By Alan P. Blood



Alan Blood

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This article reviews the theory that mycoplasma and other bacterial organisms may be involved in
masking of surface antigens and a number of other immunosuppressive and carcinogenic effects in
cancer and in AIDS. The second section discusses the theory of Rife- type electric field oscillators
as a medical treatment. We discuss the possibility that modulated induced high frequency oscillating
microcurrents on membrane surfaces may remove or disrupt the masking (eg by hCG) of tumour
antigens and also of white blood cells. Simultaneously there may be proliferation and hyperactivity of
white blood cells caused by cytokine stimulation response. The synergy of these two effects may
enhance the restoration of anti- tumour antigen immune recognition and attack in cancer, and
possibly other immunosuppressive pathways could also be disrupted. If the bacterial forms
associated with cancer or pre- cancer pathology can be successfully attacked in this type of
treatment, their immunosuppressive effects could be eliminated as well, although this has not been
demonstrated in vivo. It is believed that these hypotheses may account for unconfirmed reports of
rapid clinical remissions by Johnson et al prior to WW2, and later by Hamer *22, as well as claims
for other types of modulated or pulsed oscillator devices. An appendix section discusses some
uncertainties of interpretation of forms observed in live blood,and suggestions for new
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Mycoplasmas have several features which are different from other bacteria. They have no true cell
wall. They have a very small number of genes (genome), around 10 times smaller than typical
bacteria such as e. coli, and about the same size as the more complex types of virus. There are many
classes and species of mycoplasma. They are believed to have had a common ancestor with the
Gram- positive Orders of bacteria. Evolutionary studies on rRNA suggest that mycoplasmas may be
degenerate forms whose origins may be the hybridization of L-forms of early gram- positive types of
bacteria. Mycoplasmas show a large degree of genetic diversity and it seems that they also have a
high rate of mutation, possibly because of the loss of protection of a true cell wall. The most
researched species is the one which causes atypical pneumonia in humans. Mycoplasmas are also
known by the name Pleuro- pneumonia like organisms (PPLO). They can divide like typical bacteria,
or alternatively they can assume adult forms where nuclei continue to divide inside a single growing
cell enclosed by a sheath. Sometimes multiple adult forms develop partly fused together to give a
variety of shapes. At maturity the "adult" form can burst to release viable elementary bodies or "seed
forms". These can be extremely small, (viable free forms around 0.3 micron), and they can pass
through fine filters which do not allow bacterial forms through. For this reason they have been called
filterable bacteria. Because of this characteristic, A.Kendall in 1931 incorrectly proposed a theory of
a pleomorphic cancer virus, since filterability is a characteristic of virus. Despite the differences from
other bacteria, today none of the many types of filterable bacteria are classed as virus, because they
all have true cell phases which virus do not have. Some mycoplasmas are harmless commensal
populations of mouth or genitals. Others can also be pathogens which can live inside white and red
blood cells, especially in AIDS. Sometimes in AIDS the flask- shaped species including newly
observed M.Fermentans Incognitus strain can grow fine threads which can bud from the ends.
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Since 1920, a number of researchers have isolated and cultured filterable pleomorphic (many-
shaped) bacterial forms from a variety of neoplastic tissue *1. Various forms may often be observed
in fresh blood in cancer and in AIDS in dark- field microscopy *2. A pin- prick test can guage
cancer risk even before tumour formation (*3), by looking for these forms, as well as spots within
red blood cells. Though often dismissed as an opportunistic infection, it may be that
micro-organisms play a causative and contributing role in cancer *4,7. The link between pleomorphic
bacterial forms and cancer was first indicated by research showing tumour formation in innoculated
animals, as well as their presence in microscopic observations of cancer tissue (*1,4).

Some of the observations of cell- like or spore- like forms have been claimed not to be bacteria, but
rather membrane fragments, and researchers interested in the Rife approach ought to be aware that in
some observations this may well be the case. On the other hand, some forms isolated from cancer,
or observed in cancer or AIDS blood are undoubtedly bacterial. Kendall and Rife announced a
pleomorphic cancer virus, a theory still supported by Rife "true believers". This article points out
that their early observations of the filterable bacterial forms were not in fact virus, but rather of
mycoplasmas or of cell- wall deficient bacteria.

Over the years a variety of names and phylogeny have been suggested for the cancer isolates. Recent
film demonstrations by various independent researchers were shown at the World Cancer Congress,
including high resolution Somatoscope footage by G. Naessens. The phases of the organisms
suggest that at least some of them may be mycoplasmas, but the distinction between these and the
cell- wall deficient forms (cwdf) of other bacterial species is still not entirely clear. Other
interpretations, ie of host membrane fragments (Url), and of Endobiont forms (Enderlein) need to be
acknowledged. (See appendix discussion). Note also the probability of sexual and blood transfusion
transmission of the more pathogenic species eg M. Fermentans, M. Penetrans, and M. Pirum and
their putative role in AIDS and/ or cancer.

