TT Note: Hold on to your flu-like symptoms, folks. This doctor looks at the flu epidemic of 1918 and some researchers' findings. When compared to today's trendy virus, there appears to be some room for debate on the current flu-like symptoms. Is it really the flu?
/24-7 / -- All that is H1N1 does not glitter, at least with respect to the tireless efforts of Virologists, Epidemiologists and Health Officials to stake claim that the current "flu-like illness" pandemic is tied to "Influenza".
"The "H" and "N" of influenza sub-typing" Lawrence Broxmeyer, MD mentions, "revolves around two glycoproteins called Hemagglutin and Neuraminidase, both of which can be, and are, associated with infectious diseases such as the minuscule, viral forms of tuberculosis, a disease which ought to be high on the differential diagnosis for 'flu-like illness' . Since August, 2008, a Medline study in the Journal of Clinical Biochemistry showed that sputum neuraminidase levels over 1.0 mU per mL were proven associated with having tuberculosis in 92% of cases, previous to which bacteria closely related to TB where shown, through crystallization, to produce the same protein neuraminidase used to subtype 'Influenza'."
Furthermore, reminded Lawrence Broxmeyer MD, "Khomenko's 1993 study, showed that the explosive contagiousness of just such influenza-like forms of tuberculosis are exactly the stuff that previous epidemics and pandemics could have been made of." Khomenko was cited by Nobel nominee Lida Mattman in her textbook prior to her untimely death last year.
"That is exactly why", reiterated Lawrence Broxmeyer, MD "that in response to the present world "flu" pandemic, Japan's Health Ministry's Tuberculosis Infection Diseases Control Division deputy director Takeshi Enami went hand in hand with Yoshio Nanba, director of The Office of Pandemic Influenza Preparedness and Response, to attend a news conference in Tokyo on May 1, 2009."
But back in the US, the CDC and NIH seem to feel differently, ignoring everything but "the virus". There was much the same "Influenza" talk when in 1990, a new multi-drug-resistant (MDR) tuberculosis outbreak took place in a large Miami municipal hospital. Soon thereafter, similar outbreaks in three New York City hospitals left many sufferers dying within weeks. By 1992, approximately two years later, drug-resistant tuberculosis had spread to seventeen US states, with mini-epidemics in Florida, Michigan, New York, California, Texas, Massachusetts, and Pennsylvania and was reported, not by the American, but the international media, as out of control. Viral forms of swine, avian and human TB can be transmitted from one species to another. By 1993 the World Health Organization (WHO), proclaimed tuberculosis a global health emergency.
"No one can deny the similarities between the onset of the 1918 epidemic and that of today," mentioned Lawrence Broxmeyer MD, "Yet a Press Release, issued on August 19, 2008, by the National Institute of Allergy and Infectious Diseases (NIAID), contains a striking finding and conclusion: The 20 to 40 million deaths worldwide from the great 1918 Influenza ("Flu") Pandemic were NOT due to "flu" or a virus, but to pneumonia caused by massive bacterial infection."
Subsequently, a study published in JAMA by Talbot and Moore in 2000 showed that Mexican immigrants to the US have the highest case rates for tuberculosis among foreign born persons.
The research of Lawrence Broxmeyer MD first proclaimed that the 1918 pandemic was due to bacteria, particularly mutant forms of flu-like fowl, swine, bovine, and human tuberculosis (TB) bacteria. These forms of tuberculosis are often viral-like, mutate frequently and can "skip" from one species to another. Moreover the antibodies from such viral TB forms react in the compliment fixation and later "viral" assays. They also grow on cultures which are supposed to grow only viruses.
In a supportive 16-page-paper which appeared in Population and Development Review, University of California demographers Andrew Noymer and Michel Garenne came up with convincing statistics showing that undetected tuberculosis may have been the real killer in the 1918 flu epidemic.
Noymer's hypothesis stands sound against history. Few flu "experts" are aware that in medical texts printed circa 1918 "Influenza" was attributed not to a virus but a bacteria called Mycobacterium influenzae, discovered by Pfeiffer and Canon in 1892......not exactly a coincidence since Richard Pfeiffer worked, at one time, for Robert Koch, the discoverer of tuberculosis, a disease also caused by another bacillus called Mycobacterium tuberculosis. Both mycobacteria stained best with carbol-fuchsin, a bacterial stain commonly used in the staining of mycobacteria as it has an affinity for the mycolic acids found in their cell walls. Mycobacteria such as tuberculosis are particularly deadly because they share properties of the fungi ("myco-") as well as bacteria. TB was, not all that long ago, referred to as "captain of the men of death".
