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 Acid-Fast Bacteria In-Vivo in Prostate Cancer and the Connection between Prostate Cancer, Other Cancers, and the Kaposi’s Sarcoma Virus
Author: Alan R Cantwell, Jr (
Date:   06-03-04 12:51

Acid-Fast Bacteria In-Vivo in Prostate Cancer and the Connection between Prostate Cancer, Other Cancers, and the Kaposi’s Sarcoma Virus

Author: Alan R Cantwell, Jr., M.D.
Los Angeles, California,
contact email: alancantwell@sbc

Paper Type: Review

Please cite as: Cantwell AR Jr. Acid-Fast Bacteria In-Vivo in Prostate Cancer and the Connection between Prostate Cancer, Other Cancers, and the Kaposi’s Sarcoma Virus. JOIMR 2004;2(3):1
Published: 28 May 2004
(C) 2004, by Alan Cantwell, Jr. M.D.


Bacteria in the form of previously described “cancer microbes” were identified in a Fite (acid-fast)-stained histopathologic tissue section from a case of prostate adenocarcinoma in a 68 year-old, HIV-negative Italian-American man with a concomitant history of a solitary skin lesion of classic Kaposi’s sarcoma. The pleomorphic bacteria observed in vivo are consistent with so-called cancer-associated bacteria previously described in breast cancer, Kaposi’s sarcoma, and other forms of cancer, by various investigators over the past century. The proposed microbiology of cancer is discussed, as well as the new finding of the Kaposi’s sarcoma virus (human herpes virus-8) in the blood of up to 40% of patients with prostate cancer. Further studies of acid-fast bacteria in vivo and the KS virus in prostate cancer are sorely needed to further determine the possible role of these infectious agents in this common cancer of men.


Are infectious bacteria involved in prostate cancer? Can bacteria cause cancer? Is there a connection between prostate cancer and a cancer-causing Kaposi’s sarcoma virus common in AIDS patients? Does the presence of new viruses and unusual bacteria in the blood of healthy blood donors indicate possible contamination of the blood supply? Could blood transfusions be a hidden source of cancer-causing infectious agents? These controversial questions concerning the finding of heretofore unrecognized bacteria in vivo (within the human body) in prostate cancer are explored.

Prostate cancer is the most common form of cancer in American men, with 230,000 new cases diagnosed yearly and 30,000 deaths annually (double the number of yearly AIDS deaths in the U.S. ). The walnut-sized prostate gland manufactures the fluid portion of the semen. It lies just below the bladder and surrounds the urethra — the tubular urinary passageway that leads from the bladder down through the center of the prostate and into the penis. In many cases the cancer is slow-growing, and elderly men with prostate cancer often die from some other cause.
Autopsy studies show that thirty percent of men over age 50 already have microscopic evidence of prostate cancer; and when a man reaches the age of 80 there is an 80% chance he will have prostate cancer. If a man lives long enough, it is almost guaranteed he will have microscopic evidence of prostate cancer. The treatment is surgical removal of the entire gland (along with the portion of the urethra within it) or a series of radiation treatments to the prostate. Both procedures often result in urinary incontinence and impotence.

Since the late 1980’s the PSA (prostate specific antigen) blood test has been a widely used screening test to detect possible cancer of the gland. Previously, a rising PSA level of 4 nanograms or more signified possible cancer. However, results of a new study released in May 2004 indicates that 15% of men with PSA levels less than 4 had cancer when their prostates were assessed with biopsies. The results of this study is causing great turmoil and controversy in the diagnosis and treatment of prostate cancer.

What causes prostate cancer?

Like most forms of cancer, there is no known cause. If the cancer is confined to the prostate a cure is probable, but once it spreads to other parts of the body, there is no cure.
An April 2004 report widely heralded in the media suggests that men who ejaculate more frequently (21 times or more per month) might lower their risk for prostate cancer. However, a May 2004 report warned against male sexual promiscuity claiming that men with multiple sex partners and a history of sexually-transmitted diseases were more likely to get prostate cancer.

