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» LymeNet Flash » Questions and Discussion » Medical Questions » a Prophet is not without honour save in his own country-but this prophet is gloating

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Author Topic: a Prophet is not without honour save in his own country-but this prophet is gloating
Thomas Parkman
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Dear members of the list:

I do hope that you the honourable members and Mr. Ham who has so ably brought to the attention of the members in the thread below the latest researches of the good doctor Wormser will pardon me while I gloat. I have, as you may recall, had most unkind things to say on more than one occasion about the wretched Dr. Wormser. I have compared him to a voodoo doctor with the voodoo doctor in his loincloth or grass skirt coming out way ahead. I have even suggested that the good Dr. Wormser should really paint himself blue to drive out the evil spirits from his patients as that seems to be the only possible way he would ever be able to help anybody.

So you can imagine my sheer unadulterated venemous glee and brazen malicious joy when the good Mr. Ham cited:

posted 22 August, 2006 03:36 PM
--------------------------------------------------------------------------------
Comparative Genome Hybridization Reveals Substantial Variation among Clinical Isolates of Borrelia burgdorferi Sensu Stricto with Different Pathogenic Properties

Darya Terekhova,1 Radha Iyer,1 Gary P. Wormser,2 and Ira Schwartz1,2*

The full text will be available free in four months via this site:

http://jb.asm.org/cgi/content/abstract/188/17/6124?ct

I would cite to you paragraph seven of my memorandum on Lyme disease written with blood, sweat, toil and tears between July and November of Last year. The truth finally begins to come out in spite of it all. Ha!!!

7. These difficulties in serological testing are greatly compounded by the fact of the broad and complex genetic heterogeneity of the known pathogen, a complex of genospecies known as Borrelia burgdorferi sensu lato. This heterogeneity presents a confounding problem for the serologic diagnosis of Lyme disease.14 One study of this genetic heterogeneity in the southeastern United States identified 56 strains of B. burgdorferi broken into three genospecies, along with two hitherto unknown probable genospecies and a number of variant strains. The serological responses in patients with Lyme disease or Lyme-disease like disease were found to be variable and sometimes unpredictable with, on occasion, no response at all. The authors suggest that the genospecies B. burgdorferi sensu stricto causes some Lyme disease cases in the southern United States but that a significant number of cases of Lyme disease or a Lyme-disease like disease is caused by alternative Borrelia species or some novel uncharacterized infectious agent.3 The discovery in recent years of ``southern tick-associated rash illness'' (STARI) and of the putative agent,16 a new species of Borrelia, tentatively named Borrelia lonestari,17 would appear to confirm this hypothesis. The vector, Amblyomma americanum, (ie. the Lone Star tick) has been shown to parasitize human beings from all sections of South Carolina and Georgia, as has the vector for B. burgdorferi, Ixodes scapularis (ie. the Deer tick).18,4

Cheers. Thomas Parkman

--------------------
Thomas Parkman

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Carol in PA
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Breaking this up to make it easier to read.

7. These difficulties in serological testing are greatly compounded by the fact of the broad and complex genetic heterogeneity of the known pathogen, a complex of genospecies known as Borrelia burgdorferi sensu lato.

This heterogeneity presents a confounding problem for the serologic diagnosis of Lyme disease.


One study of this genetic heterogeneity in the southeastern United States identified 56 strains of B. burgdorferi broken into three genospecies, along with two hitherto unknown probable genospecies and a number of variant strains.


The serological responses in patients with Lyme disease or Lyme-disease like disease were found to be variable and sometimes unpredictable with, on occasion, no response at all.


The authors suggest that the genospecies B. burgdorferi sensu stricto causes some Lyme disease cases in the southern United States but that a significant number of cases of Lyme disease or a Lyme-disease like disease is caused by alternative Borrelia species or some novel uncharacterized infectious agent.


The discovery in recent years of ``southern tick-associated rash illness'' (STARI) and of the putative agent, a new species of Borrelia, tentatively named Borrelia lonestari, would appear to confirm this hypothesis.


The vector, Amblyomma americanum, (ie. the Lone Star tick) has been shown to parasitize human beings from all sections of South Carolina and Georgia, as has the vector for B. burgdorferi, Ixodes scapularis (ie. the Deer tick).

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Anneke
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Dear Thomas,

I am confused by your post.
I'm assuming your point is that the article somehow contradicts a claim made by Wormser? Would you mind explaining this a bit more?

