them the streptococcus, the pneumococcus, and even the influenza bacillus itself. The pyogenic, pus forming cocci were more generally suspected as complicating tuberculosis than other bacteria. In the British Medical Journal for July 28, 1900, the following Editorial appeared, dealing with the role of streptococci in tuberculosis: “It is a remarkable fact that………the bulk of the disturbing and dangerous  features of tuberculosis are not due to the tubercle bacillus, but to streptococci and other pyogenic organisms.” The pneumococcus, Staph and methycillin resistant staph (MRSA) are other pyogenic pathogens that have been subsequently documented.

William Crofton chafed at the ridiculous notion that in influenza, Pfeiffer’s bacillus and only Pfeiffer’s bacillus should alone be found in pure cultures. Was, he asked, the typhoid bacillus ever found in pure cultures? But because Pfeiffer’s was often found with the very same infections secondary to tuberculosis, such as streptococci and pneumocci, investigator after investigator during the Great Pandemic of 1918 was coming to the curious conclusion that Pfeiffer’s was not the primary cause, but somehow awakened to activity by some unknown primary cause. They never for a moment considered that that unknown primary cause could be tuberculosis, which not only spawned secondary infection with strep, staph and pneumocci, but Pfeiffer’s itself. Besides this, the obvious. Microbes like the Streptococci, Pneumococci or Staphylococci could produce epidemics, but never pandemics. Where was the confusion coming from?

 

New York Medical Reserve Corp; Office of Captain Victor Conrad von Unruh, MD; July 1918

Victor Von Unruh continued to see many reasons to pin a common ancestry on the two organisms. Both the influenza bacillus and quiescent TB formed Much’s granules. Much’s granules, named after their discover Hans Much,  passed through filters, then a major criteria for diagnosing a virus. Furthermore, both the Influenza bacillus and TB where mycobacteria, with the branched fungal forms characteristic of the mycobacteria. And both could stain with “acid-fast” mycobacterial stains.

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“Therefore my conclusion is that the influenza bacillus is merely a weaker or dwarfed form of the real tubercle bacillus, a strain that in this case failed of better development because of a higher degree of resistance in the host. In both tuberculosis and influenza we deal with the self-same organism that in tuberculosis is fully developed, while in influenza it lacks development. In other words, we are dealing with a difference in degree only, but not in kind.” [Ibid]

Von Unruh’s distinction is suggestive of a similar well acknowledged comparison between the damaging effects that Mycobacterium tuberculosis has, for centuries, inflicted on man in comparison to the better resistance that humans with a healthy immune system have had against bird or fowl tuberculosis (Mycobacterium avium), found in swine as well. Did forms of fowl tuberculosis in the form of Mycobacterium (Haemophilus) Influenzae suis from pigs combine additively with latent human tuberculosis to cause the deadly galloping consumption of 1918?

Victor von Unruh’s findings could have been  taken lightly, were it not for similar thoughts in the more prestigious medical journals of his time.

 

Bureau of Laboratories, Department of Health, New York City, 1918

Something was eating at Physician/researcher/Editor William Park during the carnage of 1918. Park, heading the state-of-the-art New York Bureau of Laboratories, was relied upon by both the US Government Health Corps and other major research centers across the country. Park, along with collaborator/bacteriologist Anna Williams, co-authored the important teaching text Pathogenic Microorganisms. Park at first blamed Pfeiffer’s bacillus for 1918 and reported it to the U.S. Army Health Corps. But flustered by the secondary infections, and lack of consistency in other labs in isolating Pfeiffers, Park flip-flopped, cautioning against attributing the pandemic to Pfeiffer’s solely.

By the same token Park felt uncomfortable with the muzzling of the media and medical corps by the Wilson administration regarding the ferocity of the 1918 American epidemic in general. That is until it was too late to deny its viciousness.

So although Pfeiffer’s influenza bacillus, also known as Mycobacterium influenzae, was no longer at the top of his choices for the causal agent of the 1918 pandemic, it was its association with another mycobacteria, tuberculosis, which bothered him most.  He had just put down Flicks account of what preceded both Great Pandemics.

