Microbes are all around us, on our skins, in our nasal passages and in our intestines, and even in our blood and tissues.
Usually they exist in harmless balance with the immune system. Some are even beneficent : bacteria in the human intestine help digest food, produce vitamins, and crowd out toxic pathogens. In fact, the human body contains more bacterial cells than somatic (body) cells.
Mitochondria, organelles which produce energy within human cells, have their own DNA and are thought to be descended from free-living bacteria. Bacteria are highly integrated into functions of the entire human body.
The mainstream medical community is now willing to accept that a few type of bacteria or viruses may indeed be responsible for a few forms of cancer, such as Kaposi’s sarcoma, stomach and cervical cancer, but they are unwilling to recognize that infectious agents may be inextricably linked to the development of most other tumors as well.
Yet, there scientific evidence dating back more than one hundred years which points to an bacterial cause cancer, a pleomorphic (many-formed) bacteria, related to or resembling mycoplasma, which has been seen in microscopic slides of numerous tumors.
At the beginning of the 20th century, bacterial genesis of cancer was considered a mainstream theory, and papers about it were published in the Lancet. However, it was eventually sidelined despite a large body of substantiating evidence.
Over the past century hundreds of independent researchers have noted a link between bacteria and cancer in both animals and humans, but their findings were treated as a scientific curiosity and rarely followed up by the general medical establishment.
However, the theory never went away, and individual scientists continued searching for ways to identify and eliminate the suspect bacteria.
In 1890 the German physician and bacteriologist Robert Koch formulated a standard criteria still in use today for judging whether a given bacteria is the cause of a given disease.
“Koch’s Postulates,” while not always valid, provide a useful benchmark for disease investigators.
Koch’s postulates are as follows:
The bacteria must be present in every case of the disease.
The bacteria must be isolated from the host with the disease and grown in pure culture.
The specific disease must be reproduced when a pure culture of the bacteria is inoculated into a healthy susceptible host.
The bacteria must be recoverable from the experimentally infected host.
However, Koch’s postulates have their limitations, which even Koch recognized. They may not hold if:
The particular bacteria (such as the one that causes leprosy) cannot be “grown in pure culture” in the laboratory.
Animal test subjects are immune to the infection.
In addition, a usually harmless bacteria may cause disease if:
It has acquired extra virulence factors making it pathogenic.
It gains access to deep tissues due to trauma, surgery, an IV line, etc.
It infects a patient with a compromised immune system.
Not all people infected by a bacteria develop serious disease; subclinical, low-grade infection may be more common than clinically obvious, symptomatic infection.
The different species of infectious agents linked to various cancers fit fairly well within Koch’s postulates, since they can be isolated from tumors and grown in a petri dishes or cell cultures, and they sometimes produces tumors when injected into test animals.
However, many are also found in lower concentrations in healthy subjects, and it appears that these microbes only cause disease when their host is weakened.
The host’s immune system limits the amount of damage any infectious agent can cause. For instance, H. pylori stomach infections can lead to stomach ulcers and gastric cancer, but many people are asymptomatic carries. Not every woman who has been infected with HPV develops cervical cancer.
Similarly, we should not expect all carriers of other “cancer microbes” to become ill. Also, these bacteria may have the potential to produce diseases besides cancer, since H. pylori can cause stomach ulcers as well.
History
Probably the first official mention of “cancer microbe” occurred on December 3, 1890 when William Russell, a pathologist in the School of Medicine at the Royal Infirmary in Edinburgh, gave an address to the Pathological Society of London. He described histopathologic findings of “a characteristic organism of cancer” that he observed microscopically in fuchsine-stained tissue sections from all forms of cancer that he examined, and also from some cases of tuberculosis, syphilis and skin infection.
The microbe was seen both around and within tissue cells, and ranged in size from barely visible to one and half times the size of a red blood cell. Russell felt that the large size of some of these organisms was suggestive of a yeast or fungal infection.
Russell tentatively called the microbe a possible “blastomycete” (a type of fungus); and called the round forms “fuchsine bodies” due to their bluish-red staining qualities.
Nine years later in 1899, Russell published a report in the Lancet on “The parasite of cancer,” and stated that finding the suspect bacteria present in diseases other than cancer presented a “stumbling block” to the idea of a definitive function for the organisms.