Kleineberger- Nobel noted that mycoplasma (PPLO) could proliferate in a stressed host *6.
Observations suggest that a lowering of immune competence as a result of an episode of grief can
lead to cancer in an 18 month timeframe *3. We can reasonably postulate that mycoplasma or other
bacterial proliferation subsequent to immune depression may induce cancer. Evidence of
carcinogenic effects and a variety of immunosuppressive effects from mycoplasmas have been
presented in the literature. HCG secretion by other species isolated from cancer were reported by
Acevedo et al.

Naessens has postulated that in a healthy host the so- called "Somatid" organisms are found as a
commensal population of underdeveloped coccoid and sometimes rod forms whose growth factor
secretions are controlled by humoral response. He claims that where immune function becomes sub-
optimal, an increase in the concentration of the secretions may stimulate development of the
advanced multinuclear adult forms, and may also stimulate host cell growth *7. Naessens claims that
his observations lead him to the conclusion that once a tumour acheives a "critical mass", nearby
white blood cells appear to become paralyzed, and thus the immune system cannot recognize or
challenge the abnormal cells. He attributes this effect to the secretion of "Co-carcinogenic K-factor"
by the tumour mass. This interpretation is echoed in findings that NK activity is suppressed via
hexosamine formation via deacetylase from N-acetyl aminosugars in tumour cells.

It has been reported that human growth factors can stimulate kinase release within human cells
leading to oncogenic expression. Some mammal and prokaryote growth factors are quite similar, and
it has been suspected that "mimic" bacterial growth factors may induce cancer subsequent to local
chronic infection. Indeed mycoplasma secretions have induced nuclear transformations in animal
fibroblast cell lines in vitro (*4,20), although the mechanism is unknown. In one such study viral
infection and DNA transfection had been ruled out *9. A recent 1995 study by Ushio et al reported
the sequencing of a metastasis- promoting molecule named Ag 243-5 derived from mycoplasma *33.
Multistage malignant transformation of embryo cell lines under persistant mycoplasma infection was
reported by Tsai et al *32. In 1996 Chan et al reported prevalence of mycoplasma conserved DNA
in ovarian cancer *34.

Transformed (cancer) cells should normally be attacked by both humoral and cell mediated immune
response, but we assume that they may proliferate where antigenicity is masked. A healthy immune
system can recognise and attack transformed cells, but on the other hand most human tumours tend
to attract only weak immune response. This paradox has been one of the central unsolved mysteries
of cancer research. Recently research has islated a cancer cell protein antigen which has been named
malignin. Also an antibody level test was developed *16. Other reviews confirm some antigen
expression of antigens on cancer cells coded by genes which are normally dormant. It was noted
however that the malignin antigen could often be covered over by polysaccharide substances; we
postulate that this effect may be a type of antigen masking, thus reducing the antibody contact or
white cell recognition site contact with the malignin antigen. We need to consider the questions a) to
what extent are mycoplasma polysaccharide secretions, eg galactan, involved in the masking
phenomena, especially prior to tumour formation; and b) to what extent are hCG secreting bacteria
or their cell- wall deficient forms responsible for antigen masking and local immune suppression.

Cancer cells secrete their own growth factor but require a certain critical level of factor concentration
in the interstitial fluid to trigger division. It has been demonstrated that cultured cancer cells need a
critical mass of neighbours (in culture tests) before they can build up sufficient concentration to
trigger cell division*9. Therefore it is not unreasonable to postulate that in some circumstances a
single transformed cell may not proliferate alone without a boost from bacterial secretions which
mimic host growth factors.

In 1972 V Livingstone- Wheeler discussed the discovery of "Choriogonadotropin"- like secretions
from cultured human cancer pleomorphic bacterial isolates. Human Chorionic Gonadotropin (hCG)
is secreted by the trophoblast and chorion in pregnancy. It is also secreted by human cancer cells.
Cancer research has pondered two important questions in regard to this and other similarities
between zygote cells and cancer cells. One question is in relation to the mechanism of how the
zygote brings about maternal immune tolerance; herein may lie the secret of the apparent non-
immunogenicity of cancer tissues. The other question relates to how the chorion induces blood
vessel growth, and whether this can help us understand angiogenesis.

CG- like secretions from bacteria may play some role in immune suppression. H F Acevedo
reported a direct correllation between hCG titer in normal pregnancy, chorionic carcinoma and
hydatit mole versus Immunoglobin levels and a number of other immune cell standards. He has also
demonstrated a correlation of human cancer cell lines to metastasize in nude mice models to the
degree of hCG expression of the cell line. Later we discuss Acevedo's isolation of CG secreting
"abnormal" bacteria from cancer.

At the point of tumorogenesis, before there is any significant tumour cell secretion, we may postulate
that bacterial secretions are involved in the prevention of immune response against newly
transformed cancer cells *7. According to a review by Macomber, Chorionic Gonadotropin- like
substances (*19) contain sialic acid residues which may increase membrane negative charge by
adhesion to cell surfaces of cancer, trophoblast, sperm and T- cells. This results in reduced
immunogenicity of the above cells and of the mycoplasmas. CG adhesion to white blood cells may
interfere with receptor binding in immune recognition. A role of electrostatic repulsion has been
postulated as inhibiting white blood cell response against transformed cells*4. Other
immunosuppressive pathways are briefly discussed.

