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The Return of the Cancer Parasite:
Bacteria and the Origin of the Cancer Cell
by Alan Cantwell, M.D.
October 29, 2011

The Return of the Cancer Parasite:
Bacteria and the Origin of the Cancer Cell
by Alan Cantwell, M.D.
Copyright 2011 ­ All Rights Reserved
What causes a human cell to turn cancerous? How do cancer cells become deadly killing machines? Could infectious agents, like bacteria, be involved in the process?
According to new revolutionary research by Peter Duesberg, Professor of molecular and cell biology at the University of California in Berkeley, cancer tumors are parasitic organisms which represent a newly evolved parasitic species. He says cancer cells are like parasites. They feed on us and they don't need our healthy cells to survive. And they ultimately develop chromosomes that differ from our own cells.
The prevailing view is that the cancer cell is caused by a handful of genetic mutations. But Duesberg argues that the cancer cell is initiated by a disruption of the entire chromosome, which leads to duplicates, deletions, breaks and omissions, and other chromosomal damages that alter the balance of tens of thousands of genes. The result is a cancer cell with totally new traits and a chromosomal number that differs from our normal healthy human cells, which contain a total of 46 chromosomes.
Since the 1980s Duesberg has gained notoriety for his persistent and outspoken belief that HIV does not cause AIDS. However, he hopes his new view of a cancer parasite, however disturbing, will allow medical researchers to develop more effective treatments for cancer than they have been able to thus far. For more details, see the UC Berkeley Press Release online, "Are cancers newly evolved species?" by Robert Sanders, July 26, 2011.
Surprisingly, Duesberg's idea is not new. The idea that cancer cells were parasites was popular a century ago when microbiology was in its infancy.
On Dec 2, 1911, Sir Henry Britlin's paper entitled "Unicellula cancri: The parasite of cancer" appeared in the British Medical Journal. He declared, "There is one, and only one, explanation of the conduct of the cancer cellit has become an independent creature, a new creation of a living thing."
He continued: "If the cancer cell be, in truth, a new creature, to what class of creature does it belong? It is nearest to the protozoa-so near, indeed, that it is difficult to keep it out of the protozoa." (Protozoa are the smallest one cell "animal" organisms having a distinct nucleus.) Butlin named the cancer cell "Unicellula cancri," and wrote: "I am perfectly conscious of the far-reaching consequences of admitting that unicellular bodies, derived from such a source, are a new species of created beings, but there is no alternative. The facts are plain, and cannot, I believe, be otherwise interpreted." Butlin's century-old paper is available online.
In "The Cancer Microbe" (1990), I wrote about Wilhelm Reich, the unfairly maligned and persecuted psychiatrist and cancer researcher who was sentenced to Federal prison where he died in 1957. After much experimentation he concluded that bacteria, which he called "T-bacilli," were the key to unlocking the origin of cancer.
When cells were transformed, either through injury or aging, they underwent a death process that Reich termed "bionous degeneration." As a result, deadly T-bacilli began to form within the cells. He could demonstrate these bacteria microscopically in living (and unstained) cancer cells. Injection of these microbes into animals caused inflammation and eventual death from cancer. In artificially-produced tumors, Reich observed the animal's cancer cells transform into monster cells that resembled one-celled protozoa. He believed that overwhelming infection with T-bacilli and massive breakdown of cancer tissue caused most deaths from cancer.
Reich discovered T-bacilli not only in cancer tumors, but also in the blood, body fluids, and the excreta of cancer patients. He originally thought the T-bacillus was the specific infectious agent of cancer, but he eventually found the bacteria in persons with other diseases ­ and also observed T-bacilli in the blood and excreta of normal healthy people.
The blood of cancer patients produced T-bacilli easily and quickly. In contrast, blood from healthy people produced the bacilli slowly. Reich concluded "the disposition to cancer is therefore determined by the biological resistance of the blood and the tissues to putrefaction." Reich's two revolutionary books, "The Bion Experiments on the Origin of Life" (1938) and "The Cancer Biopathy" (1948) contain details of his highly controversial biologic experiments and scientific theories, as well as fascinating insights into the origin of the cancer cell and "T" bacteria.
Reich's monster cancer cells that morphed into protozoa-like cells may have their counterpart in the HeLa cell, which was grown in tissue cell culture from cervical cancer in 1951. These cells have been used extensively in cancer and cancer virus research since that time. Due to their ability to replicate indefinitely and their abnormal number of non-human chromosomes, some geneticists now consider HeLa to be a contemporary creation of a new amoeba-like protozoal species called Helacyton gartleri. For more details on HeLa, consult the Wikipedia.
