Some are claiming that Embers et al statement about how their findings should not be used to oppose current IDSA treatment guidelines for Lyme disease is something they were asked to write - rather than something the authors included on their own.
I don't know. For this claim - whether it's true or not - I have no evidence. However, one thing I do know is that there are solid scientific reasons which back the need for more research on spirochetes which survive after prolonged antibiotic treatment.
The question, of course, which weighs heavily on every patient's mind has been this one:
Why aren't persisting spirochetes enough evidence of infection?
It's become a political hot button question, and it's a scientific question. But most people think that as long as the spirochetes Embers found are alive and metabolically active, that is enough evidence to state that yes, Lyme disease is a chronic infection - let's stop all this nonsense right now and change the treatment guidelines!
Given my own experience and how longer than standard treatment helped me improve, I totally get this. I've been there, done that - and I think that a standard course of antibiotic treatment does not work for everyone. Particularly if there is a delay in proper diagnosis and treatment. Particularly if a coinfection is present. Particularly if there is some abnormality in one's immune system.
But if you are a scientist and you are researching this phenomenon of persistence - whether you as a scientist suspect these spirochetes can cause persisting infection or not; whether the above claim by other patients is true or not - you will be called upon by other scientists to support your findings.
It isn't just going to be the IDSA or the ALDF or other organizations which deny the possibility of persistent infection as a cause of chronic Lyme disease which are going to want to know the outcome of your study.
It's going to be the American Society for Microbiology (ASM) that wants to know the outcome. It's going to be researchers in Europe like the Brorsons who study the "cyst" form of Borrelia burgdorferi and want confirmation of their own findings about persistence.
It's also going to be universities and health departments and many different organizations which may not have any particular position on whether or not Lyme disease can be chronic who will want to know the outcome of your study.
They're all going to want to know the outcome of a study such as Embers et al, so these researchers must be certain about what they found and its significance, and conduct additional research related to their findings in order to confirm them.
They must find evidence that no one can argue against - even the most skeptical - if they are to support their own hypotheses. And it may be that at this stage they genuinely do not know what to make of these persistent spirochetes and not only their ability to cause disease - but how they cause it.
I can easily imagine that Embers et al is being very cautious about the interpretation of their results and wanting further studies as easily as it is for other people to imagine that Embers at al were somehow instructed to downplay the significance of their spirochetes surviving antibiotic treatment.
Why do I say this? I say this because I have learned a few things about these stealthy bacteria and think there is good reason for Embers et al to be cautious about the interpretation and approaching their results either way.
Borrelia burgdorferi spirochetes, plasmids, and infectivity
After doing some research on this issue, the issue of whether or not these spirochetes were infectious and pathogenic or not is a more complex issue than it at first appears.
First, here's a refresher of some basic microbiological definitions. (Bear with me, I'll try to get through this part quickly.)
Infection = the replication of organisms in the tissue of a host; when defined in terms of infection, disease is overt clinical manifestation. In an inapparent or subclinical infection, an immune response can occur without overt clinical disease.
Colonization = A carrier (colonized individual) is a person in whom organisms are present and may be multiplying, but who shows no clinical response to their presence.
Pathogenicity = The pathogenicity of an agent is its ability to cause disease; pathogenicity is further characterized by describing the organism's virulence and invasiveness.
Virulence = refers to the severity of infection, which can be expressed by describing the morbidity (incidence of disease) and mortality (death rate) of the infection.
Invasiveness = invasiveness of an organism refers to its ability to invade tissue.
Now that we're past these definitions, I'll cut to the chase and say there are two important things to know upfront:
1) During in vitro passage or certain stressors, Borrelia burgdorferi can lose some of their plasmids. How soon this happens varies depending on the strain and particular isolates of Borrelia.
2) When Borrelia burgdorferi loses specific plasmids with specific genes on them, it can lose infectivity and pathogenicity. It should be noted that specific genes for specific purposes can show up on different plasmids on different strains. (For example: Bb strain N40's VlsE locus is different from the one found on commonly studied B31, and it shows up on a different plasmid than on B31.)
The essential bit of information here is that the loss of a particular gene or set of genes can affect spirochetes' ability to cause infection - and even if these genes are lost, spirochetes may still survive for a while. They can become attentuated or less infectious.Numerous studies on Borrelia burgdorferi's plasmids have shown that lp28-1 is a linear plasmid which makes Borrelia burgdorferi infectious. VlsE genes found on lp28-1 are thought to be essential for mammalian infection with Borrelia burgdorferi.