Mycobacterium influenzae was considered by most to be the cause of influenza until 1933. But there were serious diagnostic problems with Mycobacterium influenza. Stengel and Fox warned about them in their widely quoted W.B. Saunder's 1915 version of "A Textbook of Pathology". Problems with identification revolved mainly in that although the bacterial influenza occurred abundantly in the sputum of flu patients at first, it decreased in quantity as the cases advanced. And when purulent expectoration stopped Mycobacterium influenzae "disappears entirely".
In 1933 English physicians Wilson Smith, Christopher H. Andrewes, and Patrick P. Laidlaw removed secretions from the throat of a humans with flu-like symptoms thought to have "influenza" , and then filtered out a suspected infectious agent, which by virtue of the fact that it went through a filter was falsely proclaimed to be "a virus". Injecting it into ferrets, the ferrets then developed the same flu-like symptoms which Smith, Andrews and Laidlaw summarily declared as "influenza".
But to government pathologist and pioneer physician/researcher Sir John Crofton (1912-69 ), who by virtue of his office had examined some of Laidlaw's human "Flu" samples, Laidlaw's entire study was flawed. Crofton found Laidlaw's Flu samples to be laced with Mycobacteria influenza, which by then had been renamed Hemophyllis Influenza. Crofton personally confronted and challenged Laidlaw to come to his laboratory for the proof that his Influenza samples weren't viral. However historical and political momentum carried Laidlaw's study through and a great opportunity was missed to correct the record.
In a landmark study, Dr. Robert Donaldson, working out of the Pathological Society of Great Britain had ruled out that the mycobacteria now referred to as H. Influenza by itself was behind 1918, perhaps because of its disappearing nature. Yet at the same time he quickly added that there wasn't "the slightest shred of evidence" that the disease was due to a "virus" or influenza. Nor was Donaldson ever able to refute Broxmeyer and Noymer's feelings that TB was behind the many deaths in the pandemic, specifically because it is well known that secondary bacterial infections, be they from opportunistic Haemophillus influenza or any other common bacteria, are a common secondary manifestation in TB-infected lungs. During the pandemic, one-third of patients who had Haemophillus influenza where also found to have tuberculosis - keeping in mind, as always, that many other cases with TB went undiagnosed.
"In order to understand why we have this emphasis by those virologists invested in a 'killer flu' in the US today", said Lawrence Broxmeyer MD, "one must look back historically at the science itself."
In truth, until the late 1940s influenza 'viruses' were studied as infections, which, although filterable, were conceived of as analogous to bacteria, a kind of ultra or viral-like bacteria.
Not to be deterred, and still seeing Influenza as a great opportunity for virology, in 1941 virologist Hirst claimed that influenza ''virus'' could agglutinate (or clot) red blood cells of fowl and other animal species. The "H" in H1N1 comes to us through Hirst, who showed that ''virus'' particles first adsorbed to the red cells and, after a certain time, eluted again as a result of what could be interpreted as an enzymatic reaction. But 6 years later, Middlebrook and Dubos made this seem nothing more than a cheap hat trick by showing that similarly red blood cell agglutination could be produced by sera from patients with tuberculosis. Takahashi and Ono reviewed similar red cell agglutination occurring in the presence of tuberculous serums.
"As Influenza historian van Helvoort aptly pointed out", summed-up Lawrence Broxmeyer MD, "indeed, in the 1930s and 1940s the concept of 'filterable viruses', including Influenza, were subject to such criticism that Virology's very foundations were threatened. Dogmatized statements like those coming from pioneer virologist Andre Lwoff in 1957 : ''Viruses should be considered as viruses because viruses are viruses'' were totally unacceptable, and did little to help the situation.
So it was in 1952 that Cornelius P. Rhoads, Director of Sloan-Kettering Institute for Cancer Research in New York City, remarked in a conference introduction that the term ''viruses'', such as that of Influenza, had achieved ''a high professional status with doubtful credentials''.
What we have today, mentioned Broxmeyer, is a pandemic with "flu-like" symptoms. And flu-like symptoms dosen't necessarily mean Influenza is the underlying cause.
Reference: Pubmed. Lawrence Broxmeyer MD, Bird flu, influenza and 1918: The case for mutant Avian tuberculosis. Med Hypotheses. 2006;67(5):1006-15. Epub 2006 Jun 27. http://drbroxmeyer.netfirms.com/PDF%20001%20Bird%20Flu%20Editorial.pdf
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