At this point I would remind the reader that the dominant research finding is that cancer cells secrete
hCG. Therefore much of the relevant reseach on hCG in cancer will have been investigating this
connection. However the possibility of a similar model of immunosuppression and/ or antigen
masking arising from CG and other secretion of bacterial origin has generally not been considered. It
is not clear whether general immunosuppression causes a failure to mount an immune response
against tumour antigens, or whether antigen masking is to blame. It seems plausible that both play
some role in the pathology of cancer, and that they are interrelated.

Instead of a covering cell wall, mycoplasmas can protect themselves by making a slime covering.
They can secrete considerable quantities of polysaccharide substances eg of glucan or galactan
composition. Bogoch's observation of polysaccharide covering over of the Malignin antigen makes
me suspect that bacterial secretions are a candidate as a source of this material; this question would
be recommended for future investigation.

Some reviews have noted what appears to be the ability of mycoplasmas to alter their secretion
products. Also some lipid- associated membrane proteins can change the expression and size of the
antigen molecule with high frequency. A variable expression genetic system has been elucidated for
this type of control of membrane antigens. It is possible that because these antigen molecular
patterns are not constant, they can to some degree elude immune response.

Some mycoplasma galactan polysaccharide secretions bind antibodies, and inhibit phagocytosis.
Other research notes the detection of unusual products in mycoplasma infected helper T-cells. It is
known that if the helper cells fail to secrete IL-2, (a required "second message") that there can be no
T-cell activation against tumour antigens. I have not searched for studies linking mycoplasma
infection with IL-2 secretion.

Some mycoplasma species can cause membrane damage via cytadsorbtion and/ or hemolysis by
localised peroxide, sometimes with N-O secretion together forming a hemolytic "superoxide". Some
"flask- shaped" species can live inside white blood cells to escape immune attack *9. (These types
are considered some of the most pathogenic, and include those observed in some AIDS cases).
Naessens has also filmed the migration of small rod forms between red cells. Note that epithelial
basal membrane degradation has been suggested as a likely first step in angiogenesis, followed by
growth factor- like chemotactic signals from the tumour inducing blood vessel capilliary growth. A
question arises regarding a possible contributing role of local damage and / or growth promotion by
mycoplasmas in angiogenesis. The outgrowth of threads from the flask- shaped species may also be
pertinant to this question.

Once established, many types of cancer cells create their own immunosuppressive effects, eg
secretion of substances similar to p15-E retroviral proteins, which have anti-immune effects probably
including blocking macrophage chemotaxis pathways *4, 24. In addition, tumour secretion of
histamines has been shown to be immunosuppressive, and more importantly, angiogenic. (This is
now treated with Cimetidine in bowel cancer at Sydney's St George hospital) *17. Tumour lactic
acid metabolism also creates gross effects and liver load. The immunosuppresive effects of tumour
secretion make it difficult to acheive a healing response, and are the target of various approaches in
immunotherapy. But even before tumour formation, we can postulate that mycoplasma proliferation
may have triggered and supported the initiation of cancer. Therefore methods to improve immune
strength, eg nutrition, should be considered as a preventative approach *3.

Livingstone- Wheeler used autologous vaccines against the patient's own pleomorphic bacterial
isolates along with BCG (an anti- TB serum) as cancer therapy *11. In 1982 success in cancer
control was reported in animal vaccination with CG-beta subunit with tetanus toxoid and adjuvants
*9. It may also be possible to develop vaccines with isolates from sarcoid tissue and in Kaposi's
sarcoma in AIDS *27. Cantwell has reported acid- fast bacteria in KS. Recent studies have been in
conflict as to whether mycoplasmas can be isolated from KS tissue ( *30). Wheeler's vaccine
method may be of use, but her clinic was closed down by an ever- vigilant FDA. Modern research is
also investigating vaccine therapy against cancer. Various other means could be considered to
therapeutically attack mycoplasmas, eg specific antibiotics or drugs. Naessens developed a method
to inhibit some cancer cell secretions by lymphatic injections of 714X camphoramine *7. Naessens
noted NK cell "paralysis" near tumour masses, but that this paralysed condition was reversed by the

Mycoplasmas are inhibited by anionic detergents *18, and therefore saponific plants may be useful.
Perhaps this is why yucca, a cactus, has become a traditional remedy. Natural substances which
stimulate NK activity have been reported, as well as substances which stimulate T- cell activity
against tumour cells probably by IL-2 stimulation.