When the lp28-1 and yet a different plasmid, lp25, are missing from spirochetes, they are unable to infect mice. The lack of lp25 completely abolishes infectivity since this plasmid encodes a gene (bbe22) which is essential for Borrelia burgdoferi's survival in mice.
Spirochetes which lose lp28-1 plasmids will still live for a while - but the immune system tends to mop them up in a few weeks without antibiotic usage.
Specific research on mutant spirochetes with a lack of the lp28-1 plasmid has shown the following:
"While the wild-type B. burgdorferi persisted in tissues for the duration of the study, the lp28-1− mutant began clearing at day 8, with no detectable bacteria present by day 18. As expected, the wild-type strain persisted in C3H/HeN mice despite a strong humoral response; however, the lp28-1− mutant was cleared coincidently with the development of a modest immunoglobulin M response. The lp28-1− mutant was able to disseminate and persist in C3H-scid mice at a level indistinguishable from that of wild-type cells, confirming that acquired immunity was required for clearance in C3H/HeN mice. Thus, within an immunocompetent host, lp28-1-encoded proteins are not required for dissemination but are essential for persistence associated with Lyme borreliosis."To translate the above:
Normal Bb spirochetes infected C3H/HeN (mice which are specifically bred for the ability to demonstrate joint swelling and arthritic symptoms similar to those found in the average person who gets Lyme disease) mice and these spirochetes could not be cleared by the immune system despite the fact that these mice had a strong humoral response.
However, mutant Bb spirochetes which did not contain linear plasmid 28-1 were completely cleared by these C3H/HeN mice.
What's fascinating about this study is even though the mutant Bb spirochetes lacked lp28-1, these spirochetes could still disseminate. Only in severely compromised immune deficient mice (scid mice) could the spirochetes both disseminate and persist - acquired immunity must be functional in animals infected with such mutants in order to clear the spirochetes.
So, here is one example of how you can have spirochetes which are alive and metabolically active and can even disseminate - yet they are no longer causing disease. In this instance, they were cleared by the immunocompetent mice without the use of any antibiotics within a mere 18 days. (I wish I were that lucky!)
More recently, other plasmids have been found to contribute to infectivity in mammalian hosts - such as lp36. lp36 is viewed as being another major contributor to persistent infection in mice, and spirochetes become attenuated when lp36 is removed.
Linear plasmid 28-1 and lp25 have a much longer history of their role in infectivity and pathogenicity, and they are two of the most studied linear plasmids thus far - lp28-1 the most because of its VlsE genes in strain B31.
So, keep this in mind when you think of the Embers et al study, and realize why this part of their paper on Rhesus macaques caught my attention:
"A few spirochetes grew in cultures of organ tissues collected post-mortem from each animal after > 9 weeks, but we were unable to subculture any spirochetes from either treated or untreated animals due to their slow growth. We therefore pelleted these cultures to confirm their identity and test their viability by DNA/RNA analysis. Transcription was detected in culture pellets and the tissues of treated animals, indicating that the bacteria were metabolically active (Figure 6C, D). Figure 6D shows ospA transcription detected directly in tissues harvested from treated and untreated animals. We also hypothesized that persistent spirochetes may lose linear plasmid 28-1 (lp28-1), which encodes the VlsE antigen bound by the anti-C6 antibody. Transcription of a lp28-1 gene (bbf26) was verified in organ tissue from both untreated animals and one treated animal (Figure 6D).In the case of Embers et al study on Rhesus macaques, one antibiotic treated animal was found to have evidence of transcription of a lp28-1 gene (bbf26 - protein; purpose unknown) from a sample taken from heart tissue (Fig. 6D) and that transcription should only be able to occur if the lp28-1 plasmid is intact and functional. lp28-1 is a linear plasmid which is very specific to infection both in vitro and in vivo, whether a tick or needle inoculation is used.
In Embers study, in addition to transcription of a gene from lp28-1, OspA transcription from lp54 was found in three treated animals. OspA transcription was detected in two tissue samples taken from the bladder and one tissue sample taken from the spleen. Additional OspA transcription was found in different organs in two out of three of the same animals using organ tissue culture pellets.
Overall, this sounds interesting and points to the possibility of chronic infection after antibiotic treatment.
But if I have seemed cautiously optimistic about this study, it's because of a few factors*:
1) Only one treated animal had evidence of a infection where lp28-1 transcription was taking place - had more treated animals shown evidence of transcription on this plasmid, I would have been more excited. How long could spirochetes maintain these plasmids while being treated? What about lp25?
