Spiroplasma & Transmissible Spongiform Encephalopathies
By Ed Gehrman

 

Introduction
Transmissible Spongiform Encephalopathy (TSE) is identified by the plaques
of mutated amyloid protein that form within the brain tissue and destroy
synapses and neurotransmitter functions and take on a characteristic sponge
or Swiss cheese appearance. CJD, Scrapie and Kuru are all members of this
degenerative disease family, afflictions known about for over two hundred
years but not studied intently until the early sixties when they were found
to be transmissible.

Dr. Carleton Gajdusek was a young researcher looking for unusual diseases
when he visited the Fore Peoples of Papau, New Guinea during the late 1950s.
The Papuans of those years were suffering from a population density that put
a strain on very limited resources. They practiced female infanticide and
cannibalism and were in a constant state of warfare with their neighbors
over land and pigs. Severe limitations on normal heterosexual relations were
imposed; the men spent most of their time at the men1s clubhouse where they
prepared for war and engaged in homosexual relations with the young boys.
This homosexual activity was all part of an elaborate bonding thought needed
to ensure macho warriors and dependable compatriots. The warfare was brutal,
often hand-to-hand; capture meant being tortured and killed. Solidarity was
essential and achieved through the sharing of semen. The females of the
group were disrespected and often abused because they were thought to steal
the men1s strength and resolve in battle as well as their vital semen. The
malnourishment of females and young children was part of this intense
process; they supplemented their diet by eating anything that 3crawled or
crept~. Midwives ate placentas of the new born and women dug up the partly
decomposed bodies of relatives and ate and shared with young children the
flesh, brains and the accumulations of maggots and mites. This was not a
religious ceremony but an attempt to fend off malnutrition. (1) Gajdusek
observed that some of the Fore women and a few children died from symptoms
indicating a neurological disorder: dementia, frenzied behavior, blindness
and eventual agonizing death. He studied the tribal dynamics and soon
hypothesized that the condition, known as Kuru, came from their habit of
eating the brains of dead relatives; he brought some diseased brain tissue
back to the USA. Gajdusek soon discovered that when he made a broth from the
Kuru tissue and injected this mixture into lab animals, they too exhibited
the Kuru symptoms. He then processed Kuru diseased lab animals1 brains and
injected the mixture into other lab animals. They also died the same
excruciating deaths. This meant that the condition could be transmitted from
organism to organism and was therefore transmissible, hence Transmissible
Spongiform Encephalopathy (TSE). Gajdusek and his colleagues at the National
Institute of Health were never able to isolate or positivly identify the
agent that causes the TSE even though they1ve been trying since the early
sixties. Scrapie and CJD were also studied and found to be transmissible.
All this was well known underground medical information; many doctors
refused to autopsy CJD victims. For years the NIH conjectured that the
infective culprit was a slow virus. Nothing seemed to distroy the agent; not
heat, cold, or any of the normal chemical disinfectants. Nor could they find
a trace of its chemical or mocular identity. Furthermore, the virus didn1t
cause inflamation so antibodies failed to leave a calling card. Some
completely new agent was essential.
Bastian's work

Another tenacious TSE researcher is Dr. Frank O. Bastian, MD, a professor of
pathology and director of neuropathology at the University of South Alabama,
Mobile. He has published numerous research articles relating to the etiology
of Creutzfeldt-Jakob Disease and also edited a book entitled
Creutzfeldt-Jakob Disease and Other Transmissible Spongiform
Encephalopathies. (2)

In 1976,Bastian examined a brain biopsy from a patient with CJD using
electron microscopy. He saw a spiral structure foreign to the tissue. It had
features of the newly reported spiroplasmas (Spiroplasmas were only
discovered in 1976). In 1981, a team in New York reported finding a fibril
protein in scrapie-infected brain tissue. This scrapie-associated fibril
(SAF) protein was 4 nm in diameter and 200 nm long. In 1983, the team looked
at various tissues of CJD and Kuru and demonstrated scrapie-associated
fibrils consistently in these diseases but not in control tissues. These SAF
were identical morphologically to the internal fibrils of spiroplasmas.

Moreover, antibodies to SAF react with internal fibrillar proteins from
Spiroplasma and digested brain material from people with CJD, suggesting
that these proteins essentially are the same. This similarity solidified in
Bastian's mind the link between spiroplasmas and CJD.