Anneke

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brentb
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Great post. I was sure wormser,shapiro etc would one day see the light. Answers the question that if one is bitten by a borrelia carrying tick does one get "Lyme". As we see all borrelia are not the same.
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Lymetoo
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I'm too dense to figure this out. Up for help from Thomas!

--------------------
--Lymetutu--
Opinions, not medical advice!

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Thomas Parkman
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Dear members,

It is really quite simple. The species borrelia has many different subspecies and variant strains of bacteria within each of these strains. This creates a confounding problem for diagnosis by blood testing as the strains and variants of the genospecies borrelia burgdorferi sensu lato each expresse proteins slightly differently or indeed differrently.

It is as if the spirochete is a disguise or quick change con artist. It appears in one set of cloths and appearance and then when the "police" ie. the immune system, come after it it changes its clothes, make up, appearance etc. Instead of being a man (ie male) it might become a woman (ie female). It might change the color of its coat and clothes, ie the specific protein which it uses to make its outer layer.

It hides in all kinds of places in the body. It morphs into cysts and various other hard to attack shapes.

The spirochete, ie the infectious bug, will change its out layer or protein sheath at different times during its life-cycle and in response to different and very difficult environments. This means that the tests which are testing for the proteins which make up the outer sheath of the spirochete are never going to pick up all the variants and never catch all the different strains etc.

Hence negative tests even when you are infected and suffering from borreliosis. ILADS has estimated that tests in current use miss 40-50% of the people actually infected.

Thus while one strain may show up on the test, the strain which is actually causing the disease may not. These different strains may also cause different symptoms as they may aattack different parts of the body. The possibilites and variations are enormous.

The problem with Wormser, Steere et al is that they have a simple minded and simple view of a very complex family of closely related diseases caused by a highly varied and complex family of related spirochetes. Their understanding of what we have misnamed "Lyme disease" is at least ten years or more out of date.

Hence my delight that finally Dr. Wormeser has discovered what was discovered over ten years ago by researchers cited in my paper. Bb is a highly variable organism with many, many ways of evading and undermining and even turning the immune system against itself. He had been forced to admit a fragment of the truth after all.

I submit that with more and more research over time the truth will very slowly come out. But at an enormous cost in human suffering. Much of which could have been avoided if the insurance companies had not been so greedy and the ducks had not been so stupid and kept any open mind.

Lyme disease really is the "Tuskegee" of the 21st century. They could at least have admitted that we do not know and not gone after, persecuted and destroyed those brave doctors who did not stupidly swallow the party line and actually looked at patients as sick people and tried to help them.

Hope this helps make a difficult and complex subject a little easier to understand.

In plain english the duck Wormser has just confimed by his research what I have said in my research, at least part of it. So I am gloating. Now what next, Dr. Womrser? Cheers. TMP

--------------------
Thomas Parkman

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Meg
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Thank you Thomas for explaining it so well [Smile]

Did old Wormser leave any footnotes per chance?

Now if only these idgits would keep on catching up.....we might get some REAL work done to help us.

--------------------
Success Stories---Treatment Guidelines

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brentb
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quote:
Originally posted by Thomas Parkman:
Dear members,
Lyme disease really is the "Tuskegee" of the 21st century. They could at least have admitted that we do not know and not gone after, persecuted and destroyed those brave doctors who did not stupidly swallow the party line and actually looked at patients as sick people and tried to help them.


Always OK to rub it in a little [Big Grin]

Hate to be a gov't apologist but...If borrelia turns out to be as pervasive a problem as many believe it is. (imo Dr Harvey/Salvato have it right) then abx treatment for the masses is just not a practical solution.

Were stuck with two situations. Does the gov't lie (I'm convinced this is political and not scientfic) and have tons of folks with no ability to get treatment or do they tell us the truth, cause mayham and still have tons of folks with no ability to get treatment.

I have plenty of gripes about our gov't (especially the FDA) but in this case imo we are dealing with some complicated issues. Unless we have a better answer as to how this mess should have been handled imo it's tough to blame.

Just a thought before we condemn the guys for atrocities. As for the rest, outstanding post and I'm happy you finally got some vindication.

[ 24. August 2006, 03:53 PM: Message edited by: brentb ]

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treepatrol
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very good

--------------------
Do unto others as you would have them do unto you.
Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.