In the United States alone, Lawrence Flick, citing census reports leading into the two greatest world “influenza” pandemics in history, reported that out of every 1,000,000 US deaths: 242,842 males and 302,046 females died of tuberculosis. This was for all nationalities and colors. Specific subsets within these statistics revealed that among African-Americans every million deaths represented 248,179 males and 326,973 females as having died of tuberculosis. Among people of Irish parentage, 309,507 males and 375,636 females died of TB for every million deaths. And among people of German parentage its victims numbered 249,498 males and 254,958 females for every one million deaths. [19] Although Park had seen these statistics before, their effect was not lost on him. Park[20]: “Consumptives (people with tuberculosis) frequently carry influenza bacilli (Pfeifer’s bacilli) for years and are particularly susceptible to attacks of influenza.”

In 1918, with “flu” victims dropping all around them, John B. Hawes, MD of the Massachusetts General Hospital and Richard Cabot MD of Harvard wrote:”One of the diseases most frequently mistaken for pulmonary tuberculosis is influenza, chronic or acute.”  According to Hawes and Cabot, the symptoms of both diseases were often identical. [21]

Tufts Pulmonologist Edward O. Otis also caught Park’s attention. [22] Otis not only mirrored Hawes and Cabot’s view, he went a step further: “Often a patient gives the history of a previous attack of influenza which may have been an active outbreak of a latent tuberculous focus, which latter again became inactive.”

The Journal of  The American Medical Association [23]  specifically cited Liverpool Physician R. Buchanin: “Dr. R.J.M. Buchanan makes the not improbable suggestion that many of the so-called sporadic cases of influenza are really symptomatic of the initial infection of tuberculosis, or possibly an exacerbation of a latent tuberculosis previously unsuspected or undetected.”

In saying this, Buchanan had fired the shot heard around the world, and physician Walter Lindley, editor of the Southern California Practitioner, was quick to respond. [24] Lindley on Buchanan: “The author, impressed by the large number of instances in which patients have referred the commencement of their ill-health to an attack of so-called influenza, conceives that many of the so-called sporadic cases of influenza are really symptomatic of the initial infection of tuberculosis or possibly an exacerbation of a latent tuberculosis.”

Lancet’s complaint [25]  regarding an epidemic of infectious fever raging in New York, is also appropriate. The Lancet: “The name “influenza” seems to have  a strong attraction for some people. Every ache and pain, no matter where located and whether accompanied by fever or not, is at once put down as “influenza”; every headache, every coryza (nasal congestion, common cold), every sore-throat, every attack of gastroenteritis, from whatever cause is promptly self-diagnosed as “influenza,” and when the practitioner arrives upon the scene he will be expected to fall in with this view, and there is a great temptation to do so.” Lancet goes on to doubt that the rise in temperature and general malaise frequently met with in this New York epidemic was influenza at all.

Hendrickson , who practiced during the Great Pandemic of 1918, spoke more bluntly: “No doubt there were many cases of tuberculosis whose death certificates were labeled influenza during the pandemic owing to lack of time to make a diagnosis by the overworked physician.” [26]

Hendrickson reiterates that when an attack of influenza intervenes in a patient suffering from pulmonary tuberculosis, the tuberculosis process is likely to be aggravated “and very often terminates fatally in a comparatively short time.” Of more vital interest, even in the cases of dormant healed TB in which the individual has contracted the disease in childhood, he quotes Osler as Influenza being “an important exciting cause” of latent Tuberculosis. [27] At the same time Hendrickson clarifies why in certain army barracks in 1918, measles in marked analogy to influenza, could also cause the reactivation and rapid spread of dormant tuberculosis.

By 1920, with the killing fields of 1918 laid out before him, UK physician Marcus Paterson took still another jab at the “flu” epidemic. [28] Paterson: “During the time I was Resident Medical Officer at Brompton, it was usual to classify a rise of temperature in an ordinary case of “chronic” pulmonary tuberculosis as influenza, even when there was no epidemic.”