Dr. Bastian has postulated that Spiroplasma bacteria causes CJD and other
TSE. His twenty years of research indicates a role for Spiroplasma. The
evidence includes the following: spiroplasma-like inclusions were seen in
brain biopsies from patients with CJD (Arch Pathol Lab Med.
1979;103:665-669); spiroplasma internal fibril proteins are identical
morphologically to those seen in TSEs; the spiroplasma proteins show
immunological cross reactivity with the TSE proteins (J Clin Biol.
1987;25:2430-2431); and spiroplasma, when inoculated into rodents, produces
a similar neuropathology (Amer J Pathol. 1984;114:496-514).

Spiroplasmas
Spiroplasmas, are present in the hemolymph of almost all insects; there
probably are several million strains. They can also cause diseases in plants
but are usually associated with a vector. For example, a leaf hopper carries
a spiroplasma that infects orange trees.

Spiroplasmas are similar to mycoplasmas. They do not have a cell wall (cell
wall deficient) and have among the smallest genomes of any living organism.
Mycoplasma, are the smallest and perhaps the oldest life forms. These
bacteria, one cause of "walking pneumonia", are thought by many to be rather
fragile, but nothing could be further from the truth. They tolerate extreme
fluctuations in temperature, lay dormant in the soil for generations and
survive the harshest elements; only drano-like chemicals kill them
effectively outside the body. Under normal circumstances our immune system
efficiently deals with this complicated, membrane enclosed piece of DNA .

Spiroplasmas as the cause of CJD
A common phenomenon among the mycoplasmas is that the organisms bind host
proteins that often are of identical molecular weight to their surface
proteins and, therefore, are looked at by the immune system as being the
same as the host. The spiralin protein on the surface of spiroplasmas shows
a migration pattern on gel electrophoresis with a molecular weight of 27,000
Da to 30,000 Da, similar to that of the prion protein. This biochemical
similarity is compatible with spiroplasma etiology.

Bastian was able to show that spiroplasmas were neurotropic. When inoculated
peripherally into suckling rats, they will eventually localize to the brain
tissues. The organisms will produce a persistent infection and produce a
spongy change in the brain tissue of these animals. The neuropathologic
changes are similar to those seen in CJD.

Spiroplasmas are also within the size range of the agent that transmits CJD
and other transmissible Spongiform encephalopathies. Spiroplasmas will pass
through a 50 nm-pore filter. The transmissible agent's size has been
determined to be 42 nm.

The obvious way to look for an agent directly is by electron microscopy, but
this method may not be appropriate for spiroplasmas. Spiroplasmas are
similar to mycoplasmas, and it is a well-known phenomenon that mycoplasmas
are able to blend with cell membranes. What happens, possibly, is that
spiroplasmas essentially fuse with host-cell organelle membranes, thereby
blending with the background, so you would not see it unless you had a
marker to label it. Developing such as marker has been difficult because
spiroplasmas are very fastidious (difficult to cultivate)organisms.

Bastian also inoculated suckling rats with spiroplasmas, and examined their
brain tissues by electron microscopy early in the infection process; he
documented the organisms in the tissues. They appeared as membrane-bound
forms, except for the one instance where he observed the spiral form. Later
in infection, when he knew that the tissues were infectious by broth
culture, he couldn't find any evidence of spiroplasmas by looking at the
tissues extensively with electron microscopy.

Bastian insists that the infection-related protein that most researchers
refer to as a "prion" is produced by the host in response to the infection
and is not the causative agent. Prions are thought to be self-replicating
proteins. Some researchers believe prions are the cause of CJD and related
illnesses because they have found prions in brain tissue from people with
CJD and sheep with scrapie but not in normal brain tissue. Bastian states
that a shortcoming in the prion theory is that CJD and scrapie can be
transmitted without prions.

Brain material from which the prion has been removed with antibodies can
still infect animals. Moreover, the prion has been found in unrelated
disease processes, such as Kawsaski syndrome and inclusion body myositis.
Prion researchers have jumped to conclusions and have not considered any
other possibility. It is quite possible that spiroplasmas may be inducing
the formation of the prion protein to protect itself from the immune system.