2) It is unknown to me if the genetic background and/or immune system of the treated Rhesus macaques somehow played a role in their inability to clear the spirochetes which remain after antibiotic treatment. (Refer to this post on HLA-DR types, read what's before and after the "=" signs, and you'll see what I mean.)
3) it is unknown to me how different the results would be if the Rhesus macaques had been infected using ticks instead of needle inoculations. It seems to make sense to me to do this study again using ticks because that mimics what happens in nature.
On the other hand, I find it very interesting that three animals showed evidence of transcription of OspA. Given how much inflammation people experience during Lyme disease - plus evidence of later stage antibody reactivity to OspA - it at least gives me pause to think about how often OspA has been a culprit for my own symptoms, directly or indirectly.
 |
| The only kind of spirochete you don't mind getting close to. |
Is There Anything Positive To Glean From Dr. Baker?
Of Dr. Baker's two major stated issues with the Embers study, the only one now left is whether or not the spirochetes which were transmitted by ticks to new hosts (xenodiagnosis) were in fact infectious. His other concern was over the use of ceftiofur in the study rather than ceftriaxone - however, the authors of the study have since posted a correction to PLoSONE stating that ceftriaxone - not ceftiofur - was used throughout the entire study.
If there are any remaining minor issues he has with the study, he has yet to share them on the Lyme Policy Wonk blog. Mostly, he seemed to reiterate his concern about these two issues and focused on the single mention of ceftiofur in the paper repeatedly.
About the most positive response I heard from Dr. Baker on that blog thus far was about his view of how Lyme disease research should be conducted:
"...I favor a multi-disciplinary approach that moves the field in a different direction, rather than solutions based on the assumed yet to be proved existence of a persistent infection that can only be cured by antibiotics. I don’t really discount such a view; rather, I feel we are neglecting other possibilities that may provide the answers we all are looking for. A case in point, would be the recent work of good friend, Armin Alaedini — who I helped support when I was at the NIH– using specimens collected by Mark Klempner as part of his clinical trial. These valuable specimens are being maintained by Mark in a specimen repository for use in just such cutting-edge research. They are available free of charge on request."Like Pamela Weintraub, I agree that a multi-disciplinary approach to research on Lyme disease is important. And while Dr. Baker also supports a multi-disciplinary approach to research on Lyme disease and he states he doesn't discount the view of persistent infection in the above paragraph - his direct responses to patients suffering with CLD/PTLDS state that most patients are suffering from some other non-Lyme disease related condition - something I find particularly unhelpful to my situation. That and a lack of sufficient research on other treatment approaches has been an issue for ages.
In my opinion, Dr. Baker's response to the Embers Rhesus macaque study was more negative than it warranted. I wouldn't have viewed it negatively at all - I see it as a stepping stone in getting a better understanding about Lyme disease. And just because it leaves unanswered questions does not mean it was inherently flawed - which was what Dr. Baker seemed to suggest.
To quote someone else on that blog:
"My question to Dr. Baker is why don’t you and your colleagues offer some expert advice, according to your best opinions and hunches if science really has proven inadequate for your epistemic standards of validity, without having to officially disclose any sensitive data that might get you in trouble with your career, that could actually HELP these affected people lessen their pain and disability? Just disparaging some controversial or technically flawed research as being invalid does not seem helpful enough to me."Yes. This.
Regardless of anyone's opinion - Dr. Baker, or LLMDs, or my friends and family - researchers will be expected to provide evidence to the world that these remaining spirochetes are pathogenic. They will need to provide evidence that that they can cause infection and reproduce - even if they are already proven to be alive.
Researchers who are trying to work without bias will want to cover all the bases and check their postulates twice to be 100% certain that Borrelia burgdorferi either causes a chronic infection or it does not after standard antibiotic treatment.
This may be so - but I'm impatient about it.
References:
The Absence of Linear Plasmid 25 or 28-1 of Borrelia burgdorferi Dramatically Alters the Kinetics of Experimental Infection via Distinct Mechanisms. Maria Labandeira-Rey, J. Seshu, and Jonathan T. Skare. Infect Immun. 2003 August; 71(8): 4608–4613. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC166013/
Correlation between plasmid content and infectivity in Borrelia burgdorferi. Purser JE, Norris SJ. Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13865-70. http://www.ncbi.nlm.nih.gov/pubmed/11106398
High- and low-infectivity phenotypes of clonal populations of in vitro-cultured Borrelia burgdorferi. Norris, SJ, Howell, JK, Garza, SA, Ferdows, MS, and Barbour, AG. Infect. Immun. 63:2206-2212.