Acute and chronic inflammation of the prostate (prostatitis) is a common and painful condition affecting younger and middle-aged men. There is debate whether this a risk factor for cancer. The cause of chronic prostatitis is incompletely understood, although antibiotic therapy is employed in the majority of cases. A variety of bacterial species (staphylococci, streptococci, corynebacteria, and others) have been cultured from prostatitis sufferers. Benign prostatic enlargement (hyperplasia) , another common condition of older men, is not a premalignant lesion nor a precursor to carcinoma.

There is disagreement regarding the role of testosterone in the development of prostate cancer. Testosterone administration is contraindicated in prostate cancer as it is believed to make the cancer more aggressive.

Researchers have recently cautioned men about ingesting excessive amounts of zinc supplements, claiming that 100 milligrams of zinc daily could more than double the risk of prostate cancer. Zinc is normally found in the prostate, and some nutritionists have previously recommended zinc supplementation as beneficial for prostate health. DHEA, another popular supplement, is also suspect because some fear that the increased levels of testosterone seen with daily DHEA pills could stimulate the growth of a tiny prostate tumor that would otherwise have remained dormant.

Prostate Cancer and Kaposi’s sarcoma virus infection

Over the years a number of viruses (the cytomegalovirus, human papilloma virus, various herpes viruses, and the hepatitis B virus) have been suspected of causing or complicating prostate cancer. A very recent report suggests the Kaposi’s sarcoma virus, also known as human herpes virus 8 (HHV-8), might also be involved.

The KS virus is intimately connected with the epidemic of HIV and AIDS. Prior to the onset of the AIDS epidemic in gay men in the late 1970’s, so-called “classic” Kaposi’s sarcoma (KS) in the U.S. was an extremely rare cancer tumor found primarily in elderly men of Jewish and Italian extraction. Before AIDS, there was never any evidence that KS was transmitted sexually.

When AIDS began exclusively in the gay male population in America, KS skin tumors in young homosexuals became the “Scarlet Letter” indicating infection with a new infectious agent (now known as HIV) that was mysteriously introduced into this select population. Up to one-third of AIDS patients now carry the KS virus. When the epidemic began, one in three gay AIDS patients had KS skin lesions. At present, only about one in ten have KS lesions.

Infection with HIV, the virus that causes AIDS, makes patients more vulnerable to certain cancers, particularly lymphoma, KS, and uterine cancer. However, prostate cancer in HIV-infected men is uncommon.

Scientists now believe the KS virus is the cause of most cases of AIDS-related KS, as well as non-HIV-related “classic” cases and “epidemic” forms of KS seen in Central Africa. Although KS cases were first diagnosed in Europe in 1872, the KS virus was first discovered in 1994 in cases of AIDS-related KS. This KS virus has also been found in other forms of cancer, such as lymphoma and multiple myeloma.

A 2004 study by LJ Hoffman and associates at the University of Pittsburgh tested the blood of prostate cancer patients for antibodies to the KS virus antigens. Remarkably, 40% of men from Trinidad and Tobago and 20% of U.S. men tested positive for antibodies to the virus. This was considerably higher than an age-matched control group of Trinidad men (23%) and American men (5%). The researchers conclude that the KS virus could play a role in the development of prostate cancer.

In the U.S. the general incidence of KS virus in blood donors is 5%. However, a 2002 study of Texas blood donors indicated a 15% infection rate. Seroprevalence was found to be low in countries like Malaysia, India, Sri Lanka, and Thailand. However, the African countries of Ghana, Uganda and Zambia show high seroprevalences (up to 40%) in both healthy and HIV-infected populations.

The emergence of the KS virus worldwide indicates a virus that has been introduced in recent decades. The fact that both HIV and the KS virus were initially introduced exclusively into the gay American population in the late 1970s has received little comment. One can perhaps easily explain the “introduction” into gays of a new HIV virus of supposed African origin, but what is the explanation for the additional introduction of a second KS virus into a select population of young gay white American men?