Newbie Links

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Marnie
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Thomas...this is also compounded because we typically measure (count) ANTIBODIES...

We are still relying on the Western Blot or worse, the Elisa.

We measure our RESPONSE to the bacteria. The number of healthy antibodies which are present to fight this and other pathogens.

To be measured, to count them, one would suspect the antibodies would have to be "perfect".

But they aren't.

They are damaged at the top - called the "fab" portion/area.

It looks like the top of a stalk of broccoli. The stalk of broccoli being the appearance of an antibody. It is pictured somewhere on the internet. I found it along time ago, but unfortunately didn't link it/save it back then.

"Characterization of the physiological requirements for the bactericidal effects of a monoclonal antibody to OspB of Borrelia burgdorferi by confocal microscopy.

The bactericidal effect of Fab-CB2 is not dependent on the induction of spirochetal proteases but ***is dependent on the presence of Ca2+ and Mg2+.***

Supplementation of Ca2(+)- and Mg2(+)-free medium with these cations ***restored the bactericidal effects of Fab-CB2.***

The mechanism by which a Fab fragment of an antibody destroys a bacterium directly may represent a novel form of antibody-organism interaction.
PMID: 9125579

In other words, the antibodies aren't "healthy" and don't WORK...they can't destroy Bb unless they are HEALTHY and to be healthy...we need Mg and Ca...enough to last for several days.

A ``novel form of antibody-organism interaction?''

I don't THINK so!

"E. Required by immunological process. Magnesium, immunity, and allergy: Mg is required for several steps of immunological reactions
1. Lymphoblastic transformation, a prerequisite of secretion of antibodies by lymphoblasts, requires Ca2+ and Mg2+
*2. Mg is required for synthesis of proteins, immunoglobulins included*
3. Antibody-induced complement activation is Mg dependent
4. The antigen-immunoglobulin-complement reaction induces degranulation of the mastocyte

http://www.mdschoice.com/elements/elements/major_minerals/magnesium.htm

So it doesn't matter what strain/what various proteins/genes expressed are in the outer cell wall...what does matter is that we make enough PERFECT healthy antibodies to MATCH that strain.

We can't make PERFECT antibodies IF we don't have enough Mg and Ca. Ca is not a problem, as it is our most abundant mineral. Mg, on the other hand, IS a problem. We have to have enough to supply energy to our cells.

I suspect a Mg deficiency triggers Bb's gene expression "alterations" too.

We don't have enough to "spare" fast enough. Mg levels drop "significantly" at the outset to INactivate PFK and to INactivate HMG CoA reductase while awaiting the formation of HEALTHY antibodies (which takes DAYS).

Meanwhile, up goes TNF alpha...big time.

Too toxic too fast for our bodies to handle.

Likely the pathogen load and the presence of co-infections depleting the same nutrients would greatly impact the success of being cured with minimal abx. as well as the amt. of stored nutrients to support a healthy immune system. (Choline, which we KNOW Bb is after, is included too. We KNOW it helps protect us from Alzheimers...IF we have enough in storage.)

The pathogens are all parasites. They take from us specific nutrients...unfortunately we need enough of those nutrients to mount an appropriate immune response.

We MAKE our own highly, highly targeted "antibiotics"...antibodies.

IF we have the "ammo" for the "guns".

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Thomas Parkman
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Dear Marne and Members of the List:

Marnie, you have hit the nail on the head!!! I have always said that we are involved in an inherent contradiction here which is inevitably going to cause endless trouble. Whatever the technical details of it, the fact is that we are testing the immune response to a disease that evades, undermines and hides in various ways from the immune system in order to determine the presence of the disease. This is why in my paper I tried to suggest an opening to get beyond that. However the dumb duckmobile keeps its head stuck in a rut and insists that the tests will tell us the truth. HOGWASH!!!

Futher there is this huge number of variant strains and subspecies and we are assuming that an antibody/antigen test using proteins from one bug or set of bugs will automatically detect any other bug. well it ain't necessarily so.As I keep saying, those idiots at the CDC have gotten all of us in this huge mess and are now to whatever to even acknowledge that we need to get out of it. Cheers.

--------------------
Thomas Parkman

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brentb
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quote:
Originally posted by Thomas Parkman:
Dear Marne and Members of the List:

.. we are testing the immune response to a disease that evades, undermines and hides in various ways from the immune systemCheers.

Nice to hear the truth finally coming out [Smile]

mind going into this further?

