Are the British Planning a Coup To Install Blair as EU President?

LaRouche October 2 2009

October 2, 2009 (LPAC)—According to The Sun, in case of a "Yes" victory in Ireland, the EU will appoint Tony Blair as President of Europe, a function introduced by the Lisbon Treaty. A "senior government source" told The Sun: "If we get a 'Yes' vote, it will all move very, very quickly. Tony could be named by the end of October." According to the Sun, Sweden (current EU presidency) wants a president named by the end of this month. The Sun quotes French Foreign Minister Bernard Kouchner saying that Blair is, for the moment, the only candidate. A "senior French diplomat" adds: "Who will dare say no to Tony Blair?" and plays down concerns about Blair's support for the Iraq War.

However, all this could work only if three circumstances materialize in October: 1. Yes victory in Ireland; 2. Czech ratification; 2. Polish ratification. At the moment, Czech ratification is beyond the horizon, as the Constitutional Court needs time to work through a verdict on the two challenges. A sort of "coup" scenario is hinted at by the FT: "Some EU officials hope that, if the Irish result is an emphatic Yes, [Czech President Vaclav] Klaus may surprise everyone with a prompt announcement that he will sign. There has even been talk in Brussels of a special ceremony bringing together Mr. Klaus and Lech Kaczynski, the Polish President, who has also delayed signing the charter."

Is H1N1 Swine Flu Really A Virus...Or Is It A Bacteria?

By Lawrence Broxmeyer, MD 10-2-9

ABSTRACT

On June 3rd, 2009 in Global Research, a curious article by F. William Engdahl appeared entitled "Sarkozy's Secret Plan for Mandatory Swine Flu Vaccination". In it Engdahl plainly states that " The only problem with the Swine Flu (H1N1) Vaccine, is that to date, neither WHO nor the US Government's Center for Diseases Control (CDC) have succeeded to isolate, photograph with an electron microscope, or chemically classify the H1N1 Influenza A virus". Furthermore there was no scientifically published evidence that French virologists have done so either. Therefore, mentioned Engdahl, "To mandate a vaccination for a putative (supposed or assumed to exist) disease that has never been characterized is dubious to say the least."

 

Engdahl wasn't finished. "Even more bizarre is the admission by the US Government's Food and Drug Administration, an agency responsible for the health and safety of its citizens, that the 'test' approved for premature release to test for H1N1 is not even a proven test. More to the point", continues F. William Engdahl, "there is no forensic evidence in any of the deaths reported to date that has been presented that proves scientifically that any single death being attributed to H1N1 Swine Flu virus was indeed caused by such a virus."

 

Therefore, 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".

 

Both the World Health Organization (WHO) and the Centers for Disease Control (CDC) are fully aware of a far more serious and ongoing tuberculosis Pandemic in the world today. Yet they choose to downplay the link, disregarding the similar flu-like symptoms tuberculosis often begins with. Despite this, and with regards to the present TB Pandemic, WHO freely admits that there were more than 9 million new cases of TB worldwide, and approximately 1.8 million deaths from the disease in 2007, the most recent year for which data are available. The World Health Organization estimates that there are presently 13.7 million people living with TB. An infectious disease, TB has been on the rise since the 1980s. About one-third of the world's population, or two billion people, carry the TB bacteria.

 

The "H" and "N" of influenza sub-typing, revolves around two glycoproteins called Hemagglutin (H) and Neuraminidase (N), 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 were shown, through crystallization, to produce the same protein neuraminidase used to subtype 'Influenza'. Furthermore, as of 2006, it has become obvious in Menozzi's study that similar to Influenza, Tuberculosis not only uses Hemagglutin to attach to the lung's epithelial cells it invades, but requires Hemagglutin for dissemination of the disease to the rest of the body.

Furthermore, 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, 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.

 

Masked Soldiers In City, Circa 1918

AMERICA'S TAKE

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.1

 

1918 AND TODAY

No one can deny the similarities between the onset of the 1918 epidemic and that of today, 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." 2 Subsequently, a study published in JAMA by Talbot and Moore3 in 2000 showed that Mexican immigrants to the US have the highest case rates for tuberculosis among foreign born persons. Mexico is the country where Swine Flu deaths were first documented.