Another aspect of the worldwide spread of the KS virus is that the blood supply is not screened to eliminate donors carrying this cancer-causing virus. Gay men and any man who has had sex with another man since 1978 are banned as donors, and all blood is screened for HIV. Yet, persons carrying the KS virus in their blood are not excluded as blood donors. This alone is good reason for any person undergoing elective surgery to donate their own blood beforehand in the event that a blood transfusion is needed during or after major surgery.

Cancer and the Cancer Microbe

Although medical science claims the cause of most cancer is unknown, there is evidence accumulated since the late 19th century to show that cancer is a disease caused by infectious bacteria (not to be confused with viruses which are not visible microscopically). In 1890 the noted pathologist William Russell (1852-1940) reported spherical forms in histopathologic sections from various forms of cancer which he interpreted as "the characteristic organism of cancer." These forms were subsequently discredited as microbial forms but have became known to every pathologist as "Russell bodies." (For more details see, “The Russell Body: The forgotten clue to the bacterial cause of cancer”)

The most vocal proponent of bacteria as a cause of cancer was the late Virginia Livingston, M.D. In 1950, Virginia Wuerthele-Caspe Livingston and Eleanor Alexander-Jackson (a microbiologist), along with John A Anderson (head of the Department of Bacteriology at Rutgers), James Hillier (head of the electron microscopy at the RCA Victor Laboratories at Princeton), Roy Allen (a renowned microscopist), and Lawrence W Smith (author of a well-known pathology textbook used in medical colleges), all combined their talents to write a paper entitled “Cultural Properties and Pathogenicity of Certain Microorganisms Obtained from Various Proliferative and Neoplastic Diseases,” published in the December issue of The American Journal of the Medical Sciences. The characteristics of the cancer microbe in blood, tissue, and culture, were described in detail; and the extreme pleomorphic nature of the organism was revealed in photos taken with the electron microscope at a magnification of 31,000X. (The ordinary light microscope only magnifies a thousand times.)

The cancer microbe, which Livingston later called Progenitor cryptocides, was filterable through a pore designed to hold back bacteria. The filterable microbial forms were indeed “virus-sized.” However, with time they were able to revert back to the size of conventional bacteria.

The microbe was characterized as pleomorphic, that is, having more than one form and size. The smallest forms of the organism were virus-like, and the larger bacterial forms were comparable to what bacteriologists call “mycoplasma”, “L-forms” and “cell-wall deficient forms.” The largest forms of the organism resembled what Russell called “the cancer parasite.” Livingston believed the organism was closely related to the mycobacteria, the species of acid-fast bacteria that causes tuberculosis. In addition, she claimed the “acid-fast” staining method was essential to color and identify the microbe in tissue and in culture.

In a series of papers published in the 1950’s, 60’s, and 70’s, Livingston and Alexander-Jackson , along with Irene Diller (a cell cytologist) and Florence Seibert (a chemist famous for developing the tuberculosis skin test) , all continued important cancer microbe research showing the characteristic “connective tissue parasite” of cancer, the germ that could be found inside the cell (intracellular) and outside the cell (extracellular) in all cancers. From the very beginning of her research Livingston stressed that the microbe tends to involve the collagenous (connective) tissue, and the photographs presented here in prostate cancer confirm that.

Livingston’s two books, Cancer: A New Breakthrough (1972) and The Conquest of Cancer (1984) are unfortunately out-of-print. When she died in 1990 at the age of 84, she was widely regarded as a quack, particularly by the American Cancer Society which claimed her cancer microbe did not exist. Likewise, a bulletin published by the National Cancer institute on Nov 30, 1990 also declared: “There is no scientific evidence to confirm Livingston’s theories of cancer causation.”

More details covering a century of cancer microbe research can be found in my book, The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases (1990) , in Cell Wall Deficient Bacteria (1993) by Lida Mattman, Ph.D., in Can Bacteria Cause Cancer?: Alternative Medicine Confronts Big Science (1997) by David Hess, and also by initiating a computer search at and typing in “cancer bacteria”, “cancer microbe”, or “cancer-associated bacteria.”