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Lymester
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Thomas/Marnie:

Excellent.

This is a "keeper".

Thank you,

Lisa

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Lymester

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Troup Brazelton
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Then, If I understand what Marina and TParkman are saying, if a doctor considers the clinical signs and test for Mg levels to determine dx and treatment, we could have a more reliable system than what we have now. A magnisum supplement along with abx started immediately would benefit more people than waiting for western blot and pcr and reverse western blot as well. If no improvement, them MRIs and the like.
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Thomas Parkman
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Dear Members of the List:

It seems to me that somebody must devise some kind of test that will somehow just get away from the immune response. One could look for other biological markers indicating the presence of the disease. Could it be possible, for example to identify the lipoproteins that are the toxins which cause the herxheimer reation when the enough of the spirochetes die? After all in the disease some spirochetes are dying all the time. I suspect that much of our misery comes from the fact that these lipoproteins are present all the time and are poisoning us.

Further it may be of use to look at ways to strenghthen the immune system. First to test if minerals and vitamins are defficient or if there are hormonial imbalances and what not and then treat these deficiencies, whatever they may be. If for example a magnesium supplimentation could be of help, why not try it. It could not be any more costly than any other of the number of tests and medications we are taking now?

I am told on good authority that there are better tests out there but mainstream medicine does not use them. What is urgently needed is immagination balanced by a rigorous adherence to the facts. Something that is badly lacking in the present situation. We need to start thinking out of the box as the phrase is.

In my memorandum I attempted, however feebly to do just that. I suggested:

8. Paradoxically a negative test result could actually aid in proving the presence of the disease if it demonstrates not the presence or absence of infection but rather that consistent inconsistency in immune response that is the hallmark of the disease. Lyme disease, evades and undermines the immune system. As the immune response develops gradually over a period of months to years 19 persistent infection would be indicated by changing bands over time. Thus rather than just looking for proof of the infection, for this band or that band or this number of bands, in addition one should actually be looking for a pattern demonstrating that process of immune evasion in which there is a fading in and out of immune response and that variablity in results that is characteristic of the immune response observed in other diseases. While a diagnosis of Lyme disease is a clinical diagnosis and in the current state of affairs cannot be based upon test results alone, testing can provide further information to assist or confirm an accurate diaganosis.

The truth of the matter is that the doctors cannot seem to recognize that this is a fiendishly complicated bug or should I say family of bugs. It is not easily cured if at all when it becomes embedded in the biosphere of another organism, particulary one as complex as homo sapiens. But they seem to want a simple and curable disease. That Lyme disease most emphatically is not. Cheers. Thomas Parkman

--------------------
Thomas Parkman

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Thomas Parkman
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Dear members:

In her response Marnie noted:
So it doesn't matter what strain/what various proteins/genes expressed are in the outer cell wall...what does matter is that we make enough PERFECT healthy antibodies to MATCH that strain.

I must emphatically disagree. This is the problem with all of the serological testing. Even with perfect antibodies, if the strain in the patient does not match that used as the antigen base or the strain in the patient is expressing different proteins and thus stimulating antibody production to different antigens then the test will never present the presence of the disease. while it is much more complicated than that for puposes of a preliminary understanding that will suffice. That is why serological tests will always be problematic. You have a huge disconnect between the proteins by the body used to create the antibody and the preteins used to construct the antigen, ie the foreign matter, itself.

--------------------
Thomas Parkman

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brentb
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quote:
Originally posted by Thomas Parkman:
Dear members:
You have a huge disconnect between the proteins by the body used to create the antibody and the preteins used to construct the antigen

"antigen drift" going on? Is this a cat and mouse game of some sorts in which as soon as the immune system finds the protein borrelia expresses the borrelia then "switches it's coat" and hides again?

I'm also confused as to how some "strains" produce lipids which can turn off the immune system. Why use antigen drift to confuse the immune system if it can be completely turned off. Different strains?
Appreciate the expertise you provide on this very challenging topic.

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Thomas Parkman
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DEar Members of the List:

Please do not consider me an expert in anything. I, however, have done some reading and research and the matters I have cited above are based on the conclusions drawn from that research.

I am sorry, but I do not quite understand what is meant by antigen drift. Antigen change would probably be a better description of what actually happens. Given the radically different environments in which the various species or strains or variants of the genospecies live, ie blood sucking insects and warm bloodied mammals they have developed a vast repetory of changes in order to be able to survive such drastic changes.