In the 1920's Royal R.Rife of San Diego (*21, 22, 12) developed an audio- pulsed radio frequency
electric field oscillator which produced an audio intermittent or square wave modulated r.f.
oscillating electric field set up in an electrode gap within a large spherical gas plasma tube output
fired by an overmodulated a.m. signal . In the area near the tube, the so- called "Rife Ray" was
claimed to be able to kill or affect motility of various pathogens at modulations of audio frequencies
specific to each species. It could be that this claim may in fact only apply to wall- less or abnormal-
walled organisms. Rife made visual and film observation through a special high magnification
micropolariscope of his own design. In some cases Rife claimed to have observed membrane
rupture of bacteria. In 1995 Bare produced film showing the process of rupture of some Paramecia
in a sample using a variant design of the Rife device over 45 seconds *13. However this film should
not be interpreted as fully verifying Rife's claims, since it was necessary to visually track forms of
abnormal morpholgy to capture the rupture event, and other cells in the sample did not rupture.
Modified Phanotron gas tubes are now available which have been driven by conventional 100W
transmitter/ linear amp/ tuner * 13. The most powerful c 1935 Rife design was reported to be driven
by a 500 W transmitter with a 8000 V signal. Whether this Voltage was an r.f. peak value or power
supply value is not clear.

A suitable variation to this type of device for experimental cell research would be the adaptation of
an electrophoresis unit by driving it with audio- pulsed r.f., and using a non conductive sucrose
medium. Alternatively an air gap between 2 electrodes could be employed. Bare's design employs a
straight gas tube which is externally wrapped by cable from a transmitter. Each cable end is tied off
into circle or loop ends, and a gap remains between each of these loops, creating a dipole.

We could assume that an electron or negatively charged particle in the body of the patient
experiences an attraction to the anode. (Here we discuss a set-up where one electrode, ie "cathode"
is connected to common earth with the transmitter and/ or amplifier earth.) The amplitude of the
force of attraction varies at r.f.. Hydrogen ions and other positive ions will experience forces in the
opposite direction. Therefore we assume that in the area near the tube, all charges will experience
some induction due to local electric field perturbation at r.f. We also assume that most induced
current flow will occur on membrane outer surfaces, just like r.f. current concentrated on the outside
surface of a cable. Because the audio modulated intensity falls away to a low or zero amplitude for
about half the audio cycle, membranes experience a switching from surface current or excited state
to relaxed state at audio freqeuncy. This may equate to an audio oscillation of charges from interior
to exterior of the local membrane. Various speculations as to the mode of biological effect follow,
but note that testing of various claims has not been undertaken.

Recent research has suggested that at least some ion pumps utilizing ATP run at fixed frequencies
from 1kHz to 1 Mhz *19. The claimed Rife mortal oscillatory rate effect on bacteria (m.o.r. effect)
may conceivably be caused by ion pump failure by electrical resonance when subject to
synchronized oscillator output. On the other hand such a phenomenon could in theory adversely
affect animal cells, but the treatment was claimed to be safe for humans. However claims have been
made by Crane of parasite killing (ie worms at 20 Hz modulation). Post- treatment effects of
weakness or illness have been reported, but have been attributed to toxin release, or may be a
symptom of fever- like immune hyperactivity.

An alternative explanation may be that postulated by Pappas, ie that the plasma membrane exhibits
different electrical resistance depending on the direction of current flow, and that the efficaciousness
of pulsed h.f. magnetic or electric field oscillators lies in generating ion dispersion in tumour cells
such that there is an increment of one- way charge movement at each modulation pulse. Thus cells
revert to normal type membrane potentials, and thus lose the mitotic condition at low potential, as
well as becoming immunogenic *28. Pappas also claims that weak- walled and wall- less bacterial
samples have been killed by his coil magnet device. This latter recent observation seems to be in
agreement with Rife's claims of success in killing pleomorphic forms. (These were of major interest
to A.Kendall and E. Rosenow). It may be that other claims by Rife that a whole library of bacteria
and virus could succumb to his treatment at individual mortal oscillatory rates may simply not be
true. On the other hand models of immune stimulation may be plausible.

Rife claims effective modulation values at 1927 Hz for carcinoma and 2008 Hz for sarcoma. I was
interested to read Giannni Dotto (who developed the patented Dotto Ring in 1975 in USA) mention
2000 Hz frequency as a sort of cell self- tuning frequency, but no explaination was expounded.
Recently I studied nerve impulse action potentials in unmyelinated nerve cell axons. Na channels
open quickly, followed more slowly by K channels which counter the Na flow- induced potential
change. (These types of channels are Voltage- gated). It just so happens that peak depolarization
occurs 0.5 ms after the initiation of the action potential. Therefore a 2000 Hz modulated excitation
would trigger Na flow like a diode current, but K flow would not get a chance to "kick in". Cancer
cells have relatively low membrane potentials at around 15 mV, compared to 50 mV or more for
normal cells. It may be that the cancer cells are susceptible to death arising from further lowering of
this potential due to Na influx. Much of these latter speculations have not been investigated.

In addition to the concept of an antibiotic effect, it has been noted that various electrical oscillatory
applications can cause the stimulation of white blood cells, probably by causing cytokine secretion,
similar to what the blood does near the site of a wound. This effect may be of particular importance
to encouraging immune recovery by recognition and response to cancer cells. It has been claimed
that after electrotherapy white blood cells are observed to undergo rapid multiplication and to
become hyperactive for about 18 hours until dying off.

