Wednesday, February 29, 2012

12 A Personal Note From A Fellow Lyme Patient

I was going to work on a page about the Lyme disease controversy which incorporated some of the discussion about Embers et al Rhesus macaque study on the Lyme Policy Wonk blog or post something about how Viral Genetics' chronic Lyme disease treatment is supposed to work.

But I've decided for now to set that aside because now I have something to say about something more personal.

Recently, someone mentioned me online in a Lyme disease support group forum and stated that my ability to knock out 1,000 word rebuttals and look up all this research made other people with Lyme disease look bad.

I took exception to that statement, and disagreed with it.

It wasn't all that long ago that I wasn't even able to write and do research, and it wasn't until I had been treated for Babesia by my LLMD that I began to see a difference in how quickly my mind worked.

When this change took place, I wanted to take advantage of it.

I felt compelled to write and do research because I finally could do so again and I was afraid I would relapse again any day. I feared I would return to some muddy primordial brain soup that couldn't string other people's sentences together and would put down a book after two minutes of frustrated repetition that looked like reading but really wasn't.

Relapse when? Who knows. I'm still afraid of my old symptoms returning and losing ground. Relapse happened to Pamela Weintraub. Relapse happened to others. And I've already relapsed once from about 85% of my original baseline.

I was so close. So, so close to feeling normal again. And then I lost what I had gained.

I'm not 100% now and I'm not at 85% again - however, I'm still better off than I was over a year ago.

This writing I do here and other places online? It isn't a game to me. At times it has been a genuine challenge. I've done it while having headaches and muscle pain and joint swelling. I've done it in the middle of episodes of fatigue and to avoid standing up due to vertigo. I've done it at 3 am. I've done it after waking up after being crashed out for hours because I'd been in the ER all night.

It's true that I do a lot of research. And it's not hard to do because it's what I used to do for a living. To some degree, it's force of habit and was easy to return to once I was able to understand what I read again. And I'm trying to reeducate myself and learn new things so that I have a better understanding of what I write and share with you.

But just because I do this does not mean I am capable of returning to my old job. Even if I can read and write, my health is so unstable that employment has not been possible during this time. Employment requires stability.

My brain - while functioning in some ways - is not fully running on all cylinders in others. It's just not obvious how it isn't to someone who isn't living life inside my skin every day.

Care for the rest of me outside my brain can be time consuming.  Case in point: I just looked on my calendar for February to see how many appointments I had. If you add it all up, I've had 5 appointments for different health problems - either to follow up on an already existing condition or to check up on a new one.

Many if not most of my friends without Lyme disease haven't seen a doctor within the past year.

That used to be me. Not any more.

When it comes to blogging online, I think it's a great thing: In some small way, this has been my slice of "normal". No one could see how impaired I have been and how bad things can be.

Perversely, having my capability for research and writing online being pointed out by a near-total stranger is satisfying: It means that I pass as being more normal than I truly am to someone in a world where the dominant paradigm of normal = healthy - even when I'm part of a community where it's normal to not be healthy and one faces challenges daily. But it can be demoralizing and confusing to read the accusation attached to it that my doing my best is somehow reflecting poorly on others.

I'm not doing research and writing about Lyme disease to make other patients look bad. I've been doing it because it's one of the few things I've been capable of doing from my sofa during the past year. 

I've been doing it because I want to learn as much as I can about this disease and topics related to it.

I've been doing it because maybe what I learn and share with others can help them, somehow, in some small way.

I've been doing it to educate people about Lyme disease and other tickborne illnesses.

I've also done it because it keeps me saner than I otherwise might be after all I have been through. It distracts me. It gives me a goal to live for other than to drag myself through another appointment, another blood draw, and another tedious stack of paperwork.

I've been trying to do something positive with the situation I've been placed in against my will, and implied assumptions about my health and reasons for writing long rebuttals or doing research are about as useful to hear as hearing a statement such as "those with chronic Lyme disease only suffer from "the aches and pains of daily living" is useful to hear: It isn't.

And when it boils down to it, a remark about my being a bad example for knocking out long posts online doesn't even make sense to anyone when so many other patients - including ones with other medical conditions which are disabling - spend at least as much time reading, writing, and posting online as I do.