It is as if at one moment I were living in the wilds of Antartica and then a few moments later were living on a hot, torrid and humid mud flat in the middle of the African jungle surrounded by all these unpleasant and dangerous animals. Antigen simply means any foreign matter in the human body. A speck of pollen or a minute piece of a thorn in the blood stream would be an antigen.

In the case of borrelia, it changes antigens, ie the proteins which constitute its outermost layer as a part of its adaptive and protective mechanism. The process by which the species evades, undermines and hides from the immune system is only partly understood. I have used the very crude analogy by way of illustration of a con artist changing his clothes and appearance to escape the police.

There are some 16 or so proteins which the borrelia expresses during its life time. Further there are any number of different species and strains which express different proteins-ie use different proteins-at different times during their lifetimes and at different points during their lifecycles. This is a complex and very complicated business. Which makes the use of testing as a tool for diagnosis such a problematic undertaking which I suspect causes more problems than it solves. The conventional medical profession hasn't even gotten to first base in an understanding of this disease. On a recent thread there has been mention of STARI, yet another cousin in the family. So things just keep getting curioser and curioser and curioser. Cheers. Thomas Parkman

--------------------
Thomas Parkman

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brentb
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Good stuff...yep the times are getting interesting. If you have time I'd like to hear your thoughts on Barbour's work. He seams to state a vaccine is just plain stupid. If the host can't find it...

http://id.medscape.com/govmt/CDC/EID/2000/v06.n05/e0605.02.barb/e0605.02
.barb-01.html
From: Emerging Infectious Diseases
Antigenic Variation in Vector-Borne Pathogens
Alan G. Barbour, University of California Irvine, Irvine, California;

Conclusions
The requirement for vector transmission of these infectious pathogens
provides a powerful selection for mechanisms that prolong parasitemia.
Through convergent evolution, several vector-borne pathogens have
arrived at the same strategy of antigenic variation to achieve this
goal. The similarity in the genetic mechanisms that such unrelated
pathogens as African trypanosomes and relapsing fever Borrelia spp. use
for antigenic variation is remarkable.
Antigenic variation has important implications for the development of
vaccines against these pathogens. If the variable antigen is to be the
target of immunoprophylaxis, the vaccine would likely need to be
multivalent, perhaps to the point of impracticality. If the infected
host animal has not solved the problem of identifying an antigen that
is conserved among the variants, thereby neutralizing the infection
earlier, how can vaccine developers hope to do this?

A possible way to meet this challenge is to focus on the function
domains of the variable proteins. The variable antigens of both the
bacterial and parasite pathogens have other roles in pathogenesis
besides immune evasion. These include tissue tropism, shielding of
adjacent molecules, inhibition of phagocytosis, modulation of antigen
presentation, and selective adherence. Certain regions of the variable
protein may be irrelevant for these functions of the pathogen, and
consequently the encoding DNA sequences could be highly divergent among
alleles. On the other hand, the regions conferring these functions
would likely be more constrained in structure and thus comparatively
more susceptible to cross-reacting antibodies.

Another possible way to meet the challenge of antigenic variation is to
focus on the vector-specific surface antigens of these pathogens. The
repertoire expressed in the arthropod vector, which lacks an adaptive
immune system, is generally more limited than that expressed in the
vertebrate host. The Lyme disease vaccine is an example of successful
targeting of a vector-specific protein. Although B. burgdorferi has not
yet been proven to undergo true antigenic variation, there is
considerable diversity in the ospC sequences that define strain
identity within a given area in which transmission to humans occurs. A
vaccine based on OspC would likely need to be multivalent. In contrast,
B. burgdorferi's OspA protein[62], the sole protein in the vaccine, is
natively expressed in the tick's midgut but usually not during
infection of mammals[63]. Perhaps because of OspA's infrequent
encounters with the mammalian adaptive immune system in nature, there
is little divergence in ospA sequences between strains of B.
burgdorferi [64]. The OspA-based vaccine apparently works by eliciting
antibodies that kill or inhibit the spirochetes in the tick, before
expression of the more polymorphic ospC and vlsE genes in the mammalian
host[65].

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Ann-OH
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My eyes are getting crossed at such dense copy, so I have broken up your post.