It may be that binding sites or electrostatic bonds of CG- like secretions and possibly other
polysaccharide substances may be broken by induced or transduced electric oscillating currents. If
this is the case, then the combined effect of white cell hyperactivity and their access to newly
exposed tumour antigens may engender an immune recovery.

In trying to develop a theory to explain the claimed anti-cancer effects of oscillators of quite different
designs and outputs developed independently by various different innovators, it has seemed to me
most likely that in all cases an immune recovery is engendered somehow by means of induced
microcurrents. The role of hCG secreted by tumour cells, and the possible role of other bacterial
secretions, must be prime suspects in immunosuppressive mechanisms. The dispersion of these
slimy coatings by modulated h.f. local membrane microcurrents would firstly expose tumour
antigens, and secondly the coatings on T- cells would also be dispersed.

Activation of the helper T-cells would be necessary to provide IL-2 "second message" for cytotoxic
T-cell activation. This may occur naturally where accessory cells present antigen correctly, or failing
this, IL-2 therapy may prove a useful adjunct. Also IL-2+ genetically engineered anti-tumour
activated autologous CD8+ T-cell therapy has been described in in vitro models by D M Pardoll *

In searching for a means to kill A.Kendall's pleomorphs, Rife learned to force the aggregation of
viable bacterial filtrates isolated from cancer tissue by an r.f. stressing technique, using a corkscrew
or helical plasma tube as a test tube holder, and driven with unmodulated r.f.. Thus a sample of
filtrate in a test tube could be positioned so that one electrode was above and the other below the
sample. The aggregation or clumping occurs because cells stick together under r.f. fields eg in r.f.
electrophoresis. In the case of filtrates of wall- less organisms it is likely that the elementary bodies
will completely fuse. The motile aggregates could then be imaged, and a mortal audio resonant
frequency was determined by tests with the Rife Ray. Tumour formation after innoculation was
claimed to have been prevented by Rife Ray treatment. In hindsight the latter conclusion may be
open to criticism. It is true that innoculation of cancer bacterial isolates will induce tumours, and that
effective antibacterial treatment post- innoculation may prevent the tumour growth. However the link
between the cancer microbes and human cancer is not universal as Rife and Kendall were tempted to
believe. Kendall's culture technique required a pork gut medium, and we could suspect that his
culture organisms were contaminants. However their capacity to induce tumours by innoculation is
still significant. Modern research has verified that pure cultures of mycoplasma isolates do indeed
cause tumours by innoculation.

A significant number of AIDS patients are infected with mycoplasmas, and it was thought that these
were opportunistic infections after HIV immunosuppression. A new strain named M. Fermentans
Incognitus has been discovered in some 17 % of cases. CD-4 binding sites on the membrane of M.
Incognitans have been discovered, which means that the virus can be transported by Incognitans,
and it has been argued that the AIDS syndrome may in at least some cases be a co-infection based
on the sexual transmission of mycoplasmas. A revealing series of experiments with monkeys shows
that innoculation with HIV-1 alone will not kill monkeys, probably because this virus is human
specific. However when injected with M. Incognitus alone, monkeys showed wasting syndrome, and
death within 7 to 9 months. One in vitro experiment showed that a cell line infected with both M.
Arginini and HIV-1 showed HIV-1 expression at a rate 40 times greater than a control with HIV-1
only. If this is the case in vivo in AIDS, the mycoplasma co-factor link should not be ignored.We
may postulate mycoplasma pathogenicity and various immunosuppressive effects as contributing to
the disease process. Therefore the therapeutic treatment of mycoplasmas in AIDS eg by specific
antibiotics may be useful.

Interestingly, Beck claims that transduction electrotherapy prevents the capacity of the HIV virus to
attach to the CD-4 surface receptors of helper T-cells * 14. An interesting article appeared in an
Australian newspaper describing how a farmer suffering the long term effects of Ross River virus
was pushed into an electric fence by a playful calf only to discover that his symptoms were relieved.
A neighbour with the same affliction thought he'd try his luck, and was also rewarded with respite of
symptoms! Unfortunately it is unlikely that any "anecdotal " claims of this kind will attract any
follow- up research.

The mycoplasma- cancer link may be disputed on the grounds that less than half of cancer or AIDS
cases have yielded mycoplasma isolates. However we contend that the question of a link in some
cancer pathways is is still open. Even if the Mycoplasma infections in AIDS are indeed late-comers
to the disease, their contribution to the disease may be significant. The reader might like to compare
notes with a recent 1996 review on mycoplasmas in AIDS (* 30).

In his cancer treatment Rife set a protocol of 3 minute exposures with 3 day rests in order to allow
toxin elimination. There may be some danger of kidney failure or lesion haemhorrage in cases of
breakdown of tumour masses, *23 . In many cases surgury or the other tumour destructive therapies
may be indicated prior to Rife treatment. For bleeding it may be appropriate to administer
Tributyrate *26. Like other forms of electrotherapy, there is a danger of induced heart attacks as well
as epilepsy. Electrotherapy may therefore be generally be considered contra-indicated for patients
with a history of these conditions. Rife claimed that he detected no harmful effect from his oscillator
to humans. However there may be unknown hazards, and there have been reports of frequencies
which affect intestinal flora. Possible effects on early pregnancy should also be considered. Where
live blood observation indicates pre-cancer pathology, Rife treatment may similarly unmask the
bacterial forms and T- cells, thus engendering anti-mycoplasma immune response. A reduction of
mycoplasma population, particularly of the advanced phases, could eliminate the source of
immunosuppression, which would be considered a major cancer risk factor.