Cultures yielded numerous species of bacteria, and injection of the bacteria into animals gave ambiguous results. Subsequently, many scientists concluded that Russell bodies were merely the result of cellular degeneration.
In the 1920s and 1930s, the scientist Royal Raymond Rife pioneered the use of radiofrequency devices to kill bacteria. Rife discovered that a certain spectrum of radio waves was lethal to bacteria, while harmless to human tissue. He also invented a new form of microscope which used monochromatic light, and was accurate enough to see viruses without the use of electron microscopy.
Working from a laboratory in La Jolla in the 1930s, Rife claimed to have a 100 percent success rate in treating cancer. Rife’s lab was shut down due to political pressure by the American Medical association , most of his papers were destroyed, and currently the only known example of his microscopes exists in a museum.
Rife’s discovery of radiofrequency devices to kill bacteria was picked up by Hulda Clark, a Canadian scientist, who began her work in the 1960s. Clark also claimed that many other diseases, including diabetes, allergies, epilepsy, Crohn’s disease, bipolar disorder, schizophrenia, are caused by bacteria and parasites such as liver flukes.
She improved on Rife’s technology, and invented a small raidofrequency device she called the “Zapper” that she claimed eradicated bacteria and other parasites from the body. Instructions on how to build the devices were made available to the public, and can be found on the Internet today.
Clark was harassed by the American authorities until she left to set up her cancer clinic in Mexico, where in 2001 the authorities forbade her from offering alternative treatment for cancer. Like Rife, Clark claimed an extremely high success rate in treating cancer, nearly 100 percent, but no independent analysis of her claims, or those of Rife, exist.
In the 1960s, Dr. Virginia Livingston antagonized the scientific establishment by claiming to have found the microbe responsible for causing cancer, naming it “Progenitor cryptocides”, which means “hidden killer”. She felt that that the microbe had an intrinsic, symbiotic function in the human body, that was responsible for initiating life and for healing of tissue, and that the microbe was ultimately responsible for eventual degeneration and death of all life.
When the cultured organism was injected into animals, it caused tumors to develop in some, but not all, of the test subjects.
In 1974, Livingstone became the first scientist to discover that both cancer bacteria and cancer cells produce the human hormone HCG. This hormone, normally secreted by the human fetus to protect it from the maternal immune system, also protects cancers from immune system attack.
Livingstone concluded that bacteria secrete mutagenic factors such as actinomycin-D with damage human cell DNA, and that they can also interchange genetic material such as bacterial growth factors with human cells. Vaccines targeting HCG-producing and cancer-promoting bacteria deprive cancer cells of a key source of HCG.. As the levels of HCG are lowered, the immune system’s ability to launch an assault on cancer cells increases.
Livingstone cultured patients’ own bacteria from blood and urine to create “autogenous” vaccines to stimulate the immune system. She published many articles and books, such as “Cancer, A New Breakthrough” (1972); “The Microbiology of Cancer” (1977); and “The Conquest of Cancer” (1984).
Her research has been confirmed by other scientists, such as microbiologist Eleanor Alexander-Jackson, cell cytologist Irene Diller, biochemist Florence Seibert, and dermatologist Alan Cantwell, among others.
Milton Wainwright, a microbiologist at the University of Sheffield, UK, has written extensively about the bacteriology of cancer in recent publications such as: “Nanobacteria and associated ‘elementary bodies’ in human disease and cancer” (1999); “The return of the cancer germ; Forgotten microbiology – back to the future” (2000); “Highly pleomorphic staphylococci as a cause of cancer” (2000); and “Is this the historical ‘cancer germ’”? (2003).
Currently, one of the most well-known popular proponents of the link between cancer and bacteria is Dr. Alan Cantwell, who has written numerous articles and books on the subject. Cantwell isolated and reported cell wall deficient bacteria in breast cancer, Kaposi’s sarcoma and Hodgkin’s disease. He states, ” If a disease like cancer is indeed caused by microscopic bacteria, it would indicate physicians have been unable to see what was quite plain for some nineteenth and twentieth century scientists to observe using simple light microscopy.
And with powerful electron microscopes there is now little excuse for not “seeing” bacteria.”
Mycoplasma
Mycoplasma, the oldest suspect in the bacterial theory of cancer, has also been implicated as a direct cause or a signficant cofactoer in a host of other degenerative and inflammatory diseases.