As for the well-known sick feeling (malaise) and preliminary symptoms of reactivated tuberculosis, Paterson asked: “Are these symptoms any different from those of the ordinary onset of Influenza? They are not, simply because they denote, not a particular disease, but a toxemia due to bacterial action.” [Ibid]

Paterson’s reference to the confusion of sorting out  influenza from TB  gets pointed:  “Surely there is no more emphatic testimony to the clinical difficulties of a differentiation between the two diseases when one group of clinicians describes a rise of temperature in a proven case of tuberculosis to be influenza, and another section terms an arrested case of tuberculosis with pyrexia (fever) an active case of tuberculosis.”

Speaking in 1920, after the greatest pound for pound health catastrophe ever, Patterson said what every physician still learns as a resident: “Before the war, it was usual to classify a sudden onset of acute symptoms as influenza, and it is very easy to appreciate the reason.  When a person is taken ill, the patient’s friends demand to know at once what is the ailment: hence it must be given a name, and “influenza” is a good enough term for the moment”. [Ibid]

What Paterson leaves out, as a given, is the hysteria in the family and immediate community that would intrude were the diagnoses of tuberculosis rendered. Instead he summarizes that he knows of no physician who can differentiate clinically between tuberculosis and influenza. And he “shudders to think” of the number of times that “tubercle bacillus have been classified as influenza without further investigation”. To Paterson, this represented countless opportunities to cure the real cause, masked under the designation “influenza”. His conclusion: “There is no research required here. It is a known fact that what is at present called influenza is often tuberculosis. But the knowledge is not practically applied. It is information of inappreciable value lying idle. It is no new discovery, or its import would ring throughout the world.”

In fact, for Paterson, much like for von Unruh, “influenza” was simply the first indication of tuberculosis. [Ibid p.224]

Many years later, well after influenza was proclaimed “a virus”, influential Johns Hopkins head of Pathology, Arnold Rich, summed things up best: “In relation to the question of the effect of influenza upon tuberculosis, it should be pointed out that in many cases in which pulmonary tuberculosis has been thought to have followed an attack of influenza it is altogether probable that the supposed attack of influenza was, in reality, a manifestation of an existing tuberculous infection; for tuberculoprotein, whether absorbed from a spreading lesion or injected into the body, can cause constitutional symptoms (fever, malaise, headache, joint pains, anorexia, prostration) quite like those of influenza.”[29] Rich concluded: “The writer has seen attacks closely simulating influenza occur in healthy, tuberculin-positive laboratory workers as a result of the accidental inhalation of the vapor of boiling tuberculin”. [Ibid v. Chapter XI]

 

Department of Animal and Plant Pathology, The Rockefeller Institute for Medical Research, New York, 1931

Richard E. Shope was in direct communication with UK investigators Smith, Andrewes and Laidlaw at Mill Hill and sent samples of his flu virus and Pfeiffer’s bacillus. But the English group , in return, wasn’t being 100% supportive.

Virologists like Shope and Laidlaw of the British group saw a great opportunity provided by the 1918 pandemic for virology.  Shope began the first salvo on swine ‘‘influenza”, again falling back on the stale conception that the mild disease and flu-like symptoms created in pigs by what he felt to be a filterable virus [30]. Shope had the singular advantage of realizing that since 1918, pigs had been coming down with the same ‘‘Influenza” each year. Having lived in Iowa, he had grown up with the knowledge. But beginning his investigations in earnest, Shope became perplexed. Not a virus, but a bacteria kept cropping up in swine’s mucous secretions and it resembled the Pfeiffer’s bacillus or Haemophillus Influenza (H. Flu) more than anything else. The problem was he couldn’t infect most of his subjects with the bacteria. So he took the mucous secretions of sick pigs and put it thru a filter which he felt would only yield a virus. However, incredibly, even the filtrate from the discharge just gave low grade symptoms. So if it wasn’t a ‘‘virus” that had caused the deadly strains of flu and it wasn’t the bacteria present in most malignant ‘‘flu”…..what could it be? To Shope, possibly both, working in conjunction with one another. So he introduced both into animals which subsequently came down with just the deadly ‘‘flu” complicated with pneumonia that killed between 20 and 100 million people in 1918.