Because the emphasis is on immune response, various natural therapies, exercise, vegetable juices,
anti-oxidant vitamin and mineral supplements, herbs, nutritional protocol, substitution of refined salt
for sea salt, etc, medical immunotherapies and even psychotherapy are considered necessary
adjuncts to the Rife therapy. Conventional immunosuppressive therapies (ie X ray and
chemotherapy) may counteract the desired immune response in the short to medium term, but could
be considered nonconcurrently. Surgery, on the other hand, may be indicated as an early treatment,
and would be expected to assist the process of immune recovery. Critics may suggest that these
comments constitute a danger to the public should they be tempted to avoid seeking qualified
treatment. Such debate is dealt with by other commentators. However there is no excuse for the
ongoing failure of the "establishment" to grant funding to undertake impartial investigation, eg for the
Wheeler vaccine, nor for the many "snow jobs" that have recently been exposed, eg on Sheridan's

A number of products using skin- contact electrodes (transduction devices) go by the name of Rife
devices, but in fact use only audio currents. These have been reported to be of use in pain relief in
arthritis at 5000 Hz, and would be expected to stimulate white blood cells, but have not been
demonstrated to be of use against cancer. "Hulda Clark Zappers" use high frequency unmodulated
currents, supposedly against a pathogenic fluke parasite. Although her theory is most likely flawed
by misinterpretation of radionic signatures, it may nevertheless come to be shown as a useful
therapy. I have thought she may be reading "slime" rather than liver flukes (or reading AIDS, which
has often mistakenly been the case). Various other designs have been produced including magnetic
field oscillators, some of which are legal to use and have demonstrated physiological effects.
Because of the prevalent prejudice in the scientific establishment, there appears to be no peer
reviewed literature to prove or disprove the various claims, and no doubt no adequate funding for
such research. Inevitably this boils down to "assignment of priorities", and the prejudice becomes
invisible. If anyone has relevent literature or data, please let me know!

The public are often warned to avoid unproven therapies, and perhaps rightly so. However in view
of the acknowledged poor results of orthodox treatments, it must be in the public interest to properly
investigate new alternatives. Other authors have pointed out that this logic conflicts with corporate
and professional interests. While this unfortunately may have tended to be the case at certain times in
many countries, it is to be hoped that compassion and common sense will prevail in the future.

A good deal of controversy and misinterpretation has dogged this study, from as far back as
Bechamp over 100 years ago, and is still unresolved. Research collated in V. Livingstone- Wheeler's
"Microbiology of cancer" contains various speculations as to the classification of these organisms,
including mycobacteria, mycoplasma, Actinomycetales, as well as the then mysterious L-forms or
cell- wall deficient forms (cwdf). Wheeler's "folly" was to declare a new species called Progenitor
Cryptocides, What appeared to be a definitive elucidation was later presented by Acevedo et al, who
reported the isolation and identification of a number of non-mycoplasma bacterial species from
cancer *29. The American Cancer Society publication CA in its criticism of Wheeler made an
unreferenced comment to the effect that Wheeler's organism was not a new species, but a collection
of common and rare known types.

A closer reading of Acevedo's paper is warranted. The paper reports the expression of hCG- like
material, or fragments thereof, from 7 bacterial species isolated from cancer, and cwd forms of 2
bacterial species from non- cancer patients. (I might add at this point that mycoplasmas, had they
been present, would not have been isolated by standard culturing techniques.) From Acevedo: "
Electron microscopy of these 9 strains" (including comparison of CG negative controls of these
strains (sic)) "revealed morphological alterations in the bacterial cell walls and cytoplasmic material
and/ or bizzarre forms of reproduction in 6 of the 9 strains expressing hCG- like material including
the 2 cwd variants."

Majnarich and Wheeler reported the transmission of CG+ characteristic between bacterial species
which suggested the transmission of a CG+ plasmid. While this suggestion may be verified in future
work, we may speculate on a role of mycoplasmas as a possible CG+ plasmid vector. Acevedo's
description of morphological and reproductive alterations in his CG+ isolates begs the question of
the mechanism of this manifestation. Is this an effect of CG on the cell? The latter question could be
reasonably simply tested by adding CG+ extracts to CG-neg strains in vitro. For the purposes of the
current discussion we shall assume that this is not the case. I have found no literature to suggest CG
production in mycoplasma studies. Perhaps mycoplasma supernatants and sonicates could be added
to Acevedo's CG neg strains to determine any effects. Co- culturing of mycoplasmas with CG neg
bacteria could be investigated for plasmid transfection or new products from re-isolated bacteria.
Co- culturing of mycoplasma with CG pos bacteria could be studied as well to look for any plasmid
transfection or other effects eg abnormalities. Other studies could probe for CG plasmids or gene
amplification in the CG+ strains, as well as in mycoplasma isolates from cancer. Here we note a
reported capacity of mycoplasmas to "take" entire sequences in plasmid transfection in "co-integrate
structures" (with the genome), implying their capacity as vectors for a whole range of genetic
material of host origin, and possibly indirectly as infective vectors for cancer.