On December 3, 1890, William Russell, a pathologist at the Royal Infirmary in Edinburgh, gave an address to the Pathological Society of London outlining his findings of "a characteristic organism of cancer" that he observed microscopically in fuchsine-stained tissue sections from all forms of cancer that he examined, as well as in certain cases of tuberculosis, syphilis and skin infection.
The parasite was seen within the tissue cells (intracellular) and outside the cells (extracellular). The size of Russell's parasite ranged from barely visible, up to "half again as large as a red blood corpuscle." The large size of some of these bodies suggested a fungal or yeast-like parasite. Russell called them "fuchsine bodies" because of their bluish-red staining qualities.
In the late nineteenth century, it was generally thought that each microbe could only give rise to a single disease. Thus, the idea of a cancer germ (especially one that could also be identified in TB and syphilis) was received cautiously. Nine years later, in yet another report on "The parasite of cancer" in The Lancet (April 29, 1899), Russell admitted that finding cancer parasites in diseases other than cancer was indeed a "stumbling block." By this time a considerable number of opposing scientists concluded that Russell bodies were not organisms, but were merely cellular degenerations of one kind or another. Furthermore, no consistent microbe could be cultured from cancer tumors; and when these microbes were inoculated into animals the results were often conflicting or negative. Russell was not trained as a microbiologist, and he avoided getting into the bacteriologic controversies regarding the various microbes grown from cancer.
After three years' work at the New York State Pathological Laboratory of the University of Buffalo, Harvey Gaylord confirmed Russell's research in a 36-page report titled "The protozoon of cancer," published in May 1901, in the American Journal of the Medical Sciences. Gaylord found the small and the large round or oval forms characteristic of Russell bodies in every cancer he examined. The tiniest forms were the size of ordinary cocci (around 1 micron in size); the large spherical bodies attained the amazing size of 50 microns in diameter! In addition, he found evidence of internal segmentation within the larger bodies "after the manner recognized in malarial parasites." Thus, the size range of Russell bodies was enormous.
Russell's 1899 paper ended his writings on a cancer parasite, but his "fuchsine bodies" became well-known to pathologists as "Russell bodies." These bodies continue to fascinate researchers and physicians (like myself) up to the present time. Russell's 1890 paper can be found online by Googling: brmedj04652-0016.
Virologists now believe viruses cause cervical cancer, and cancers like Kaposi's sarcoma. Hepatitis viruses are thought to promote liver cancer; and the AIDS virus (HIV) is considered a cancer-causing virus. But could bacteria infect a cell and transform it into a parasitic cancer cell? Stomach-ulcer causing bacteria have been implicated in gastric cancer; and in October 2011, two independent research teams have found a link between infection with fusobacteria and colon cancer.
By the early part of the twentieth century, the idea of a "cancer parasite" was soundly rejected. The most influential physician to speak against it was James Ewing, an American pathologist. In 1919 Ewing declared that "few competent observers consider it (the parasitic theory) as a possible explanation in cancer." According to Ewing, cancer did not act like an infection. Therefore, microbes could not possibly cause cancer.
As a result, few researchers dared to contradict Ewing's dogma.
Nevertheless, some die-hard physicians remained convinced microbes were at the root cause of cancer and wrote about it convincingly in medical journals. The long history of this research is recorded in my two books, "The Cancer Microbe" (1990) and "Four Women Against Cancer" (2005). A wealth of information on the microbiology of
cancer can also be found by Googling "cancer microbe."
In the late 1970s microbiologist Guido Tedeschi at the University of Camerino discovered "granules" in the red blood cells of healthy and ill people that could be cultured in the laboratory. Some of the staphylococcal and corynebacteria-like bacteria cultured from the red blood cells were acid-fast and cell wall-deficient, a staining and growth characteristic shared with the cancer microbe. This research has been confirmed by newer studies suggesting that bacteria reside in blood in healthy as well as sick individuals. These findings cast great doubt on the long-held idea that normal healthy blood is "sterile."
Light microscopes can magnify objects 1000 times. Although electron microscopes (which have been used since the 1950s) have the ability to magnify objects tens of thousands of times, the exact significance and function of Russell bodies still remain an enigma.