 

The research of Lawrence Broxmeyer MD first proclaimed4 that the 1918 pandemic was due to bacteria, particularly mutant forms of flu-like fowl, swine, bovine, and human tuberculosis (TB) bacteria

http://drbroxmeyer.netfirms.com/001pdfBIRDFLUEDITORIALPUBLISHED.pdf 

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.5 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 Michael Garenne came up with convincing statistics showing that undetected tuberculosis may have been the real killer in the 1918 flu epidemic. 6

 

THE ROOTS OF HISTORY

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 Pfeiffer7 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". And it never lost its potential to kill.

 

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 Fox8 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, whether the disease was still active or not, Mycobacterium influenzae "disappears entirely".8

 

In 1933 English physicians Wilson Smith, Christopher H. Andrewes, and Patrick P. Laidlaw9 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, from the onset, 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". In addition Sir Christopher Andrewes 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.

 

But to government pathologist and pioneer physician/researcher William M. Crofton, who by virtue of his office as County pathologist 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 the bacillus Mycobacteria influenzae, which by then had been renamed Haemophilus Influenzae. To Crofton this bacilli was the common denominator for the Pandemic of 1918 he had witnessed, although the bacteria could be accompanied by an array of opportunistic organisms such as Staph and Strep. Crofton publically and personally confronted and challenged Laidlaw to come to his laboratory for the proof that his Influenza samples weren't viral. Crofton was convinced by the confirmation of scientists like Calmette at Pasteur regarding how certain forms of tuberculosis, appearing both minuscule and viral, could pass through the smallest of filters. Crofton himself then established that tuberculosis could disappear into tissues as viruses did, and then go through filters which stopped cold even most of those "now invariably called viral disease". "Surely, then", Crofton concluded, "Tuberculosis has more right to be considered a true virus than these."10 So, at a time when viral forms of TB where scantily being documented, Crofton struggled to link H. Flu with the TB it so often infected in coordination with, as historical and political momentum carried Laidlaw's study through for posterity. A great opportunity was missed to correct the record.

 

Frank Macfarlane Burnet was the first to grow "Influenza" in a laboratory setting; in 1940 he grew influenza in embryonated chicken eggs, using the allantoic sac. He obviously considered such a technique "Influenza" specific, never bothering to consider that such an allantoic site might also be an excellent site for culturing the viral or Cell-Wall-Deficient (CWD) forms of tuberculosis and the mycobacteria. Viral TB, in fact grows there as early as 6 hours after introduction into such a place in chicken embryos.11

Furthermore, some of the filamentous forms of tuberculosis mentioned by Corper12 appear similar to those attributed to ''Influenza'' by biochemist and Influenza guru Burnet.13

 

It wasn't because Burnet didn't know that bacteria could assume viral forms. The first, and for a time the only virologist in Australia, it was Burnet who discovered bacteria in viral forms of Q-fever14. And in that same paper, proclaiming Virology as an Independent Science , and after admitting that viruses, including influenza, are composed of the same sorts of material as bacteria, Burnet struggles to differentiate Influenza by the fact that it ''probably has no DNA'' and was therefore exclusively RNA.(Ibid.). But, according to Xalabardar, some cell-wall-deficient mycobacterial forms also are exclusively RNA. Furthermore, points out Xalabarder, such cell-wall-deficient tubercular forms are true antigens, all of which, similar to Influenza, induce the production of specific antibodies detectable by complement fixation tests, such as those originally used to detect Influenza.5

 

CONCLUSION

In a landmark study15, 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 Haemophilus influenza or any other common bacteria, are a common secondary manifestation in TB-infected lungs. During the pandemic, one-third of patients who had Haemophilus influenza were 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, one must look back historically at the science itself. 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 Hirst16 claimed that influenza ''virus'' could agglutinate (or clot) red blood cells of fowl and other animal species. Such a hemagglutinin discovery, in turn, led to fast assays of what is thought to be Influenza. 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 Dubos17 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 Ono18,19 reviewed similar red cell agglutination occurring in the presence of tuberculous serums.