Over the past four decades various personal papers published in medical journals have confirmed the presence of cancer bacteria in the tissue of various cancers, including breast cancer, Kaposi’s sarcoma, Hodgkin’s disease, mycosis fungoides, as well as non-cancerous diseases like scleroderma, lupus erythematosus, and sarcoidosis. Additional papers on the microbiology of cancer are presented online at the Journal of Independent Medical Research web site ( References and abstracts on 10 cancer microbe medical publications can be found at the National Library of Medicine’s “PubMed” web site (Type in a query of “Cantwell AR + cancer bacteria”.

Livingston stressed that the cancer microbe was present in the blood, tissue, excreta, and body fluids of all human beings. When the immune system was functioning normally these microbes did not cause disease. However, when tissue was damaged or weakened these microbes became aggressive and pathogenic, producing hardening and thickening of the tissue (such as found in scleroderma and heart disease), inflammation (autoimmune diseases and sarcoidosis) and proliferative and cancerous changes. According to Livingston, the cancer microbe is essential to our life biology. When conditions are adverse, it emerges and reverts to its pathogenic form .

Livingston’s research is connected with newer microbiologic findings indicating that the blood of all human beings is indeed infected with a variety of so-called “cell wall deficient” bacteria. The tiny, virus-like forms of the cancer microbes are undoubtedly related to the tiniest of newly-discovered bacteria currently called nanobacteria. These previously neglected and largely-unstudied nanobacteria, which lie in size between the normal-sized bacteria and the smallest viruses, are thought to be involved in a variety of skin and heart ailments presently labeled as diseases of unknown etiology. An excellent source of up-to-date nanobacteria research can be found at the Nanobac Pharmaceutical web site ( ).

Detecting Acid-Fast Cancer Bacteria in Prostate cancer

In December 2003 my partner of 30 years was diagnosed with prostate cancer. He is a 68 year-old Italian-American who has always been in good health. His PSA was abnormally elevated to 9, and a digital rectal examination by the urologist revealed a hardened area on the right side of the gland. Multiple biopsies were preformed from six areas of the prostate gland and three were positive for adenocarcinoma.

Two months before the prostate cancer diagnosis, he had a skin biopsy performed on a small reddish skin lesion on the right lower leg. The pathology report was interpreted as Kaposi’s sarcoma. The lesion totally disappeared after the biopsy site healed and there has been no recurrence.

In view of the frequent association of KS with AIDS, an HIV test was performed and was negative. Thus, his KS diagnosis was consistent with the pre-AIDS “classic” type of KS which, although rare, is found most often in elderly Jews and Italians in America. His blood was not tested for the KS virus. However, blood tests did reveal past asymptomatic infection with the hepatitis B virus, and he has a history of recurrent skin infection with herpes simplex virus.

A prostatectomy, along with removal of the surrounding lymph nodes, was performed in March 2004. Microscopic examination of this tissue showed the cancer entirely confined to the prostate with no cancer detected in the nodes. Approximately 25% of the gland was involved with invasive adenocarcinoma. Cancerous prostate glands removed at surgery often tend to be multifocal, meaning that more than one part of the gland is affected by cancer.

In view of my previous cancer microbe studies, I requested that the pathologist supply me with a Fite-stained tissue section of his prostate tissue. The Fite stain is an “acid-fast” stain traditionally used for the detection of acid-fast tuberculosis-type bacteria. It is the essential staining technique required for the detection of cancer-associated bacteria. One of the reasons pathologists do not identify bacteria in cancer is that the hematoxylin- eosin tissue stain, routinely employed by pathologists, does not stain cancer microbes.

Because bacteria are so small, it is necessary to study the tissue under oil immersion. That is, a drop of oil must be put on the slide and the tissue must be studied carefully using the oil-immersion lens of the light microscope in order to visualize the material at the highest possible magnification. This allows tissue examination at the highest magnification possible, a magnification of 1000 times.

Having retired from dermatologic practice a decade ago, I had done absolutely no microscopic work. Although I had studied various types of cancer related to dermatology, I had never had the opportunity to study prostate cancer, the leading cancer of men. I had previously reported on bacteria in vivo in various types of KS. I was aware of the association of the KS virus and prostate cancer, and I was determined to see if microbes could be identified in my partner’s cancer, particularly because he had the rarest of cancers — the non-AIDS related classic form of KS seen in elderly Italian men .