Plasmid Stability during In Vitro Propagation of Borrelia burgdorferi Assessed at a Clonal Level. Dorothee Grimm, Abdallah F. Elias, Kit Tilly and Patricia A. Rosa. Infect. Immun. June 2003 vol. 71 no. 6 3138-3145 http://iai.asm.org/content/71/6/3138.full
Experimental assessment of the roles of linear plasmids lp25 and lp28-1 of Borrelia burgdorferi throughout the infectious cycle. Grimm D, Eggers CH, Caimano MJ, Tilly K, Stewart PE, Elias AF, Radolf JD, Rosa PA. Infect Immun. 2004 Oct;72(10):5938-46. http://www.ncbi.nlm.nih.gov/pubmed/15385497
The critical role of the linear plasmid lp36 in the infectious cycle of Borrelia burgdorferi. Mollie W Jewett, Kevin Lawrence, Aaron C Bestor, Kit Tilly, Dorothee Grimm, Pamela Shaw, Mark VanRaden, Frank Gherardini, and Patricia A Rosa. Mol Microbiol. 2007 June 1; 64(5): 1358–1374. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1974800/?tool=pubmed
Basic Epidemiology. Beaglehole R, Bonita R, Kjellstrom T. World Health Organization, Geneva, Switzerland, 1993
* Factors which concern others but I did not originally think of are included in comments below.
[Edited March 9, 2012 - Removed item above about brain tissue after reviewing Embers paper again - multiple brain samples were taken; one treated animal was positive for B. burgdorferi RNA in both heart and brain.]
This work by Camp Other is licensed under a Creative Commons
Attribution-NonCommercial-ShareAlike 3.0 Unported License.
Questions and observations about this study which came from someone else which bear mentioning:
ReplyDelete" I am puzzled by the data of Figure 2, groups A and B. Why are the kinetics so different for the two groups BEFORE treatment -- or sham treatment-- that begins at 27 weeks? One would expect them to be very similar. Were the animals randomized for the type of treatment they were given or were those with the highest C6 index from 10-27 weeks selected for antibiotic treatment? "
"I am puzzled by the fact that inflammation was noted ONLY in 3 animals (Table 1). What is remarkable is that these 3 animals were found in the antibiotic treated group, not the sham-treated group where one would have anticipated that the frequency of inflammation would have been much higher. What is the explanation for this?"
"f the RT-PCR data of Table 1 provide a valid measure of "viable" Borrelia in the tissues examined, wouldn't one expect most--if not all-- of the animals in the sham-treated group B to be positive?"
These questions are not mine and belong to someone else - namely "Henry", who has stated he is a bacteriologist. I thought I'd put them up here for further consideration and to see if anyone else reading has comments about them.
" I am puzzled by the data of Figure 2, groups A and B. Why are the kinetics so different for the two groups BEFORE treatment -- or sham treatment-- that begins at 27 weeks? One would expect them to be very similar. Were the animals randomized for the type of treatment they were given or were those with the highest C6 index from 10-27 weeks selected for antibiotic treatment? "
ReplyDeleteWouldn't it be explained by the fact that the sham-treated group was split into two distinct groups for analysis, selected to show the two distinct response? Combining the two as one "sham-treated" group might yield a similar pattern pre-treatment.
"I am puzzled by the fact that inflammation was noted ONLY in 3 animals (Table 1). What is remarkable is that these 3 animals were found in the antibiotic treated group, not the sham-treated group where one would have anticipated that the frequency of inflammation would have been much higher. What is the explanation for this?"
That is interesting. Do antibiotic treatment indirectly cause the inflammation?
"[i]f the RT-PCR data of Table 1 provide a valid measure of "viable" Borrelia in the tissues examined, wouldn't one expect most--if not all-- of the animals in the sham-treated group B to be positive?"
It might not be a sensitive measure for detection, but still a valid measure that organisms are viable when detected. I would also expect most detection in the sham-treated group, but that doesn't make it less valid a measure of viability, does it?
TicksSuck
TicksSuck,
ReplyDeleteThanks for taking a shot at it. The questions were raised and I hope more people are willing to give it their own shot.
You said,
"Wouldn't it be explained by the fact that the sham-treated group was split into two distinct groups for analysis, selected to show the two distinct response? Combining the two as one "sham-treated" group might yield a similar pattern pre-treatment."