It is also relevent to point out that critics have stressed that any isolates from cancer may merely be
opportunistic infections, and this may also be the case for Acevedo's isolates. This argument is
countered by the induction of tumours by innoculation, and claims by some oncologists that the
blood forms are to be found before any sign of tumour. Of the 7 strains isolated from cancer by
Acevedo, none were reported to be cwdf. How can we reconcile this finding with the extensive list
of reports of extremely pleomorphic forms by other workers? Critics have suggested that such
observations are the result of "contaminations". This thinking may have some justification due to the
infamous ability of mycoplasmas to contaminate bacterial and cell cultures. Indeed the early special
serum supplemented media developed by Wheeler's associates cannot be considered as contaminant
free, and the same caution must apply to interpretations of Kendall and Rife. However the live blood
observations and innoculation experiments are overlooked by the critics, and therefore the whole
issue should again be thrown open to debate and research. The divide between proponents of the
bacterial link to cancer versus a powerful orthodoxy in denial are extreme. The ACS critic claimed
that one authority had never encountered the presence of bacteria as described by Wheeler in cancer
tissue, and that they simply "do not exist".

Mycoplasma research has isolated various strains from some cancer tissue, and from blood in
AIDS, but not in a majority of cases. I would very much like to see Naessens' organism genotyped.
To ensure that any putative mycoplasmas are not discounted yet again as suspected contaminants, it
may be appropriate to employ a micromanipulator to individually select the pleomorphs in blood.
Also I would like to see Acevedo's work repeated with an emphasis on the culturing requirements of

Under high resolution light microscopy, Naessens has defined a 16 stage life- cycle for the Somatid,
much of which appears similar to mycoplasma phases. However there are controversial differences
to Kleineberger- Nobel's PPLO cycle. Dancing dots are shown in Naessens' films which he assigns
as Phase 1. These were said to contain no DNA. They were stable when heated, whereas
chylomicrons (lipid /protein micelles) were not. If these particles are membrane fragments, their
composition would be a mix including proteins not present in the chylomicrons, and may therefore
remain stable under the heat test. In orthodoxy, the smallest viable elementary bodies are around 0.2
micron, around the size of Naessens' Phase 2. The phase 1 would seem unlikely to be a bacterial

The Somatid cycle as observed in in vitro culture were reported to go from the "spore" (phase 2,
normally kept underdeveloped in vivo by antibody attack against its growth factors) through to rod
form (pathological in vivo) which grows out to a mycobacteria- like form with which goes on to
develop a bubbled cytoplasm and later bursts. The released substance was said to form "levurid" or
yeast like forms which grow out to 4 to 7 micron spherical forms. (In vivo films showed forms like
this attached to red cells or free in the plasma in cancer pathology). These grew out in culture to
larger long bulbous forms which peristaltically ejected the cytoplasmic content at maturity, and left
the sheath or thallus behind. These thalli could be observed in blood in advanced cancer.
Kleineberger- Nobel's work focused on M. Pneumoniae. She describes only one bursting stage at
maturity, and therein lies an apparent discrepancy. It is possible that Naessens has isolated more than
one species, or grown contaminants. The larger adult phase resembles the flask-shaped species of
mycoplasmas, and it may have grown out more slowly. Alternatively, changes in culture conditions
over time may have given rise to altered morphology of later maturing forms. The observed thalli in
pathology may arise from either bursting form. Naessens commented on different in vitro
morpholgy; a snake- like long thin form was filmed in vitro. It may be that Naessens cycle is indeed
basically accurate. Since mycoplasma research has been far from comprehensive, this is not entirely

Demonstrations of hypotonically stressed or heat stressed healthy red blood cells showed the
outgrowth of chains, which could coalesce into more spherical forms, and both forms could break
away. Similar outgrowths were also demonstrated by W.J. Clifford by the addition of minute
dilutions of toxic metals to blood in isotonic solution. It was claimed that similar phenomena could
be observed in cancer, and Naessens assigned the chain shapes as bacterial phase Somatids. W. Url
argues that these outgrowths consist of the cell membrane, but not any bacterial form. Naessens' film
also clearly shows spots in red cells and these were assigned as cancer or pre- cancer indicators.
These have also been noted as "sclerotic inclusions" in the work of Enderlein.