For the first 15 minutes of study I searched the most cancerous area of the gland and found nothing. However once I searched the connective tissue areas (the stroma) adjacent to the main tumor mass, the bacteria were easily detected.

Figure 1 (left): Tiny, tightly-packed intracellular coccoid forms in the stroma (collagen) of prostate cancer. Fite stain, magnification x400
Figure 2 (right): Additional view of tightly packed coccoid forms in prostate cancer. Fite stain, magnification x400

Prostate cancer bacteria are primarily observed in the connective tissue stroma in tightly-packed clusters of round “coccoid” forms seemingly embedded in a matrix. Sometimes a cell nucleus can be clearly observed with the coccoid forms surrounding it (Figure 1). Often no nucleus is visible (Figure 2). Extracellular forms, forms that escape from the tight bacterial clusters and scatter in the tissue, are also visible (Figure 3). The size of these round coccoid forms vary. Most are the size of ordinary staphylococci. Some are so tiny they are barely visible to the naked eye.

Figure 3 (left): Extracellular, scattered coccoid forms on left and a cluster of coccoid forms on right in prostate cancer. Fite stain, magnification x400
Figure 4 (right): Large coccoid forms resembling the size of yeast spores in prostate cancer. Fite stain, magnification x1000, in oil

The photos emphasize the varied size of the pleomorphic coccoid forms in the prostate, as well as the preference of the microbe for “collagen” — the “glue” protein that helps hold together the cells and tissues of the body. Could this affinity of the microbe for collagen and the resultant biochemical change be the basis for the elevated protein antigen detected by the PSA test? Particularly when antigens are often defined as foreign substances produced by bacteria and viruses.

Cancer Microbes and human blood

Although doctors and the blood supply companies would like the public to believe that the blood is “sterile” and free from harmful infectious agents, in reality human blood is an aquarium filled with various known and unknown viruses and bacteria. Currently, healthy blood donors are screened for syphilis, hepatitis B and C, HIV-1 and 2, and HTLV-1 and 2. There is no routine screening for other known pathogenic viruses, such as transfusion transmitted virus (TTV), hepatitis G, the KS virus, parvo B 19 virus, and others.

It is now increasingly recognized that everyone’s blood contains bacteria. Some of the species of blood bacteria (staphylococci, streptococci, corynebacteria) are similar to the kinds of bacteria found on the skin. These types of bacteria are also closely related, if not identical, to what are termed “cancer-associated bacteria” reported by various investigators over the decades. Except for the bacteria that cause syphilis, the blood is not screened for any of these bacterial agents.

A December 2001 bulletin published by America’s Blood Centers indicates that blood suppliers are well aware of bacterial contamination of the blood. In fact, “the estimated rates of bacterial contamination of components are 50 to 250 times higher than those of viral infection. While many bacterially contaminated components produce no clinical morbidity, consensus is developing that it is under-recognized and the most important infectious complication of transfusion.”

Blood suppliers do not appear to recognize that staphylococci, streptococci and corynebacteria, as well as a host of tiny and difficult-to-culture “nanobacteria” are normal constituents of the blood. Blood contaminated with staphylococci and corynebacteria are assumed to originate in skin contamination when the blood is drawn, rather than having an intrinsic origin within normal and diseased blood.

According to the Pall Corporation which provides products to solve complex contamination problems in the blood industry, “less than 5% of the U.S. population donates blood, making the supply very precious. The reality is that if all these contaminated units were to be discarded, there would be an insufficient supply to meet requirements for donor blood.”

With its intrinsic infectious viruses and bacteria, the transfusion of blood undoubtedly causes harm to some patients, particularly in light of the fact that persons who need blood transfusions have stressed immune systems are not in the best of health. The extent to which blood transfusion causes future pathological diseases is not known, nor is it even considered.