Mycoplasmas are frequently found in the oral and genito-urinary tracts of normal healthy subjects, with females four times more frequently infected than males, which just happens to be the same gender-skewed incidence rate as rheumatoid arthritis, fibromyalgia, Chronic Fatigue and other related auto-immune disorders.
In 1997, the National Center for Infectious Diseases, Centers for Disease Control and Prevention’s journal, Emerging Infectious Diseases, published the article, Mycoplasmas : Sophisticated, Reemerging, and Burdened by Their Notoriety, by Drs. Baseman and Tully who stated:
“Nonetheless, mycoplasmas by themselves can cause acute and chronic diseases at multiple sites with wide-ranging complications and have been implicated as cofactors in disease.
Recently, mycoplasmas have been linked as a cofactor to AIDS pathogenesis and to malignant transformation, chromosomal aberrations, the Gulf War Syndrome, and other unexplained and complex illnesses, including chronic fatigue syndrome, Crohn’s disease, and various arthritides.”
The first strains of mycoplasma were isolated from cattle with arthritis and pleuro-pneumonia in 1898 at the Pasteur Institute. The first human variety was isolated in 1932 from a wound abscess.
The first connection between Mycoplasmas were identified as a cause of rheumatoid diseases in 1939 by Drs. Swift and Brown. In the late 1950′s a specific strain was identified as the cause of atypical pneumonia, and named Mycoplasma pneumonia.
The association between immunodeficiency and autoimmune disorders with mycoplasmas was first noted in the mid 1970s in patients with primary hypogammaglobulinemia (an autoimmune disease) due to infection with four species of mycoplasma localized in joint tissue.
Since that time, more than 100 different mycoplasma species have been identified and recorded in plants, animals, and humans.
There are hundreds of studies from scientists all around the world linking various species of mycoplasma with cancer.
The research of Dr Shy-Chung Lo at the Armed Forces Institute of Pathology in Washington, D.C., confirms the multistage, malignant transformation of embryo cell lines persistently exposed to mycoplasma infection as well as animal models so exposed.
According to research by P.J. Chan, published in Gynecologic Oncology (1996), “The oncogenic potential of mycoplasmas was only recently realized when they were shown to cause chromosomal changes and in vitro cell transformations through gradual progressive chromosomal loss and translocations.” Chan and colleagues also report the prevalence of mycoplasma DNA in ovarian cancer.1
In 1993, a research team led by C. Ilantzis at the McGill Cancer Centre, Montreal, Canada analyzed cancer-related markers which are specific to various organs in the body. These markers, called “organ-specific neoantigens” (OSNs), elicit specific immune responses. After analyzing OSN proteins from human colon adenocarcinomas, researchers found the OSNs to be mycoplasmal in origin.2
——————————————————————————————————————————————————————
(1). Chan P.J et al Prevalence of Mycoplasma Conserved DNA in Malignant Ovarian Cancer Detected Using Sensitive PCR-ELISA Gynecologic Oncology 1996 pp. 258-260(3)
(2). C Ilantzis, DM Thomson, A Michaelidou, S Benchimol Identification of a human cancer related organ specific neoantigen Microbiol Immunol, 1993;37(2):119-28
Microscopic Findings
The “cancer bacteria” have a variable appearance, both in tissue samples and in cultures. They can appear as cocci (spheres) 0.1 micrometer in size (a micrometer is 1/1000 of a millimeter), called “ultramicroscopic” since they can still be seen by an ordinary light optical microscope.
Scientists have used the term “nanobacteria” to describe extremely small bacteria which range from .05 to 0.2 micrometer in size. Viruses, which measure 0.01 to 0.02 micrometers, can be viewed only with an electron microscope. The smallest forms of bacteria pass easily through a standard viral filter with pores 0 .2 micrometers in size, which microbiologists assumed (until recently) would catch all bacteria, which tend to be much larger.
Once these tiny cocci are placed in a petri dish and the resulting culture is observed over time, the bacteria also produce larger rods and branching, fungus-like strands.
Mycobacteria are known to exist in different forms, and the tuberculosis microbe, Mycobacterium tuberculosis, is a good example of this complex life cycle. Some forms of the bacillus are round “coccoid” forms; other forms are more typically “acid-fast” and “rod” forms. All mycobacteria form a phylogenetic link or bridge between the bacteria and the “higher” fungi. “Myco” is Greek for fungus. This is the origin of the term “mycobacteria.” Mycoplasmas also have a flowing plasma-like structure without a cell wall – hence “plasma”.