As noted, Russell bodies can be found in cancerous and non-cancerous diseases. In 1954 RG White, in "Observations on the formation and nature of Russell bodies," experimentally produced Russell bodies in animals by injecting them with different species of bacteria. He then studied the ensuing development of these bodies in the spleen, lymph nodes and plasma cells of the injected animals.
Various current theories of origin of Russell bodies include their derivation from lymphocytes, from plasma cells with later degeneration, from the mitochondria of cells, and even from a red blood cell swallowed up by a plasma cell. (Plasma cells are specialized forms of white blood cells that normally produce antibodies.) Most researchers currently believe Russell bodies are composed of immunoglobulins (proteins that acts as antibodies), but an electron microscopic study by SM Hsu in 1981 has cast some doubt on this belief. No modern researcher has ever considered the possibility that Russell bodies might represent unusual large growth forms of cell wall deficient bacteria (also known as mycoplasma or
Bacteria are unicellular microorganisms that lack an organized nucleus. By contrast, protozoa are classified as larger single cell "animal" forms with a nucleus. There are many different kinds of bacteria but only one type has been consistently observed and studied in cancer for over a century. The cancer microbe within the body is cell wall deficient and pleomorphic, meaning it has various forms, some of which appear as the tiniest of granules barely visible microscopically. The most common primordial form in tissue is the size of ordinary staphylococci; and the largest fungus-like round spherical spore-like forms mimic the various sizes of Russell bodies.
As mentioned, some Russell bodies enlarge to truly gigantic proportions, many times larger than the size of the smallest cocci or granules. In addition, the microbe has exceedingly small filterable submicroscopic virus-like forms approaching the size of viruses, and visible only by use of the electron microscope. This was demonstrated by Virginia Wuerthele-Caspe Livingston and colleagues in a landmark 1950 report in the American Journal of the Medical Sciences, entitled: "Cultural properties and pathogenicity of certain microorganisms obtained from various proliferative and neoplastic diseases." (For details, Google the cancer research of Virginia Livingston.)
Scientists who have extensively studied cultures of the pleomorphic cancer microbe claim it most closely resembles the "acid-fast" mycobacteria that cause tuberculosis. Because mycobacteria are closely related to fungi, they can exhibit fungal-like forms. There is still controversy as to whether the fungal-like mycobacteria can produce "spores", similar to what fungi do.
During the 1960s microbiologist Louis Dienes popularized the terms "cell wall-deficient" and "L form" to encompass bacterial laboratory growth stages that range in size from filterable virus-sized forms, up to large spherical forms that he termed "large bodies." I believe Russell bodies found in cancer and non-cancerous tissue represent infection with pleomorphic forms of cell wall deficient bacteria within the body.
What do we mean by the term "parasite?" The word in microbiology is a general and non-specific term meaning any form of life that feeds on another.
Viruses are submicroscopic, can only replicate inside a cell, and can't be seen with a light microscope. There is controversy as to whether viruses are living or dead. Bacteria do not contain a nucleus and are considered the smallest forms of life. Fungi are larger than bacteria, and they produce spores. Protozoa are one-celled life forms which have a nucleus.
There are an estimated 100 trillion cells in the human body. Ninety percent of these cells are microbial cells, primarily bacterial cells. These body bacteria live peacefully within us in "symbiosis." However, when the immune system is weakened and/or or when tissue is damaged, these bacteria can proliferate and cause cellular inflammation. Inflammation is a precursor to the development of cancer.
Cancer microbe researchers believe that it is these primordial symbiotic body bacteria that are involved in cancer. Unfortunately, when looking for "a cause of cancer," cancer experts generally ignore these trillions of bacteria as causative agents. Also ignored are the many reports showing these intra- and extracellular bacteria in cancerous tissue. These bacteria can also invade the cell nucleus, thereby gaining access to the cell's genetic material. This should be of great interest to geneticists and molecular biologists searching for reasons why genes mutate and chromosomes break.
In his 2011 Press Release on the cancer parasite, Duesberg states: "Cancer is comparable to a bacterial level of complexity, that is, it doesn't follow orders like other cells in the body, and it can grow where, when, and how it likes. That's what species are all about."
Cancer is a new form of life within the human body; and bacteria are the ancestors of all living things. For details on the connection between the two, see my article "Bacteria, cancer, and the origin of life," available online.