The origin of “cancer microbes” in cancer tissue may very well be derived from blood bacteria. The microbiology of cancer, although presently ignored by science, will ultimately have to be explored in relationship to the equally-ignored microbiology of human blood.

Cancer: One disease or many?

The cancer establishment believes that cancer is not one disease but many different diseases, each with their special risk factors, and each with their own special treatment. However, if cancer microbes turn out to be etiologic agents in cancer, cancer may prove to be essentially one disease and not many different ones. For example, tuberculosis bacterial infection confined to the skin is a very different clinical disease from extensive tuberculosis infection of the lungs. Yet both diseases are the same because they are caused by the same agent.

Figure 5 (on left): (Click here to enlarge image) Arrows point to variably sized coccoid forms in breast cancer. Kinyoun’s (acid-fast) stain, magnification x1000, in oil
Figure 6 (on right): Additional view of closely-packed coccoid forms in breast cancer. Kinyoun’s (acid-fast) stain, magnification x1000, in oil

Breast cancer and Kaposi’s sarcoma are considered very different diseases. However, cancer bacteria in vivo have been reported in both diseases. Figures 5 and 6 show the appearance of variably-sized coccoid forms in breast cancer (infiltrating ductal carcinoma), and Figure 7 shows the acid-fast stained appearance of Staphylococcus epidermidis cultured from the tumor when it metastasized to the skin. The size of some of the coccoid forms in the tumor are exactly the size and shape of the staphylococci bacteria cultured from the tumor. Figure 8 shows the appearance of the same cocci stained with Gram’s stain.

Figure 7 (on left): Smear of culture isolated from a metastatic skin lesion from breast cancer and identified as Staphylococcus epidermidis. Note the similar size and shape of these cocci to the coccoid forms seen in the primary breast tumor, as shown in Figures 5 and 6. Ziehl-Nielson (acid-fast) stain, magnification x1000, in oil
Figure 8 (on right): Smear from same Staphylococcus epidermidis culture shown in Figure 7 but stained with Gram’s stain and showing Gram-positive cocci (dark purple) and Gram-negative (pink-stained) cocci. Magnification x1000, in oil

Figure 9 shows coccoid forms in vivo within a skin lesion of KS in a patient near death from AIDS. Figure 10 shows the appearance of Streptococcus G cultured from his blood shortly before death. If one compares the size and shape of the blood streptococci, they appear similar in size and shape to the coccoid forms seen in vivo in KS (Fig 9).

Figure 9 (on left): Figure 9: Coccoid forms in the deep dermis of a skin lesion of fatal AIDS-related Kaposi’s sarcoma. Fite stain, magnification x1000, in oil
Figure 10 (on right): Smear from culture of streptococcus G isolated from the blood of the patient with KS (Fig 9). Note that the size and shape of the streptococcus are similar to the size and shape of the coccoid forms seen in the KS tumor. Ziehl-Nielson (acid-fast) stain, magnification x1000, in oil

Until the recent study associating the KS virus with prostate cancer, there was no relationship between KS and prostate cancer. Likewise, mammary gland breast cancer and prostate cancer (found exclusively in men) have nothing in common except they are the most common forms of cancer (other than skin cancer) in men and women. Both are secretory glands making body fluids that are excreted externally, and both glands and both cancers are hormone-fueled. However, the pleomorphic coccoid forms seen in vivo in both cancers resemble each other greatly, suggesting that bacteria are involved in the production of both cancers.

Cancer microbes provoke a variety of tissue responses, including fibrosis and thickening of the connective tissue (as in scleroderma), cellular infiltrations (as seen in autoimmune diseases), and the formation of tumors. The fact that similar-appearing bacteria can be identified in vivo in so many different types of diseases, as well as in healthy individuals, makes them admittedly an unprecedented type of infectious agent.

Why does the medical establishment ignore cancer microbe research?

Despite a century of credible cancer microbe research, the medical profession generally ignores all aspects of research implicating bacteria in cancer. One exception is the 1982 discovery of certain bacteria in the stomach (Helicobacter pylori) that are now accepted as the cause of stomach ulcers that can sometimes progress to gastric cancer and gastric lymphoma. This remarkable discovery completely transformed our understanding of the microbiology and pathology of the human stomach. This microbe can be found in normal as well as in diseased stomachs.