If I've actually improved - if I've actually been doing better than I used to be doing - that is a good thing. When anyone else shares the news that they are doing better, I tell them I'm happy for them. I don't tell them they set a bad example. That doesn't make sense.

A lot of us struggling with disabilities are in the same boat. Former lives are broken and may not come back together the same way again. It sucks, all the way around.

I don't know what the future holds.

In the meantime, though, I am going to make good use of this time to research and write if I can, and do the best I can do at what I'm capable of doing.

How can anyone salvage something out of this situation? You do the best you can.

I encourage you to do likewise. Life is short.
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0 A Win For Free Access To Publicly Funded Research

A couple weeks ago I posted about the Research Works Act, and how it would force the public to pay twice for research their hard earned tax dollars already funded.

Today, I'm glad to report that the Research Works Act was rejected. Representatives Issa and Maloney pledged not to move the legislation forward. Infojustice's web site posted about this turn of events, and scathing commentary has ensued concerning the pay wall that is Elsevier.

Read about it here:

Also, see this article in The Scientist

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Monday, February 27, 2012

0 Blog Log: Spirochetes Unwound On Persisters

Well, our favorite spirochete blogger has posted about the magic of antibiotic tolerance today - an apropos choice for this evening's post to follow on the heels of the discussion about Embers et al paper, "Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection".

While this entry on persisters in Spirochetes Unwound is not specifically about Borrelia, it is an interesting read for those who wish to learn more about the mechanisms related to antibiotic tolerance and how some bacteria can be dormant and survive its wrath.

"Bactericidal antibiotics are effective at killing proliferating bacteria as long as they don't carry mutated or acquired genes that encode resistance to the antibiotics. Unfortunately even antibiotic-sensitive bacteria can tolerate antibiotics under some circumstances. Bacteria that are in a nondividing "dormant" state often survive antibiotic exposure. When the antibiotic is removed and growth resumes, the bacteria regain susceptibility to antibiotics.

At first glance antibiotic tolerance appears to be a passive process in which nondividing cells survive simply because the target of the antibiotic is inactive. However, this is not correct. Antibiotic tolerance requires an active response by the bacteria. The nondividing bacteria that survive antibiotic treatment are called persisters. Persisters may account for infections that are difficult to eradicate with antibiotics..."

Read more here:

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Saturday, February 25, 2012

5 Debate About Embers Non-Human Primate Chronic Lyme Disease Study Continues

UPDATE - Feb. 27:  I did receive a response from Dr. Baker. See comments below this post.

There is some heated discussion going on at CALDA's web site regarding Embers et al study, "Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection (2012)".

I wrote about this study last month and commented on some of the findings and the need for further research and confirmation of the findings in this study. (I recommend reviewing that post and comments made on it.)

CALDA's Lorraine Johnson has questioned Dr. Phillip Baker, who was Program Officer for the NIH's Lyme disease research division at the time the Embers study began (then known as Mario Phillip's study; Baker retired from NIH in 2007 and is now in charge at the ALDF), over the 12 year delay of Embers et al publishing the results of this study.

Dr. Baker himself decided to respond to Lorraine's questions and respond to a number of the comments and questions patients and advocates shared on CALDA's Lyme Policy Wonk blog.

Interestingly, a number of people have discussed this study on Lymenet Europe - with one member, Henry, questioning the use of ceftiofur when Embers study was supposed to emulate Klempner's chronic Lyme study. This issue happens to be one of of main issues Dr. Baker also raises on the Wonk blog about the Embers study. (Warning: There are seven pages of spirited discussion on this topic at LNE thus far - some of which may raise blood pressure in readers.)

To follow the discussion and see an example of different points of view over the issue of chronic Lyme disease, read here:

In the meantime, I have submitted my own questions and comments to CALDA's web site for Dr. Baker. As of this writing, my post has just cleared moderation and I await a response from Dr. Baker.

I want some answers. Not just about oversight for how the study was designed but about the lack of treatment studies for chronic Lyme disease patients.

Even if your position is that chronic Lyme disease is not caused by a persisting Borrelia infection, there is no reason why more research cannot be completed to provide evidence that this is or is not the case in some circumstances. And even if your position is that chronic Lyme disease's persisting symptoms may be caused by other factors, there is no reason why more treatment research cannot be completed to provide evidence either for or against these factors playing a role...