 

As Influenza historian van Helvoort20 aptly pointed out, 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''21 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''.22

 

Perhaps in his authoritative text, The Pathogenesis of Tuberculosis, Johns Hopkin's 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.23

 

As Professor Hans Rosling http://www.youtube.com/watch?v=V8bUtbODV-Q 

has so aptly pointed out: during the initial 13 days that WHO started gaining data on Swine Flu Deaths, April 24-May 06, 2009, 31 people died of Swine Flu. 29 of these were in Mexico and 2 in the US. During this same 13 day window, 63,000 people, around the world died of tuberculosis. http://www.who.int/research/en

What we have today, is a pandemic with "flu-like" symptoms. And flu-like symptoms doesn't necessarily mean "Influenza" is its underlying cause.

Readers interested in the subject of Influenza/TB can also go to Dr. Ron Paul, MD's take at:

http://informationclearinghouse.info/article22507.htm

Other relevant links include:also applicable to the current Swine Flu epidemic include:

http://www.frequencyfoundation.com/2009/07/bird-flu-influenza-and-1918-case-for.html

And:  http://www.frequencyfoundation.com/2009/07/swine-flu-do-we-really-have-right.html#links

 

REFERENCES

Talay F Kumbetli S Altin S Factors associated with Treatment Success for Tuberculosis Patients: a Single Center's Experience in Turkey   Jpn. J. Infect. Dis., 61,25-30, 2008.

DM Morens et al. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: Implications for pandemic influenza preparedness. The Journal of Infectious Diseases DOI: 10.1086/591708 (2008).

Talbot EA Moore M McCray E Binkin NJ Tuberculosis Among Foreign-Born Persons in the United States, 1993-1998 JAMA. 2000;284:2894-2900.

Broxmeyer L. Bird flu, influenza and 1918: The case for mutant Avian tuberculosis. Med Hypotheses. 2006;67(5):1006-15. Epub 2006 Jun 27

Xalabardar C, Formas L. Publicaciones Del Instituto Antituberculoso Francisco Moragas. 7, Barcelona; 1970. p. 1 83.

Noymer A, Garenne M. The 1918 influenza epidemic's effects on sex differentials in mortality in the United States. Popul Dev Rev 2000;26(3):565 81.

Chester FD  A Manuel of Determinative Bacteriology Macmillan & Company Ltd, London 1901 p.351. 401ppgs.

Stengel A Fox H A text-book of Pathology 6th Edition Philadelphia and London WB Saunders & Co 1915 1039 ppgs P298

Smith W, Andrewes C, Laidlaw P. A virus obtained from influenza patients. Lancet 1933;2:66 68.

Crofton WM The True Nature of Viruses 2nd Edition, Staple Press, London 166pgs 1939

(Balan V.F. (1991): The use of chicken embryos for the culture of L-forms of mycobacteria tuberculosis . Problemy Tuberkuleza i Bolezni Legkikh, 2, 59 60.)

Corper HC. In discussion following mutation forms of the tubercle bacillus. JAMA 1926; 9(October):1210 11.

Burnet F. Filamentous forms of influenza virus. Nature1956; 177(4499):130.

Burnet F. Virology as an independent science. Med J Australia 1953; 40(223):841 5.

Donaldson R. The bacteriology of influenza: with special reference to Pfeiffer's Bacillus. In: Crookshank, editor. Influenza. London: Heinemann; 1922. p. 139 313. 144.

Hirst GK. The agglutination of red cells by allantoic fluid of chick embryo infected with influenza virus. Science ;xciv:22 3. 1941.

Pound A. Observation on the agglutination and haemolysis of red cells treated with extracts of Mycobacterium tuberculosis: an evaluation of methods. J Pathol Bacteriol 1952;64(1):131 43.

Takahashi Y, Ono K. Hemagglutination reaction by the phosphatides of the tubercle bacillus. Kekkaku no Kenkyu (Tuberculosis Res) 1957;7:1.