The idea of a cancer parasite was forcefully rejected in the early years of the twentieth century. The most influential physician condemning cancer-associated bacteria was James Ewing, a noted American pathologist and author of the widely read textbook, Neoplastic Diseases (1919), in which he wrote that “few competent observers consider it (the parasitic theory) as a possible explanation in cancer.” In Ewing’s view, cancer did not act like an infection. Therefore, microbes could not possibly cause cancer. As a result of his edict, few doctors dared to contradict Ewing by continuing cancer microbe research.

Ewing co-founded the American Cancer Society in 1913 and in the 1930’s he was the director of Memorial Hospital, now better known as Memorial Sloan-Kettering Cancer Center in New York City, one of the most prestigious cancer hospitals in the world. Ewing died in 1943 from bladder cancer, at the age of 76.

Although bacteria were dismissed as causative agents one hundred years ago, viruses are now considered as likely causes of cancer — despite Ewing’s contention that cancer did not act like an infectious disease. What Ewing did not know is that pleomorphic cancer microbes have characteristics of both bacteria and viruses. As mentioned, a half-century ago Livingston showed by electron microscopic study that the microbe is virus-like and invisible in the light microscope in one of its stages. Although physicians easily accept the idea of microscopically invisible viruses in cancer, they seem unable to conceive of a microscopically visible bacterial agent in cancer.

Undoubtedly, the acceptance of cancer bacteria would put cancer research and treatment into a tailspin because the alleged benefits of radiation and chemotherapy would have to be reevaluated as a rational treatment for bacterial infection. Because current antibiotics cannot rid the body of cancer-causing bacteria, this would necessitate the development of new cancer treatments designed to minimize this infection.

It may be left to future medical historians to explain why cancer microbe research has been ignored for a century, despite the millions of cancer deaths yearly and the billions of dollars spent trying to uncover the cause of cancer.

In the meantime, as a retired physician I will continue to bug (pun intended) my colleagues in medicine to get out their microscopes and search for bacteria as I and other cancer microbe researchers have done. The only requirements are an acid-fast stained histopathologic slide of the malignant tissue, a drop of oil on the slide, the use of the oil-immersion lens, and an open mind.

To ignore cancer bacteria because a powerful pathologist told his students a century ago that there were no microbes to be found in cancer is simply irrational and bad science. Re-search means to search again. After many decades of failure to uncover a cause for cancer, surely it is time for a second look at bacteria that can be easily found in this dread disease.


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The microphotographs of the prostate cancer were performed by microscopist James D. Solliday of Santa Ana, California.

Key words:

Bacteria, pleomorphic
Breast cancer, infiltrating ductal carcinoma
cancer-associated bacteria
cancer, origin
cell wall-deficient bacteria
Histopathologic findings
Human Herpes Virus-8
Kaposi’s sarcoma, cutaneous
Kaposi’s sarcoma virus
Prostate cancer, adenocarcinoma
Staphylococcus epidermidis
Streptococcus G

 Formal Peer-Review Assessment
Author: Greg Blaney MD (
Date:   08-07-05 15:43

It is my opinion that:
1. This manuscript is of a scholarly nature
2. It provides a significant contribution to the literature
3. It is not obviously incorrect or incomplete
4. It is of general interest

I believe that "the scientific community is better served by publishing .. this .. manuscript" and I unreservedly recommend that it be accepted and published. Greg Blaney MD, 7 August 2005, Vancouver, BC, Canada

Author: Trevor (
Date:   08-10-05 15:06


This is a Medical Journal, not a discussion forum. If you have a valid peer review to offer, then please make sure your identity is clear on the review and also that your professional qualifications and affiliations are clearly shown, in such a way that they can be readily verified by the Editorial Board.

Guidance for writing an Open Peer Review is at this link.

Reviews not fulfilling these requirements will be deleted from the record.

Trevor G Marshall, PhD
Managing Editor

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