Unlike common bacteria, the suspected cancer microbe Mycoplasma has no cell wall. It invades tissue cells, and uses the cell to replicate itself, much like a retrovirus. When the Mycoplasma breaks out of the cell, it takes a piece of the host cell membrane with it. When the immune system attacks the Mycoplasma, it may also mistakenly attack the host cell, causing an autoimmune condition. It can invade the Natural Killer cells of the immune system, causing immune system disorders. Because it can hide deep within cells, it is extremely difficult to detect and eradicate.
Treating Mycoplasma With Antibiotics
Antibiotic treatment must be tailored to the specific bacterial infection. Many bacteria, especially mycoplasma, are unaffected by many common antibiotics. However, some targeted treatments which are known to kill specific cancer-causing bacteria have proven effective, at least in the early stages of disease.
Mycoplasmal infections are treatable with long cycles of high-dose antibiotics such as doxycycline and tetracycline, followed by a long period of low dose antibiotics. Due to their lack of cell walls, mycoplasma are unaffected by penicillins. Since the organism is a slow-growing, intracellular species with a long life cycle, several long term courses of antibiotics may be necessary. The infection may need to be treated for several months or years, much the same protocol as for Lyme Disease.
No clinical trials have been published in regards to the treatment of cancer with antibiotics against mycoplasma.
Vaccines Against Mycoplasma
Maruyama vaccine is similar to BCG vaccine, both of which are made from mycobacteria tuberculosis isolates. Both have been used extensively as immune system stimulants in cancer patients. Murayama vaccine is made from mycobacteria tuberculosis isolates, and BCG is derived from an attenuated bovine tuberculosis bacillus. However, BCG has more side effects than Maruyama vaccine.
Maruyama vaccine, invented by Dr. Chisato Maruyama more than 50 years ago, can be used by itself or in combination with standard therapies. Some Japanese physicians claim to have achieved complete remissions in poor-prognosis cancers, but no large scale clinical trials exist. No negative side effects from the vaccine have been reported.
Murayama vaccine is approved by the FDA to treat terminal cancer patients. Some forms of health insurance will cover the cost if the vaccine is used as part of standard therapy, because it is officially approved only as an immune system stimulant to counteract the side effect of bone marrow suppression caused by radiotherapy.
Maruyama vaccine is supplied by The Research Institute of Vaccine Therapy for Tumors and Infections Disease, Nippon Medical School Hospital in Tokyo, as long as the patient supplies a request from their physician. It is not expensive, approximately 9000 yen (100 USD) for a 40 day course of treatment.
According to an article published in Cancer Detection And Prevention, 2003, by Tetsuo Kimoto M.D., Ph.D., Maruyama vaccine does not have direct cytotoxic effects on tumors, but rather causes their encapsulation by collagen fibers.
This leads to the containment and sometimes necrosis (death) of tumors and their metastasis. Survival time increased in both animal and human subjects with tumors, and Kimoto stated that Murayama vaccine “may benefit patients in whom the tumor is inoperable and resistant to conventional chemotherapy.” 1
——————————————————————————————————————————————————————
(1). Tetsuo Kimoto M.D., Ph.D The antitumor effects of Maruyama vaccine (SSM) Cancer Detection and Prevention Volume 22 Issue 4 Page 340 – August 1998 .
Herpes Virus
Cervical cancer, caused by the human papilloma virus, strikes more than 10,000 U.S. women each year, killing more than 3,700. A new vaccine against the virus, Gardasil, was approved by the FDA in 2006. The vaccine is effective against HPV types 16 and 18, which cause approximately 70 percent of cervical cancers and against HPV types 6 and 11, which cause approximately 90 percent of genital warts.
Less well known is the fact that HPV is also implicated in squamous cell head and neck cancers, especially cancer of the tonsils. 1,2 Researchers at the Johns Hopkins Oncology Center tested tumor tissues from 253 patients with head and neck cancers and found 25 percent of the cases were HPV-positive. In 90 percent of those HPV-positive tumors, HPV16, the type of virus most often associated with cervical cancer, was present.3
Multiple studies confirm the link between HPV and head and neck cancer. Approximately 31,000 people in the United States are diagnosed each year with cancer of the oral cavity and pharynx, which causes 8,500 deaths annually.