Dr. Baker,

First of all, I want to thank you for being here and presenting your view in the presence of Lyme disease patients who have different points of view than your own and who are at a minimum questioning your opinion about Lyme disease and at a maximum - quite angry.

This isn't an easy thing to do. I recognize that. But this is a necessary thing to do, and I wish that more dialog occurred between people with differing views even at the risk of it becoming contentious. It is often the only way opinions get aired and heard and questions get answered - even if we don't like the answers we hear.

I have a few questions for you, and hope I did not miss the boat on getting a response from you at this late hour:

1) Just so the storyline is clear: Who determined that ceftiofur should have been used in Embers et al study on NHP and is this decision something that NIH would have had to give approval - or is this a decision that would have been made at the individual level of the PI/researcher and not require any approval from the NIH? Would any independent governing scientific board outside the NIH been expected to approve of the study design including methods and materials? It seems that in order to emulate the Klempner study, the antibiotic chosen should either be the same as used in the original study or have, as you've stated, PK and PD that are pretty much indistinguishable from ceftriaxone.

2) In your opinion - and in the opinion of others at the ALDF - would you have to see studies separately completed on ceftiofur that provide you with evidence that its PK and PD in NHP are functionally equivalent to the use of ceftriaxone in humans? If these studies are conducted and they are found to be equivalent, then would you say that the results of the Embers et al study are valid? (Even if - according to your position - they don't yet prove a persistent infection/persister cells are the cause of patients' symptoms.)

3) The central point on which a lot of this debate hinges is whether or not spirochetes which remain after antibiotic treatment are viable and infectious. I've never gotten the impression that the majority of researchers out there have debated the existence of spirochetes after abx treatment - the impression I've had is that they either didn't think they were the cause of persisting symptoms in patients or did not know one way or the other if they were the case of persisting symptoms.

Parallel to demonstrated survival of some spirochetes after abx treatment, some research has indicated that a combination of Borrelial strain, host genetics, immune system response, and in some cases, molecular mimicry - may be causative factors for persisting symptoms. I myself think that based on evidence I've read to date, both persisting spirochetes and immune system changes can lead to persisting symptoms. I am particularly intrigued by HLA-DRs and variable immune response in this regard (see "HLA-DR alleles determine responsiveness to Borrelia burgdoferi antigens" by Bettina Panagiota Iliopoulou, Mireia Guerau-de-Arellano, and Brigitte T. Huber. Arthritis Rheum. 2009 December; 60(12): 3831–3840.).

My questions are:

When is the NIH-NIAID going to conduct more studies aimed towards this end? And also, if you and others are convinced that chronic Lyme disease patients are not suffering from persisting infections - why hasn't more treatment research been conducted that supports your point of view of what is or what are the causative factors for such symptoms?

Why are patients, advocates, and Lyme disease advocacy organizations having to donate money to Dr. Karen Newell Rogers and Viral Genetics to find alternative treatments to long-term antibiotics - why isn't the NIH-NIAID pursuing these alternative approaches now, if the argument is that long term antibiotics do not work and you consider them unsafe (Which in my opinion debatable in my eyes - I have personally benefited from more than the guidelines recommend - and I do not think the use for or against more abx is applicable to everyone because this is a heterogenous patient population. The patients need to be characterized into subgroups first rather than boxed into meeting CDC specific requirements before designing new trials.)?

I have been offended with the letter to the Lancet about Lyme disease patients and advocates supporting pseudoscience when so many of us have wanted to fund more research and get answers. When a number of our friends and families have donated their money to research even when they have already paid so much for treatment.

Some of the answers are already there. If more than one hypothesis is solid enough for testing, I'm for it. Test different combinations of antibiotics. Create drugs which have the anti-inflammatory properties of these antibiotics and use them as a control against combinations of antibiotics. Use higher doses of orals, if the fear of line sepsis freaks you out (it does me, and I have not had a PICC line by choice). Try testing thymus peptides and altering the distribution of B cells to see if that helps patients.

What I see as an observer is that Lyme disease treatment research has been shut down unless it's for acute Lyme disease. We need more late stage untreated Lyme disease research, and I'm with Fallon on this one - more specific neuroborreliosis research. His suggestions for those trials seem worthwhile.

