- Comment
Spiroplasmas and Mad Cow Disease - NOT
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- From moonbeam@earthling.net
12-24-00
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- Recently, an article posted at your website suggested
a possible role of Spiroplasmas as a causative agent in Mad Cow Disease/CJD.
It is true that Spiroplasmas cause the same type of holes in the brain
as Mad Cow Disease, yet Spiroplasmas seem quite easy to kill with antibiotics,
yet the agent that causes Mad Cow Disease/CJD seems almost impossible to
kill, resisting all known antiseptics and drugs.
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- This article shows that Spiroplasmas are easily killed
by antibiotics, whereas Mad Cow Disease is not killed by antibiotics.
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- Source: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=287 7430&dopt=Abstract
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- 1: Pathol Biol (Paris) 1986 May;34(5):360-3 Sensitivity
to various antibiotics of spiroplasmas isolated from mosquitoes in France.
Abalain-Colloc ML, Le Goff F, Abalain JH, Chastel C
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- Mainly on the grounds of morphologic evidence, spiroplasmas
have been incriminated in the genesis of human Creutzfeld-Jacob disease.
We recovered six strains of Spiroplasma sp. from 1927 female mosquitoes.
In vitro susceptibility of each strain to the following antibiotics was
studied: tetracycline, oxytetracycline, doxycycline,erythromycin, chloramphenicol,
rifampin, kanamycin, gentamicin and pefloxacin.
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- Each of the six strains was found to be highly susceptible
to tetracycline, oxytetracycline, doxycycline, erythromycin, chloramphenicol
and pefloxacin (MICs less than or equal to 0.16 microgram/ml, 0.63 microgram/ml,
0.08 microgram/ml, 0.16 microgram/ml and 0.32 microgram/ml respectively).
From our results, spiroplasmas seem to have more or less the same susceptibility
to antibiotics as mycoplasmas.
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- Hello Jeff,
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- Note the second paragraph: a New York team. Where else
would they study tse in New York? On our favorite island (Plum).
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- Patty
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- Dr. Bastian's Work
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- 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)
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- 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.
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- 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.
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- 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).
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- Spiroplasmas
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- 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.
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- 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 .
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- Spiroplasmas as the cause of CJD
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- 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.
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- 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.
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- 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.
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- 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.
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- 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.
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- 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.
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- 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.
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- 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."
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- 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.
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- 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.
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- ENDNOTES
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- (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
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- (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,".
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- [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.
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- 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.
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- 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.
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- (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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- Visit my website "Emerging Diseases" and message
board http://goddess-of-fire.tripod.com/index-1.html http://disc.server.com/Indices/93896.html
Patricia Doyle, PhD Investigator of Emerging Diseases
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