I saw that. The researchers said that the antibody responses in the untreated group either oscillated but never declined steadily (5 out of 12 macaques) and they scored positive on the C6 - or they returned to background levels (7 out of 12 animals in that group) but their return to background levels wasn't the same as the treated group's decline in antibody response. (Slower decline vs. rapid decline)
This where I begin wondering if the untreated animals have different genetics which predispose them to a different immune/antibody response. There's not enough information here to know that, though.
(I've surmised both host genetics and spirochete genetics (strain) are important here.)
Now I want to get out my tests and look at them and see if they oscillated. I haven't looked at them in a while.
"That is interesting. Does antibiotic treatment indirectly cause the inflammation?"
It might be this response where the antibiotics affect the spirochetes and the spirochetes trigger inflammation? At least initially. This is something I'm trying to understand? I think if this was an RST1 strain of Bb and not RST 2 strain, then there is a risk of greater inflammation upon treatment. The inflammation could be sustainable past antibiotic treatment, too, so it doesn't have to just be an initial "spike" of inflammation.
See: <a href="http://spirochetesunwound.blogspot.com/2009/12/genetics-of-both-host-and-pathogen.html>http://spirochetesunwound.blogspot.com/2009/12/genetics-of-both-host-and-pathogen.html</a>. Make a note of Joanne's comment there, too.
I know it's about inflammation and autoimmunity, but I keep thinking that this sort of mechanism can continue while spirochetes are present at low levels.
I'll get to the third question later... right now, I have to go.
Bah. Try this: http://spirochetesunwound.blogspot.com/2009/12/genetics-of-both-host-and-pathogen.html
ReplyDeleteBut think of it in terms of simultaneously occurring, potentially, with a low level infection. I keep thinking about those three treated animals where transcription of OspA was found.
Okay, have a few more minutes, then I really have to go...
ReplyDeleteI'm going to say that second one is puzzling me, too. I need more data.
For anyone looking for the shorter answer to the question, "Why aren't persisting spirochetes enough evidence of infection?", here it is:
ReplyDeleteBecause when spirochetes lose specific plasmids, they can continue to live in their host but either become less infectious and/or less virulent - or they can lose their ability to be infectious entirely.
(And you might think this is strange, but spirochetes can disseminate widely in their host but still not be that virulent or that infectious. These conditions can occur independently.)
A somewhat longer more detailed answer:
The period of time these spirochetes live and where they live in the host depends on which plasmid or plasmids they lose. Linear plasmid 25 (lp25) is needed for persistence, and its presence is connected with infection in the joints. Linear plasmid 28-1 (lp28-1) is needed for persistence, and its presence is connected with a more system-wide infection in mice.
These two plasmids are often the first to get "lost" during in vitro cultivation of spirochetes. That one of them was found in a living spirochete transcribing a gene after months of antibiotics in an in vivo study is a bit surprising for some.
This shortened explanation is somewhat of an oversimplification of the bigger picture. This is what I know about these particular plasmids' operation from animal models. What happens in people? Good question.
More notes, taken from the book, Borrelia, 2010, Horizon Press:
ReplyDelete"Low infectivity B31 clones are associated with absence of lp25, whereas intermediate infectivity phenotypes retained lp25 but were missing lp28-1 (Labandeira-Rey and Skare, 2001; Purser and Norris, 2000; Xu et al, 1996). The critical infectivity determinant on the B31 lp25 plasmid has been defined as a nicotinamidase (PncA) (Purser et al, 2003). The lp28-1 determinant for reduced infectivity has not been defined, but is widely believed to be related to the VlsE locus. Loss of this plasmid results in a phenotype that requires a higher infectious dose. The spirochetes remain capable of disseminated infection, but are more vulnerable to host medicated clearance, or may have altered tissue tropism (Elias et al, 2003; Grimm et al, 2004a; Labandeira-Rey et al, 2003; Lawrenz et al, 2004; Norris et al, 1995; Purser and Norris, 2000; Xu et al, 1996; Zhang et al, 1997)."
Barthold et al, Borrelia, pg. 384
CO,
ReplyDeleteI doubt that "autoimmunity" is a valid concept.
Best example may be RA (rheumatoid arthritis): Immunologist Prof. Alan Ebringer et al. (King's College, London) almost 3 decades ago in The LANCET presented evidence that RA is caused by infection with P(roteus) mirabilis.