The immune system is very important in the pathogenesis of CJD. The agent
replicates in the spleen and lymph nodes and occasionally causes an
immunologic reaction. Auto-antibodies are characteristically seen in the
late stages of experimental and naturally occurring disease. The gene for
the host protein is located on the chromosome in the region of the major
histocompatibility complex (MHC) in the mouse. "Occasionally, you see
elevation of immuno globulins; there are morphological alterations of the
leukocytes; there is leukopenia," Bastian explains, "and auto antibodies are
characteristically seen in the late stages of both experimental and
naturally occurring infection. There is partial MHC restriction in both
human and animal disease." "The immune reaction seen in these Spongiform
diseases can be explained by super antigen activity, Bastian says. He notes
that, normally, an antigen is presented to the cell surface in the MHC and
interacts with the T-cell receptor--the antigen lying in a groove in the
T-cell-MHC sets in motion the standard reaction. A super antigen, on the
other hand, binds outside the groove of the T-cell and interacts with the
MHC. This results in some immunoglobulin production, but only transiently.
The major effect is clonal deletion of T cells, resulting in a state of
immune tolerance. Autoantibodies can also form. In Spongiform diseases, PrP
presumably acts as a super antigen. It is noteworthy that inclusion body
myositis, a condition in which prions are seen, is an established super
antigen disease."

Dr. Bastian also notes that investigators have reported transmitting a TSE
to mice from hay mites gathered from farms in Iceland where scrapie is
endemic (Lancet. 1996;347:1114). He is virtually certain that these hay
mites contain spiroplasma, noting that the investigators have not so far
found PrP in the mites.

If hay mites can cause TSE, why couldn't the same be true for the maggots
and mites on the Fore corpses? (3) Could Gajdusek have overlooked the main
factor connecting Kuru to the Fore women and children? Was the initial cause
of Kuru the ingesting of large quantities of maggots and mites by protein
famished women and children? We know that the maggots and mites contain
spiroplasma. By eating the brains of the Papuans that died from Kuru, the
disease(Spiroplasma) was retransmitted to those remaining, in a deadly
cycle. Transmissible Spongiform Encephalopathies will continue to be
misunderstood unless we begin to study and understand these simple
connections.

ENDNOTES
(1) This information comes from several sources. It is well known to
anthropologists that these conditions existed among the Fore peoples and
many other New Guinea tribes like the Sambia. I know it's hard to believe in
these modern times but we must if we are to understand the world in which we
live. My main source is Our Kind by Marvin Harris; Harper & Row; 1989. He
took much of his information from Shirley Lindenbaum, Kuru Sorcery: Disease
and Danger in the New Guinea Highlands; 1979; Mayfield

(2) JAMA August 14, 1996 DC Capital Conference spring 1996 A dissenting view
on the cause of mad cow disease Bastian regards the prion theory as a red
herring. The cause of transmissible Spongiform encephalopathies (TSEs), he
says, is a conventional microorganism--a mollicute or, more specifically, a
spiroplasma. "The infection-related protein is produced by the host in
response to the infection,".

[Infectious Disease News Homepage] (June 1996) Spiroplasma may cause
Creutzfeldt-Jakob Disease An interview with a leading expert in infectious
diseases, Frank O. Bastian, MD,. In 1992, Bastian arranged an international
symposium on bovine Spongiform Encephalopathy.

I used information, quotes, and descriptions from the above article and
interview to weave together Dr Bastian's ideas, knowledge and words, with my
own research and interviews. I edited and rearranged both words and sequence
for coherence sake. I did the best I could to convey this important message.

I've had three phone conversations with Dr Bastian. He was cooperative and
helpful at first and sent me much useful information which I have included.
But he cut a scheduled interview short when I began to suggest that
biowarfare research might inadvertently help to spread the TSE agent. I
called one more time and he refused to talk. He has refused to answer a long
letter I wrote. I thought it both rude and arrogant, but even with that
nonsense, I still believe Bastian's elegant hypothesis is far more rational
than any I've studied.

(3)Common arthropods occuring on dead bodies: The Acari, or mites as they
also are called, are small organisms, usually less than a mm in lenght.
Mites occur under the dead body in the soil, during the later stages of
decay. Many mites are transported to the body via other insects, such as
flies or beetles. Other mites are soil dwelling forms which can be
predators, fungus feeders or detritus feeders. Most species will be found in
soil samples from seepage area under the body. Sarchophagidae Among the
Sarcophagids we find the large flesh-flies with red eyes and a
grey-checkered abdomen. These flies does not deposit eggs, but larvae on the
corpse. They are, together with the Calliphorids, among the first insects to
arrive at the corpse. The larvae are predators on blowfly larvae, as well as
carrion feeders. Many Sarcophagids are feeding on snails and earthworms.

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If you wish to contact Ed Gehrman, he is available at egehrman@psln.com 




 

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