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CANCER AND BACTERIA IV
Cancer and Bacteria
 
Although the idea of a cancer microbe is medical heresy, there is ample data to show that cancer patients are highly prone to bacterial infection. A PubMed computer search (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi)
of "bacteria + cancer" elicits 49, 244 citations contained within 2,463 web pages. According to a 2003 article by Vento and Cainelli, patients with cancer who are undergoing chemotherapy are highly susceptible to almost any type of bacterial or fungal infection.
Why are physicians, and especially pathologists and bacteriologists, so unaware, so disinterested, or so antagonistic to credible cancer microbe research? Why have pathologists failed to consider Russell bodies as large forms of bacteria?
For over 30 years I studied various forms of cancer and skin diseases "of unknown origin", as well as autopsy cases of cancer, lupus, scleroderma, and AIDS. In all these diseases I was able to detect bacteria, although pathologists would never mention bacteria in any of their official biopsy reports. In my experience, they simply could not conceive of cancer and collagen disease (and AIDS) as a bacterial infection, nor did they seem to be aware of bacteriology reports pertaining to "large bodies" and pathologic effects produced by the "tuberculosis virus." In short, they were trained to see and report only the typical rod-shaped acid-fast (red-stained) "typical" form of mycobacteria, , but they were not trained to look for or to recognize other growth forms of the same bacteria that might be hidden in their pathologic tissue specimens.

Photo #7: Pleomorphic growth forms (L-forms) of tuberculosis mycobacteria photographed with an electron microscope. Note the darker staining tiny coccal forms (similar in size to ordinary staphylococci) and the larger clear balloon-sized "ghost" forms similar in size and shape to Russell bodies found in tissue. These forms are all characteristic of "cell wall-deficient bacteria" and totally unlike the well-known "typical" acid-fast rod forms of Mycobacterium tuberculosis. Reproduced from L-forms of Mycobacteria and Chronic Nephritis (1970), by Dr. C. Xalabarder P., page 51

When objects like Russell bodies are observed in a wide variety of diseases and in "normal" tissue, the significance is lessened. Doctors expect "normal" tissue to be free of microbes. I suppose they also conclude that Russell bodies cannot be an infectious agent because it would be impossible for an infectious agent to appear in so many different kinds of diseases and in so many different forms of cancer.
 
For most of the last century stomach ulcers were thought to be non-infectious because pathologists could not identify bacteria in the ulcers and because doctors believed bacteria could not live in the acid environment of the stomach. This thinking all changed gradually after 1982 when Barry Marshall, an Australian physician, proved most stomach ulcers were caused by a microbe called Helicobacter pylori, which could be identified microscopically with special tissue staining techniques in ulcer tissue. On the other hand, many people normally carry this stomach microbe without any ill effects. Not surprisingly, pathologists are now reporting numerous Russell bodies in plasma cells in some ulcer patients, giving rise to a previously unrecognized tissue reaction called "Russell cell gastritis."

Russell bodies and bacteria
 
When bacteria are threatened by the immune system or by antibiotics they may lose their cell-wall and assume a different growth form that renders them less susceptible to attack by the immune system. Some Russell bodies elicit little or no inflammatory cell response. This lack of cellular response is yet another reason why physicians have a hard time believing Russell bodies could be microbes.
 
I have observed the largest and most complex Russell bodies in tissue where there was almost a total lack of inflammation. My photographs of such "large bodies", some with obvious internal structure, that I observed in patients with scleroderma and pseudoscleroderma, were published in the American Journal of Dermatopathology in 1980. The first case of fatal scleroderma I studied in 1963 had numerous "large bodies" in the fat layer of the diseased skin that were unlike anything ever seen in dermatology. The patient had been hospitalized for pulmonary tuberculosis 7 years before developing scleroderma. The mystery of these "yeast-like" bodies deep in his skin was solved years later when I first learned about the existence of "large body" forms of Mycobacterium tuberculosis. When this patient died, Mycobacterium fortuitum, an "atypical" form of mycobacteria was cultured from his scleroderma tissue.

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