Meanwhile they have deciphered all the molecular details - but rheumatologist simply ignore this work...
(O'Dell et al. in Nebraska have shown high effectiveness of mino- and doxycycline in early RA - but "state" that MMP inhibition is the mode of action (matrix metallo proteases), not atibiotic.)
RA is a multi billion business, or probably multi dozen billlion...
Or take MS: more than 80 years ago Prof. Gabriel Steiner at the university of Heidelberg documented spirochetes (morphologically borreliae) in the MS lesions of deceased patients (see G.Steiner: "Die multiple Sklerose", Springer Verlag 1962 for an overview on his decade long research). Those patients may have lived many years, possibly decades with MS - and there were spirochetes in their MS lesions, most probably borreliae.
Or take the much more recent work of the Brorsons: B.b in the CNS of MS patients...
Or take the much more recent work of Judith Miklossy: lot's of different species of spirochetes (including B.b) to be found in Alzheimer's brains - which is a disease known to develop over decades!
Autoimmunity is not a valid concept. It's a concept to keep victims and critical minds from geting to the root cause, chronic infection - which can be cured or at least stopped / controlled by antibiotics available in the pharmacy at the corner. Doxy has been available for close to half a century, and it get's into the CNS (as does minocycline) and is the first line AB in LD / NB in Sweden. (The Swedes are intelligent people!!! At least many of them.)
Why feed those lab researchers with millions... billions? Why not study if doxy can control late NB IN HUMANS?!?!?
Everyone answers there is no drug company to finace such trials. Of course not. I know from a presentation of "molecular biology" work by a clinician that he clearly stated: we will NOT do simple clinical research as long as drug companies pay for studying their new substances. That is "big business", not "peanuts".
So if clinical research in medical universities (and even outside...) is controlled by the rich drug companies: who could do what needs to be done in CLINICAL research, i.e. in therapy of late NB?
"Forget" the concept of "autoimmunity", "forget" most of the lab science if you are looking for a solution of the needs of ?millions of late LB victims around the world.
To me it's 99% clear that it's persistent infection, and this can be controlled by readily available drugs, doxy in case of B.b (and lot's of other infections, "co-infections").
chen-men
"Henry" is McSweegan. He has many alias, like Satan.
ReplyDeleteChen-men,
ReplyDeleteI think I've answered your comment elsewhere, by stating that I suspect that a combination of infection and an immune modulation problem underlie patients' persisting symptoms. I've also said that this is my speculation. The issue for both of us - you with your hypothesis, me with mine - is that they need to be put to the test. Who is going to do it? Who is going to conduct the research which tries to provide evidence for our hypotheses?
You say don't bother with the studies. I say we do, but crowdfund them and use them in an animal model first. Consistently show people it works - not in just one person who has used them for 15 years (your account taken from another comment of yours on this blog) but with many people who have suffered from persisting symptoms due to Lyme disease.
You don't have to have NIH funding or pharma funding to do research - though admittedly, more money helps. But I think one way or another, you'll need to conduct a study somehow. Someone will have to provide evidence your hypothesis applies with a big group of people in order to satisfy medical professionals at large and convince them to try the same treatment in their patients who come to see them with Lyme disease.
I know what the Brorsons, Miklossy, etc have written about morphological changes in Borrelia and Borrelia persistence. Pretty familiar with their papers. But what you have to do is get additional researchers out there to confirm their findings and validate them. Get them to take more of an interest in studying Borrelia and repeating their experiments; create a bigger brain and tissue bank to show samples where Borrelia have survived treatment. (I think Dr. Andrew Dwork Columbia University Lyme and Tickborne Disease Research Center is supposed to be working on such a tissue bank - they may be a good place to start for preliminary studies.)
CO
Hi Anonymous and welcome to Camp Other blog.
ReplyDeleteYou wrote:
""Henry" is McSweegan. He has many alias, like Satan."
Interesting. A number of us on Lymenet Europe who have wondered who is who there did not come to the same conclusion you did. A number of us have pretty much thought Phil Baker was Henry. Being that Henry claimed to be a bacteriologist and McSweegan has not, this didn't seem that far fetched.
If you want to have an even weirder moment, someone claiming to be the REAL McSweegan posted openly to Lymenet Europe recently, to tell everyone there that he was being impersonated by someone else on LymeNet USA and wanted us to look into it.
Very, very strange post. And I responded to this "McSweegan for whom I had no evidence was McSweegan" the best I could.
If you didn't see it, I recommend checking it out sometime.
CO