As late as 1944, Shope insisted that pandemic influenza was this meld of “virus” plus Pfeiffer’s bacillus. [31] But opposed to today’s revisionist history, the idea wasn’t really his. When Shope was a teenager, the announcement that hog cholera [swine flu] was due to the combined action of a bacterium and a virus, stimulated Felix d’Herelle in 1917 to publish his discovery of bacteriophages, viruses which live in and can destroy or alter the shape of bacteria…………followed by d’Herelle’s classic book on such bacterial viruses in 1921. [32]

Actually Richard Shope had switched his interest from tuberculosis to virology only well after joining the Rockefeller institute. And originally he was looking for simply a bacterial cause such as Pfeiffer’s bacillus for “swine influenza” 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’s bacillus), which also appeared ‘viral’. To accept Shope, an exception had to be made. That there wasn’t a single cause behind 1918, but two: a virus and a bacteria.

 

His Majesty’s Medical Research Committee, Virology section, A farm near Mill Hill 1932

British virologists Smith, Andrews, and Laidlaw had started out by falsely trying to link the virus which caused dog distemper to human influenza. Nor was the fact lost on many that British virologist Patrick Playfair Laidlaw’s group, seemed to directly fly in the face of Shope’s multi-factorial conclusion, which said that both a virus and Pfeiffer’s bacillus from swine were necessary to acquire the flu.  Just the “virus” itself was necessary claimed the British trio. [33]

Christopher Howard Andrewes, who would subsequently receive the lion’s share of credit for discovering the human influenza virus, thought that he had discovered the viral cause of rheumatic fever at the Rockefeller Institute as far back as 1923. [34] When that didn’t pan out, and back in England, he, similar to Shope in America, put his efforts into finding the virus behind cancer. Again this proved wrong. But when Walter Fletcher, first secretary of Britain’s MRC (Medical Research Committee) started a new program, Andrews soon found himself at Mill HIll under virologist Patrick P. Laidlaw and his colleague Wilson Smith. Originally founded as a consequence of the recommendations of the Royal Commission on Tuberculoses, the Medical Research Committee under Fletcher had apparently gone viral.

The attentions of Andrewes and Smith were soon drawn to an influenza epidemic in their midst and they worked out a plan of action designed to reveal their hypothetical virus. In the midst of this Andrewes began to feel unwell with flu-like symptoms. Immediately, Smith, having passed Andrewes respiratory secretions though a filter, began to inject these intracerebrally and intratesticularly into mice, rabbits, and guinea pigs. Nothing happened immediately but just afterwards Laidlaw was informed by the director of Wellcome laboratory, one of their reference labs, that some of their Ferrets appeared to be suffering from influenza at the same time the epidemic of influenza was raging among Wellcome’s staff. It turned out that these Wellcome ferrets didn’t have influenza, but suffered from distemper.

Not to be dismayed, Smith then inoculated several  other ferrets through the nose with filtrates from Andrewes, and shortly afterwards influenza appeared. Subsequently Wilson Smith himself came down with a flu that the rest of the group suspected was from a ferret. From the filtrate of this the strain WS (Wilson Smith) was isolated. All of these experiments were carried out at a farm near Mill Hill.

But, as head of a government lab, Dr. William M. Crofton had actually examined the famed WS strain that Wilson Smith came down with. Today, this is still being used in research, bearing the alphanumeric notation A/WS/1933, for Influenza A/Wilson Smith/1933.

Crofton, of all people, knew that there was nothing “viral” about the WS strain, nor anything to do with “influenza”. During the summer of 1918, and winter as well, he was isolating Pfeiffer’s bacillus from 100% of cases of influenza. But to do so he was using improved special growth agents, and a sufficiently high powered microscope. Crofton’s “moist-chamber method” kept his culture medium warm and moist. If the microbe wasn’t kept warm, Crofton found, then it couldn’t be isolated in every case. Pfeiffer’s bacillus was clearly pleomorphic (many forms) with viral-like forms that could easily pass a filter. So in 1938, he cornered Andrewes, who was presenting a paper before the Epidemiological Section of the Royal Society of Medicine:

“I asked him how then he knew that his colleague Wilson Smith, from whom was first isolated the virus, had, in fact 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 influenza had been discovered. I told him that I had ascertained that Wilson Smith had, in fact, influenza, because he was swarming with (bacterial) influenza bacilli. I asked him why no cultures on proper medium were made from the infected ferret to ascertain if the Pfeiffer bacillus could be grown, as it would have been inevitably, if, in fact, influenza had been transmitted. Andrews replied not one word and the authorities of the section would not publish my criticism.” [35]

Apparently, the fix was already in through powerful governmental forces at Mill Hill’s MRC. Christopher Andrewes, flushed with victory, suggested, with the help of Burnet and Bang, that the term “myxovirus”, meaning “mucous virus”, be incorporated into a family name for the influenzas. This, one imagines, was because the organism came from mucous secretions.

By May of 1935 Laidlaw, in an article seemingly titled to assure himself (“Epidemic Influenza: A Virus Disease”), would give the only credence he saw fit to Crofton and the many scientists like him, by saying that although he felt that it was “gradually” being proven that a “filterable virus” was primarily responsible for epidemic influenza, that: “Pfeiffer’s bacillus or Haemophilus influenzae is still regarded by many observers as the prime cause of the disease and many of its complications.” [36]

William M. Crofton was convinced by scientists like Calmette at Pasteur that like Pfeiffer’s, certain forms of another mycobacterium, tuberculosis, appearing both minuscule and viral, could pass through the smallest of filters. (IBID) So, at a time when viral forms of TB where scantily being documented, Crofton struggled to link Pfeiffer’s bacillus with the TB it so often infected in coordination with. Pfeiffer’s strongly resembled TB, it was just smaller.

 

The Rockefeller Institute for Medical Research. Office of Margaret Pittman, Ph.D. January 1933

After the pandemic of 1918, Pfeiffer’s Bacillus or Mycobacterium influenzae’s name was officially changed to Haemophilus influenzae. Bacteriologist Margaret Pittman, [37] who later defined the two major strains of H influenzae: encapsulated and  unencapsulated,  pinpoints the influenza bacillus’s name change to CEA Winslow’s 1920 Committee of Nomenclature of the American Association of Bacteriologists.

In the same Rockefeller paper Pittman admits that pleomorphist Philip Hadley, poster scientist for the many forms in bacterial life cycles, had contributed “new and important knowledge concerning variations in bacteria”, knowing full well that her own findings on the different virulence of “smooth” and “rough” forms of H. Influenzae were probably held up for decades by the extent to which Koch and CEA Winslow’s monomorphist dogma held sway.

By any stretch, CEA Winslow was far from the ideal choice to head a panel to rename Mycobacterium influenzae to Haemophilus Influenzae. Not only was Winslow an avid one-form only bacteriologist [38] which left very little room for a microbe which could appear in both fungal and bacterial forms, but his unique thought  processes had became obvious when as Professor of Public Health at Yale, Winslow said he believed that posture was a neglected cause of tuberculosis, a disease known since antiquity for its spine-bending changes.

Not only did CEA Winslow and his colleagues decide to ignore Pfeiffer’s previously documented fungal forms, but they concluded that unlike the mycobacteria,  it stained Gram-negative and liked hemoglobin. But neither was accurate enough to warrant the name change Winslow had in mind.

Expert Stephen Maher [39]: “All non-acid coccal and bacillary derivatives of the tubercle bacillus are, strange to say, Gram-negative”. Krylow  [40] confirmed Maher’s observation that TB could stain gram-negative. The Gram stain, developed by Hans Christian Gram, separates bacteria based on their cell walls. The thick layers in “Gram-positive” cell walls stain purple, while the thin “Gram-negative” cell wall appears pink. Like other Bacillus, cultures of TB, on the other hand, could be Gram-positive when young, but might become Gram-negative as they age. Hans Much saw this in 1907, and Chandrasekhar reported it in 1982. [41] Therefore, the fact that Pfeiffer’s influenza bacillus was Gram-negative still didn’t rule it out as a bacillary derivative of the tubercle bacillus.  Furthermore, the organism was arbitrarily named Haemophilus influenzae (from the Greek Haemophilus, meaning “blood-loving”). But it grew on the same blood-based cultures that Mycobacterium tuberculosis  had long thrived on. [42]