Takahashi Y, Ono K. Study on the passive hem agglutination reaction by the phosphate of M. tuberculosis. 1. The reaction and its specificity. Am Rev Resp Dis 1961;83(2):

van Helvoort T. History of virus research in the 20th century: the problem of conceptual continuity. Hist Sci1994;32(2):185 235.

Lwoff A. The concept of virus. The third Marjory Stephenson Memorial Lecture. J Gener Microbiol 1957;xvii:239 53.

Rhoads CP. Introduction {to a conference on viruses as causative agents in cancer}. Ann NY Acad Sci 1952;liv:872 3.

Rich, AR  The Pathogenesis of Tuberculosis  2nd Printing. Charles C. Thomas Publisher. Springfield, Illinois 1946. 1008 pps.P.627

 

Lawrence Broxmeyer, MD

Whitestone, New York 11357

nyinstituteofmedicalresearch@yahoo.com

New PETA investigation exposes suffering in dairy industry

(These guys do an amazing job, join their cause, I did!)

After blowing the whistle on the abuse that she saw, a wonderful woman working at a Pennsylvania dairy factory farm went undercover for PETA for months. This allowed us to investigate and record the suffering of cows and calves at this Land O'Lakes, Inc., supplier.
Hundreds of cows on this factory farm were subjected to routine cruelty. Our investigator witnessed lame cows struggling to stand and walk as they were herded to the milking machines; cows who could not stand on their own being kicked, jabbed in the spine with a blade, and electro-shocked; and dying cows who were denied even a mercy killing to relieve their pain.
For these cows and all the other poor animals who are being abused in farm sheds and crates, PETA—and you—are the only hope. Please help us confront the hidden cruelty inflicted on animals by donating online to our Factory Farming Challenge, and have your gift doubled dollar for dollar.
As you may know, a group of PETA's most dedicated friends has put up $200,000 of their own money and challenged us to raise a full $400,000 to combat the suffering of animals abused and exploited on factory farms. We're already 46% of the way there, but this special challenge will end in only a few short weeks. We will only reach our goal if enough caring members like you act today.
The meat, egg, and dairy industries don't want anyone to know the kind of hellholes factory farms are and how deeply and routinely animals suffer on them. But they can't stop PETA—with your help—from exposing their cruelty. Our investigation of this Pennsylvania dairy farm has enabled millions of people to see with their own eyes the suffering that goes into every glass of milk. And it has already helped us save at least two lives.
When our investigator first saw a sweet little calf named Jerry, the animal was in pitiful condition. His legs were deformed, and he was extremely thin, infested with lice, and nearly blind—most likely as a result of pinkeye, a bacterial infection that's often spread in the filthy conditions on factory farms.
Peter, another calf on the same farm, was found nearly unconscious and close to death. He was just skin and bones and was covered in ringworm fungus. Peter's plaintive moo was a gurgled moan because of a bacterial pneumonia that's common on dairy factory farms, and his skin was raw and scalded from being soaked in urine and feces in the filthy pen that he could not escape from.
Today, Peter and Jerry are thriving at a peaceful sanctuary where, thanks to your support, PETA pays for upkeep and the calves' monthly care. Their coats are growing thick and shiny, their bodies are filling out, and they can eat fresh grass and breathe clean air for the first time in their lives. Both Jerry's and Peter's health is steadily improving, and they are now the very best of friends.
I wish we could rescue all the hundreds of suffering cows from this dairy factory farm, and there's no knowing how many animals will be saved because of this case. Of course, it's important to point out that we can stop the worst abuses of cows and other animals used for food by making their plight known to people around the world. But we can't do it without you.
I hope you will take this opportunity to support our Factory Farming Challenge with the most generous contribution that you are able to give. Your gift will have double the impact when it comes to PETA's efforts to help people see exactly what happens to animals like Jerry and Peter in these hellish places.
Thank you. Your commitment means the world to us and the animals we serve.
Kind regards,

Ingrid E. Newkirk
President
P.S. Animal abuse can't be stopped if it remains hidden. Your support helps PETA tear down the factory farm walls and lets the light in so that public pressure will result in meaningful changes in the lives of billions of individual animals. Please donate today to have your gift doubled and to help us expose the hideous abuse inflicted on animals.