One can only wonder why Duesberg and the cancer establishment continue to ignore a century of "cancer microbe" research implicating a pleomorphic virus-like, bacteria-like and fungus-like intracellular microorganism which is a perfectly equipped killing machine capable of genetically transforming our human cells into parasites of cancer.
The varied forms of the pleomorphic "cancer microbe" defy the rules and tenets of traditional bacteriology. Many scientists still profess that bacteria have only one form; and they reproduce by splitting in two to produce two similar-appearing microbes. Undoubtedly, this widespread belief in bacterial "monomorphism" has made the proposed microbiology of cancer difficult, if not impossible, for medical science to comprehend and accept. Human cell life and reproduction is complex. So too is the complexity of our bacterial ancestors that we carry in our bodies.
Figures 1-4 show examples of these intracellular and extracellular coccoid forms in breast cancer, prostate cancer, Hodgkin's lymphoma, and AIDS-related Kaposi's sarcoma. Figure 5 shows a collection of large pink-stained spherical bodies, reported as "African eosinophilic bodies" in pre-AIDS and AIDS-related Kaposi's sarcoma. They are also comparable to Russell bodies. Figure 6 shows the close relationship between the intracellular small round forms and the extracellular larger forms of Russell bodies in an enlarged lymph node from a case of AIDS. Figure 7 shows medium-sized intracellular Russell bodies, as well as large clumped Russell bodies in the same AIDS lymph node. The size and shape of large forms of Russell bodies can mimic the size and shape of fungal spores. Figure 8 shows a beaded "string of pearls" formation composed of small round coccoid forms in the connective tissue of a fatal case of Hodgkin's lymphoma.
Figure 1. Breast cancer. Tissue section showing intracellular round coccoid forms in breast cancer. Fite (acid-fast) stain, magnification, x1000, in oil.
Figure 2. Prostate cancer. Tissue section showing a cell packed with intracellular coccoid forms. Fite (acid-fast) stain, x1000, in oil.
Figure 3. Hodgkin's lymphoma. Autopsy necroscopic tissue section from a fatal case showing intra- and extracellular variably-sized round coccoid forms bursting out a cell in the connective tissue. Fite stain, x1000, in oil.
Figure 4. AIDS-related Kaposi's sarcoma of the skin. Arrows point to extracellular coccoid forms in the tumor in Fite stained tissue section, x1000. Compare the size and shape of these round forms with the Gram-stained coccal forms of Staphylococcus epidermidis cultured from the skin tumor, as seen in the insert.
Figure 5. AIDS-related Kaposi's sarcoma of the skin. Tissue section showing, in center, a tightly-packed collection of pink-stained variably-sized larger spherical bodies compatible with Russell bodies. Hematoxylin-eosin stain, x1000, in oil.
Figure 6. AIDS-related "reactive lymph node hyperplasia" showing intracellular small coccoid forms (arrow) and nearby larger extracellular Russell bodies (RB) in the lymph node. Gram stain, x1000, in oil.
Figure 7. AIDS-related "reactive lymph node". Same tissue section as Figure 6 showing an intracellular collection of medium-sized Russell bodies at top left; and a clump of very large Russell bodies at bottom. Gram stain, x1000, in oil.
Figure 8. Hodgkin's disease. An autopsy necroscopic tissue section showing, at right, a fungus-like "string of pearls" collection of variably sized-coccoid forms in the connective tissue. Fite stain, x1000, in oil
[Alan Cantwell is a retired dermatologist. He writes frequently about the bacterial origin of cancer and AIDS. He is the author of "The Cancer Microbe" and "Four Women Against Cancer" and other books, all published by Aries Rising Press, PO Box 29532, Los Angeles, CA 90029. His books are available from and through Email:]
Suggested reading: (These articles can be found on by using the website's search engine)
Broxmeyer L and Cantwell A: AIDS: "It's The bacteria, stupid!" (2008)
Cantwell A: Cancer is an infection caused by tuberculosis-type bacteria. (2008)
Cantwell A: All human blood is infected with bacteria. (2007)
Cantwell A: Do TB-type bacteria cause AIDS? (2007)
Cantwell A: Immortal HeLa cells and the continuing contamination of cancer and vaccine research. (2010)
Cantwell A: The Russell Body; The forgotten clue to the bacterial cause of cancer. (2003)
Cantwell A: The 'Star Cell'; The microscopic indicator of bacterial infection in cancer, AIDS and chronic disease . (2011)
Cantwell A: Virginia Livingston, MD; Cancer quack or medical genius? (2006)

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