The vaccine against HPV only works if it administered before infection, indicating the importance of immunization before potential exposure to the virus. Also, Gardasil does not protect against less common HPV types not included in the vaccine, thus routine and regular pap screening remain critically important to detect precancerous changes in the cervix to allow treatment before cervical cancer develops. It is a preventative measure, not a treatment for existing cervical or head and neck cancer.
——————————————————————————————————————————————————————
(1). Paz IB et al., Human papillomavirus (HPV) in head and neck cancer. An association of HPV 16 with squamous cell carcinoma of Waldeyer’s tonsillar ring. Cancer 1997 Feb 1;79(3):595-604.
(2) Klussman JP et al., Human papillomavirus-positive tonsillar carcinomas: a different tumor entity? Med Microbiol Immunol (Berlin) 2003 Aug;192(3):129-32. Epub 2002 Sep 14.
(3). Gillison ML, Koch WM, Capone RB, Spafford M, Westra WH, Wu L, Zahurak ML, Daniel RW, Viglione M, Symer DE, Shah KV, Sidransky D, Evidence for a causal association between human papillomavirus and a subset of head and neck cancers. Journal of the National Cancer Institute. 2000 May 3;92(9):709-20
Stomach Cancer
In the December 2000 edition of the Journal of The National Cancer Insitute, a research team led by Columbian pathologist Pelayo Correa reported that antibiotics, vitamin C, or beta-carotene (precursor of vitamin A) can reverse precancerous stomach conditions caused by Helicobacter pylori.
Stomach cancer is the second most common cancer worldwide, and is most common in countries such as Colombia and China, where H. Pylori infects more than half of the population in early childhood. In the U.S., where H. pylori is less common, stomach cancer rates have decreased since the 1930s.
The two main risk factors for stomach cancer are H. pylori infection, and a diet low in vitamin C and beta carotene, which the body converts to vitamin A. There is also ample evidence that a diet including fresh fruits and vegetables, which are rich in those nutrients, protects against stomach cancer.
In 1992, the researchers studied 631 patients with aberrant gastric cell growth, which falls into one of three successive premalignant stages–multifocal nonmetaplastic atrophy, intestinal metaplasia, and dysplasia.
Patients received either a placebo pill, a vitamin C or beta-carotene supplement, or antibiotics against H. pylori. Some others received a combination of drugs and supplements.
The scientists took stomach biopsies of the patients after 3 and 6 years of treatment. Patients with atrophy were roughly five times as likely to experience regression of this premalignant cell growth as those getting a placebo.
Among those with metaplasia, the volunteers who were taking supplements or drugs were three times as likely to improve as those getting placebos were. However, patients with dysplasia, the last stage of stomach disease before cancer, showed no significant improvement with any of the treatments. “The earlier in the process [that we intervened] the better the chance of regression,” Correa said. 1
This study is encouraging because it shows that treating carcinogenic bacteria produces clear benefits against precancerous conditions. However, once the tissue damage caused by infection had progressed to the premalignant stage, the antibiotics produced no benefits, and would likely produce no improvement in cases of outright malignancy either.
——————————————————————————————————————————————————————
(1). Correa, P., et al. 2000. Chemoprevention of gastric dysplasia: Randomized trial of antioxidant supplements and anti-Helicobacter pylori therapy. Journal of the National Cancer Institute 92(Dec. 6):1881-1888
Lymphoma
The common antibiotic doxycycline effectively treats a type of ocular lymphoma associated with chlamydia infection, according to a study published in the October 4 issue of the Journal of the National Cancer Institute.
A team of researchers led by Andres J. M. Ferreri, M.D., of the San Raffaele H Scientific Institute in Milan, Italy, gave 27 patients with ocular adnexal lymphoma (OAL) a 3-week course of doxycycline therapy, whether they tested positive or negative for chlamydia.
The researchers observed for tumor progression every 6 months, and found that doxycycline caused caused lymphoma to regress in patients regardless of whether they tested positive or negative for chlamydia.
The study suggested that doxycycline is a useful therapy even in patients where other treatments have failed, and it is a valid alternative to chemotherapy and radiation without causing the same toxic side-effects. Patients treated with doxycycline had a 66% rate of disease-free survival. 1
——————————————————————————————————————————————————————
(1). Andr