[quote]
Good stuff...yep the times are getting interesting. If you have time I'd like to hear your thoughts on Barbour's work. He seams to state a vaccine is just plain stupid. If the host can't find it...

http://id.medscape.com/govmt/CDC/EID/2000/v06.n05/e0605.02.barb/e0605.02
.barb-01.html
From: Emerging Infectious Diseases
Antigenic Variation in Vector-Borne Pathogens
Alan G. Barbour, University of California Irvine, Irvine, California;

Conclusions
The requirement for vector transmission of these infectious pathogens
provides a powerful selection for mechanisms that prolong parasitemia.

Through convergent evolution, several vector-borne pathogens have
arrived at the same strategy of antigenic variation to achieve this
goal.

The similarity in the genetic mechanisms that such unrelated
pathogens as African trypanosomes and relapsing fever Borrelia spp. use
for antigenic variation is remarkable.

Antigenic variation has important implications for the development of
vaccines against these pathogens. If the variable antigen is to be the
target of immunoprophylaxis, the vaccine would likely need to be
multivalent, perhaps to the point of impracticality.

If the infected
host animal has not solved the problem of identifying an antigen that
is conserved among the variants, thereby neutralizing the infection
earlier, how can vaccine developers hope to do this?

A possible way to meet this challenge is to focus on the function
domains of the variable proteins.

The variable antigens of both the
bacterial and parasite pathogens have other roles in pathogenesis
besides immune evasion. These include tissue tropism, shielding of
adjacent molecules, inhibition of phagocytosis, modulation of antigen
presentation, and selective adherence.

Certain regions of the variable
protein may be irrelevant for these functions of the pathogen, and
consequently the encoding DNA sequences could be highly divergent among
alleles.

On the other hand, the regions conferring these functions
would likely be more constrained in structure and thus comparatively
more susceptible to cross-reacting antibodies.

Another possible way to meet the challenge of antigenic variation is to
focus on the vector-specific surface antigens of these pathogens.

The repertoire expressed in the arthropod vector, which lacks an adaptive
immune system, is generally more limited than that expressed in the
vertebrate host.

The Lyme disease vaccine is an example of successful targeting of a vector-specific protein.

Although B. burgdorferi has not
yet been proven to undergo true antigenic variation, there is
considerable diversity in the ospC sequences that define strain
identity within a given area in which transmission to humans occurs.

A vaccine based on OspC would likely need to be multivalent.

In contrast,B. burgdorferi's OspA protein[62], the sole protein in the vaccine, is
natively expressed in the tick's midgut but usually not during
infection of mammals[63].

Perhaps because of OspA's infrequent
encounters with the mammalian adaptive immune system in nature, there
is little divergence in ospA sequences between strains of B.
burgdorferi [64].

The OspA-based vaccine apparently works by eliciting
antibodies that kill or inhibit the spirochetes in the tick, before
expression of the more polymorphic ospC and vlsE genes in the mammalian host[65].[end quote]

Ann - OH

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Thomas Parkman
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Dear People,

I cannot say that the idea of a vaccine is just plain stupid. I do not have the technical expertise to make such an assertion. I do know that they did attempt about six or so years ago to make a vaccine using the OSPA and the result was an unmitigated disaster. If you wish I can send you the cites about it. Further as the pathogen changes into a mammalian millieu it changes or shifts if you wish from OSPA to OSPC and others. It becomes a very complicated situation indeed.

So let us say, and this is one of my central conclusions and is my opionion only, since we are actually dealing with a whole family or group of closely and perhaps not so closely related pathogens causing in essence a series of related and very similar diseases, the idea of a single vaccine, as vaccines are currently understood and constituted may be wishful thinking, an unrealistic impossiblity in the light of present understanding or, indeed, just plain stupid. Cheers.

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Thomas Parkman

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TexasChaos
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Okay, here's what I want to know:

How the *heck* are y'all comprehending all this through the brain fog?!

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Corgilla
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Hah! Here's the trick when you have brain fog. Read every fourth word and it all makes sense! [Big Grin]

Thanks Thomas. This is great info. Can't wait to read the whole thing.

Take care,

Corgilla

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"I'll never forget good old Whatsisname."

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brentb
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It's an interesting "vaccine" isn't it...Have you checked out sci.med.lyme lately? Good stuff on immune suppresion.
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ConnieMc
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treepatrol
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This has been put in Newbie Links Page 1.

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Do unto others as you would have them do unto you.
Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.

Newbie Links

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