PamRotella.com

The bacterial model of Mad Cow Disease
[Posted 26 September 2004, last updated 19 November 2004]

The mainstream media has embraced the prion theory of Mad Cow Disease since BSE ( Bovine Spongiform Encephalopathy, known as Mad Cow Disease) became an epidemic in the 1990s.  Other than a few alternative news sources, the press largely ignores other theories of the disease.  The bacterial model of Mad Cow Disease is a competing theory with extensive supporting scientific evidence.  In his article Is Mad Cow Disease caused by a bacteria?, Lawrence Broxmeyer, M.D., presents documentation supporting the Bovine Tuberculosis model of Mad Cow Disease.

Broxmeyer is a researcher who has concentrated much of his time on Tuberculosis (TB), and is familiar with how TB can cause symptoms like those found in the Spongiform Encephalopathies.  His full article Is mad cow disease caused by a bacteria? (.pdf version) can be found by clicking here.*  The text version (does not include epidemic maps) can be found by clicking here.

Bovine TB has a long history in Great Britain, with symptoms often similar to those of Mad Cow Disease.  The deformed "prions" implicated in other research may be another symptom of the disease and not the cause, according to Broxmeyer, and "many animals that die of spongiform TSE's never show evidence of misfolded proteins."  Broxmeyer says the infectious capability of a protein without genetic material is unlikely, and "Prions" were found to be proteins occurring naturally in normal tissues, although changes were sometimes noticed in the diseased animals.  However those prion changes wouldn't explain damage to healthy tissues, and a causative agent is needed to explain prion "misfolding" at the outset.  Moreover, prions have not been proven as necessary to cause the disease, and an increased level of prions in laboratory experiments has not been shown to increase the likelihood of infection.  What researchers are calling prions, according to Broxmeyer, could in fact be "amyloids," a type of "deposition that took place due in the course of chronic inflammatory disease, mainly tuberculosis, the usual precipitating cause."  Britain's historical battle with Bovine TB is documented by Broxmeyer, with the disease often appearing in the best stables, and creating a slight risk of infection to humans consuming the flesh of diseased animals.  Broxmeyer provides maps to show that the concentration of bovine TB in the southwestern area matches the outbreak of mad cow disease.  He claims that the link between eating beef diseased with Bovine TB and the human disease is well established. 

Broxmeyer, a doctor who has treated TB in patients and studied it extensively, cites symptoms of TB which match the encephalopathy and neurological damage seen in Mad Cow Disease (BSE), Scrapie in sheep, and CJD in humans.  He explains that Tuberculosis often assumes "L-forms," or cell-wall deficient forms, which are hard for researchers to detect using standard methods, and evade the animal's immune system.  (This is also related to the bacterium's pleomorphic nature.)  Mad Cow tissue was shown to be infectious in experimentation even without "prions" present, which could indicate that an agent like L-forms are at work.  Bovine TB can also cause "downer cows" and both meningitis and encephalitis in cattle and humans.

Current mad cow diagnosis lies solely in the detection of late appearing "prions", an acronym for hypothesized, gene-less, misfolded proteins, somehow claimed to cause the disease.  Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses.  Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed the causative virus or bacteria.  Therefore, even if samples appear to infect animals, it is impossible to prove that prions are causative.
Lawrence Broxmeyer, M.D., Is mad cow disease caused by a bacteria?

I asked Dr. Broxmeyer about Mark Purdey's theory of Mad Cow Disease, the organophosphate/manganese poisoning model.  Purdey's theory of an organophosphate-Mad Cow link started with the very compelling observation that Purdey's organic herd, untreated with organophosphate pesticides, did not contract Mad Cow Disease, whereas a non-organic herd of his own which had been treated and his neighbors' treated herds all contracted Mad Cow Disease.  Also, the Mad Cow epidemic immediately followed the British government's mandatory treatment of cattle with organophosphate pesticides in order to "eradicate" the warble fly parasite.  This was a very strong observation, and usually such observations are eventually proven correct by science. 

Although Broxmeyer doesn't think that the actual cause of Mad Cow goes beyond Bovine tuberculosis, and that blaming disease on agents such as organophosphates was a traditional flaw even in the history of discovering the real cause for tuberculosis, he admitted that there could be an indirect linkage with not only organophosphates but a host of other chemical and physical irritants.  According to Broxmeyer, "Mankiewicz and Livingston's colleague Alexander-Jackson (1965) established that bacteriophages (also called phages), the viruses which live inside pathogens such as bovine and human tuberculosis could in and of themselves cause cytopathogenic change, even pre-malignancy in otherwise normal healthy mammalian tissue. Lwoff (1962) and early phage masters showed how the phages inside Mankiewicz's mycobacteria could be activated by a host of chemical and other agents, some pesticide-like, including organophosphates.  Organophosphates therefore could be one of many irritants causing Mad Cow clinically in bovine tuberculosis infected cattle by causing them to activate the phage viruses within this disease. And since Nelson and Pickett (1951) showed that it was attack by these very same phage viruses which seemed to cause the majority of Klieneberger's cell-wall-deficient (pleomorphic) forms thru breech of the cell wall, organophosphates would indirectly cause them to propagate and the underlying disease in Mad Cow, central nervous system bovine tuberculosis would become aggravated."

Broxmeyer however, because of the intricacies of such an organophosphate relationship and the fact that he felt Bovine TB itself, and not organophosphates, causes Mad Cow, chose not to cover that particular issue in his article. On the other hand, he draws freely from the "concept of Klieneberger and Livingston's viral (pleomorphic) forms of Bovine tuberculosis" to explain why some investigators might interpret that a virus is behind Mad Cow.  "Of all the pathogens," he relates, "the preferred form of any tuberculosis or the mycobacteria is the cell-wall-deficient or pleomorphic state, a strategy they [the bacteria] have devised to create dormant forms which both go beneath the body's radar of detection and mean guaranteed survival."  Obviously, with pleomorphism a forbidden yet well-known secret in the scientific community, little research would be funded or published to back such claims.  Broxmeyer is one of the few researchers brave enough to cite Virginia Livingston as it is.  (See my article on the Genetic Fad for a brief explanation of pleomorphism.)

There is no known disease which better fits into what is occurring in Mad Cow and the spongiform encephalopathies than bovine tuberculosis and its blood-brain barrier penetrating, virus-like, cell-wall-deficient forms.
Lawrence Broxmeyer, M.D., Is mad cow disease caused by a bacteria?

Even more troubling than Bovine TB, another variety of Tuberculosis, "Mycobacterium avium" (fowl tuberculosis), can infect a range of other animals including cattle and man, and is even more resistant to heat than Bovine Tuberculosis.  It is found in a substantial number of cattle.

Through years of his research on Tuberculosis varieties, Broxmeyer was well-prepared to recognize symptoms of the disease.  He makes a good case for seeing it again in the Mad Cow epidemic.


*(Note:  You'll need Adobe Acrobat, a free program that your PC probably already has, to read this one.  If you click on the above link and find that you don't have it, you can download the free version from the Adobe web site.)

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Essential Fatty Acids, the "healthy fats" we all need
Copper: What aneurysms, white hair, and wrinkles have in common
Mad Cow and Mark Purdey's Organophosphate theory
Multiple Sclerosis: The mercury/parasites model
Alternative medicine vs. the common cold and flu
Hulda Clark: A cure for cancer and AIDS?
Vegans and the B-12 deficiency myth
Aspartame, MSG, and other excitotoxins
Sickle Cell Anemia: Dr. Agbai and B-12 deficiency
Jake Beason on children and boredom

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