To many in the lay and scientific community bacterial names and classifications are hallowed ground. But Sneath and Brenner’s 1992 paper for the American Society of Microbiology[43], clarified that there was no such thing as an official classification of bacteria or “approved lists” and that even Bergey’s Manual is not “official”- but merely the best consensus at the time. Therefore, Sneath and Brenner said, bacterial lists and classifications (called “taxonomy”) are partly a matter of judgment and opinion, as is all science, and until new information is available, different bacteriologists may legitimately hold different views. In the same vein Fox and Wisotzkey remind us that even regarding today’s sacred 16SrRNA sequence identity as a criteria for species identification, that 16S RNA may not be sufficient alone to guarantee species identity.[44]

Regretfully, no attempt at bacterial nomenclature, since its inception, has left room for a microbe such as Pfeiffer’s, which exists in more than one form – both bacterial and fungal, true to its original mycobacterial designation. The price of this to the world’s future health and welfare would be substantial.  Today, we are carefully taught that Pfeiffer’s bacilli, historically  Mycobacterium influenzae, was erroneously thought to cause and be behind the great pandemic of 1918. We are not taught that Pfeiffer’s bacillus itself has a viral cell-wall-deficient phase. Nor are we taught that its original difficulty in cultivation on normal media alone, without blood’s hemoglobin, almost classified it, a priori,  as a “virus” in the minds of those who relentlessly tracked a virus for influenza.  

 

Conclusion:

It was in 1952 that Cornelius P. Rhoads, Director of the Sloan-Kettering Institute for Cancer Research in New York City remarked in the introduction to a conference on viruses and cancer that the term ‘‘virus” had achieved ‘‘a high professional status with doubtful credentials”[45].

Papers such as that of Peter Palese of the Mount School of Medicine in Manhattan, reminds us that even in 1992, millions in China already had antibodies to H5N1 meaning that they had contracted it and that their immune system had little trouble fending it off.

And as van Helvoort aptly points out, by the 1950s the word ‘‘virus” had become so mouldable a concept that one could speak of virus workers without the existence of any consensus whatsoever of what viruses were [46]. Extremely supportive of this mouldability among virologists was Max Delbruck’s subtitle for “Virus, 1950″, a conference held at the California Institute of Technology, called: Proceedings of a conference on the similarities and dissimilarities between viruses attacking animals plants and bacteria [47]. Indeed, in the 1930s and 1940s the concept of ‘‘filterable virus” was subjected to such criticism that its very foundations were threatened. Statements like those coming from pioneer virologist Andre Lwoff in 1957 such as: ‘‘viruses should be considered as viruses because viruses are viruses” were unacceptable [48]. Also under the gun was Thomas M. Rivers, the Father of American Virology, who said you could differentiate viruses by three things, namely, their invisibility under the ordinary microscope, their ability to pass the finest filters because of this small size, and their inability to propagate themselves in the absence of susceptible cells [49].

Many scientists disagreed. Twort, working on Johne’s bacillus, presently itself suspected of being a tuberculosis-like mycobacterium, had to add special factors before this bacteria would grow on a lifeless medium and Sweeny’s JAMA study which showed that certain virus-like forms of tuberculosis met Rivers criteria as well. Rivers, who would become head of the Rockefeller Institute, was wrong.  In fact Klieneberger-Nobel showed just the opposite, that some bacteria could pass through filters that some of the larger viruses could not [50]. Wade and Manalang proved this with mycobacterial forms of Pfeiffer’s.

 To say the history of the theoretical underpinning of Virology has been a tortuous one, is probably an understatement and, incredibly, many virologists, even to this day, persist in using the flawed reasoning that that which passes thru a microfilter is a virus.

 Certainly one exception to these is world-renowned virologist Stephan Lanka, who, to this day, questions the very existence of H1N1 as a swine flu virus altogether.

Should the Pandemic of 1918 return, what are the implications of mistaking a virus such as Influenza A for what viral-like mycobacterial disease in the form of tuberculosis and Pfeiffer’s is actually causing? They would be unfortunate, with useless treatment and preventative stockpiles, and moreover, precious time wasted. The obvious need for further investigation is presently imminent and pressing.

 

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