The Enderlein school describes various forms observed by dark- field microscopy in cancer blood,
but I have not studied this material in detail. Endobiont lifeforms are purportedly symbioses of
Aspergilla and Mucor, which can "copulate" from assigned lower forms to a series of higher forms
(Beilin). A system of medical therapy including Homoeopathics have been developed to treat cancer
via the treatment of the Endobionts. Enderlein developed innoculations of lower forms to induce
devolution of native forms. In common with Naessens, Enderlein also ascribes a very small
precursor; the protit. The tiny dancing forms would seem to have lively motion, which Naesens
attributes to electrostatic repulsion. Perhaps this characteristic caused Enderlein in the 1950's to
believe them to be cell precursors. However the weight of modern orthodox opinion would go
against such an interpretation. Some blood pictures show these dancing dots, and others, even in
advanced cancer, do not. In some cases such forms are seen only after treatment with 714X. I have
heard naturopaths ascribe these forms to a result of leaky gut syndrome.

Although the pioneering work of many early researchers may have led them to advance theories
which we may view as uninformed or even arcane, we must acknowledge the detail of their
observation and consider the general thrust of their findings. The history of science shows many
"rediscoveries" of the research of scientists which had fallen into obscurity. The approaches of
Livingstone- Wheeler, Rife, G.Dotto, G. Lakhovsky, A.Priore may well set the stage for a new wave
of therapeutic approaches.

*1 T.J. Glover, M. J Scott, 1925; Wuerthle-Caspe et al 1953 etc; See Refs in *4 von Bremer 1938,
Enderlein 1954 etc; See Refs in *7
*2 Enby, Url; World Cancer Congress 1994. Naessens; WCC 1995
*3 Kostler, Url; WCC 1995
*4 P. B. Macomber, 'Cancer and cell wall deficient bacteria', Medical Hypothesis, U.K. 1990 32, 1-9
*6 E. Kleineberger- Nobel,'PPLO'
*7 G. Naessens, COSE, Film, 'Somatidian Orthobiology' http://www.cose.com/enhome.htm /> *8 Torture et al, 'Introduction to Microbiology'
*9 'Recent Advances in Mycoplasmology', 1988 QR 201.M97 I57 1988 pp 145 pp 202-212
*11 V. Livingstone- Wheeler, 'Conquest of Cancer' also'Microbiology of Cancer' .... a compendium
of papers
*12 A. Blood, correspondence on Rife microscope http://www.europa.com/~rsc/tech.htm /> *13 J. Bare , http://www.rt66.com/~rifetech.htm http://www.rt66.com/~rifetech/kaboom.avi
*14 Beck, ref links http://www.europa.com/~rsc/ /> *15 W. Barnes, WCC 1995
*16 Bogoch, San Francisco Medical Research Foundation. 'An accurate test for cancer';
http://www.newagenet.com/LightParty/ProjectHealth/DETECT.html /> *17 ABC TV Australia, "Quantum" program Nov 1996
*18 Biology of Mycoplasma, Smith p. 195 QR352.S65 1971
*19 Acevedo H F et al. "Immunodetection of CG- like antigens in bacteria isolated from cancer
*20 Diller I.C., Diller W.F. "Intracellular acid fast organisms isolated from malignant tissue" Trans
Am Microscop Soc 84: 138. 1965 also in *11b
*21 Barry Lynes "The Cancer cure that worked"
*22 Mark Simpson "The Rife Way III"
*23 Wilhelm Reich "The Cancer Biopathy"
*24 Cianciolo G.J. "Antiinflammatory proteins asssociated with human and murine neoplasms."
Biochem Biophys Acta 865:69, 1986
*25 Rios A, Simmons R.L. "Immunosuppressive regression of various syngeneic mouse tumours in
response to neuraminidase-treated tumor cells." JNCI 51: 637, 1973
*26 Tributyrate by Swedish Pharmaceuticals, US. H.Cederberg, WCC 1994
*27 Cantwell A, "The Cancer Microbe"
*28 Pappas P.T and Wallach C, "Effects of pulsed magnetic field oscillations in cancer therapy"
*29 Acevedo H F et al, J. Gen. Microbiol. 133: 783-791 (1978)
*30 http:\\www.bioscience.org/1996/v1/e/brenner1/htmls/42-54.htm
*31 http:\\www.catalog.com/bri/bri.htm
*32 Tsai S; Wear DJ; Shih JW; Lo SC. Mycoplasmas and oncogenesis:persisten infection and
multistage malignant transformation. Proceedings of the National Academy of Sciences of the United
States of America, 1995 Oct 24, 92(22):10197-201.
*33 Ushio S; Iwaki K; Taniai M; Ohta T; Fukuda S; Sugimura K; Kurimoto M.
Metastasis-promoting activity of a novel molecule, Ag 243-5, derived from mycoplasma, and the
complete nucleotide sequence. Microbiology and Immunology, 1995, 39(6):393-400.
*34 Chan PJ; Seraj IM; Kalugdan TH; King A. Prevalence of mycoplasma conserved DNA in
malignant ovarian cancer detected using sensitive PCR-ELISA. Gynecologic Oncology, 1996 Nov,
*35 Drew M Pardoll "Genetic approaches to the induction of antitumor immune response", GMCRF
Accomplishments in cancer research 1991, ed.J G Fortner et al, Lippincott, Philadelphia


Rife Units

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