But for God's sake, something has to be done. Some people are seriously impaired. I am doing somewhat better now and have my mind back to a large degree and don't need a wheelchair. But I am not yet well enough to work due to pain and fatigue with normal amounts of exertion. Something is broken there.

Dr. Baker's response to me:

Hi Campother,
Even though I feel that some have their minds made up and will not believe anything that I have to say, I will try to answer your questions:
1. Dr. Philipp received a small grant (AI042352) to conduct an experiment in NHPs to replicate the Klempner clinical trial, except of course for the manner in which the NHPs were infected. Because the grant was a small one (about $250K as I recall), Dr. Klempner was able — with support from the drug company– to provide him with the ceftriaxone and doxycycline to be used; these antibiotics were from the same lots used in the human study. Fair enough? That made working on a small grant a bit easier. 
Since NHPs are rather expensive to use and maintain, not too many could be used in the Philipp study because of limited funding. Furthermore, NHPs were in short supply at that time because of increase competition for use in studies on AIDS. The grant was funded for a 4 year period of time, during which time Dr. Philipp reported to me that he was having technical problems, especially with the strain of Borrelia that he had been using in past experiments; it appeared to have “lost its punch” and was no longer eliciting an infection of the same magnitude and character as noted in previous studies. This meant that he would have to re-drive the strain and test it in other NHPs to confirm that it was suitable for use in the definitive studies planned for the grant; that of course would take a great deal of time — and additional NHPs–to do. 
Although situations like this are unfortunate, they do happen and are part and parcel of the realities of doing scientific research — if you want to do it right. 
So, as far as Dr. Philipp’s original grant is concerned, it expired — after the 4 year period– with no data that he felt was was ready and complete for publication at that time. Obviously he continued with his NHP studies and apparently received funding from other sources; note that research Resources grants like RR00164 are designed for the purchase materials, equipment, and supplies, in this case, more NHPs I assume. But, I was “out of the picture” at that point — as far as Dr. Philipp’s research on NHPs was concerned. Keep in mind that as Program Officer, I was not the czar of NIH’s entire research program on Lyme disease, even though so people have the mistaken notion that I had such “power”.
So, you ask who made the decision to use ceftiofur instead of ceftriaxone? I honestly don’t know. 
You will have to ask Dr. Philipp, whose e-mail address is provided in the Embers paper. During the time that Dr. Philipp was doing his work under AI042352, it was being done in accordance with the terms of that grant indicated above. Whatever else he did — or may have done– must have been accomplished afterwards and with other support that did not involve me or NIAID. I must say that I find it strange that the term ceftriaxone is used throughout the Embers et al. paper, and it is only in the first paragraph on page 9 that it is first mentioned that ceftiofur was actually used. I find that very strange indeed.
As stated before and in other postings on this site, I have two major — and legitimate– concerns with the work reported by Embers et al. . First, since so little is known about the PK, PD, and MIC of ceftriofur, was the treatment adequate to eliminate the massive infection induced by needle inoculation? Since the author did not provide such assurances, that is a major and significant unknown. Second, if the therapy was adequate, there is no evidence to indicate that the “persistors” are able to infect other animals and produce disease. They might just be sitting there, for all we know, doing nothing harmful to the host. In view of these considerations, the PCR, RT-PCR, and xenodiagnosis data are not informative. In fact, there are no real differences between the antibiotic treated and sham-treated groups in terms of the objective signs of infection (pathology) noted ; that makes me wonder if the therapeutic regimen was truly effective. So, if I were reviewing this paper for publication in a journal, I would have to reject it publication for these and other deficiencies that I will not elaborate on at this time.
2. Since ceftiofur and cetriaxone differ significantly in chemical structure, I would not be at all surprised if they had different PD/PK properties; those who do drug design research find that the addition of a single chloride atom is enough to alter the properties of some drugs. What is certain is that ceftiofur is not approved for use in humans and there is no published evidence on its efficacy for treating borreliosis in animal models. Obviously, the use of ceftiofur is a big unknown. My best advice, if someone wanted to replicate the Klempner studies in an animal model would be to use ceftriaxone and doxycycline in the same manner that he did and not introduce another variable like ceftiofur– unless you plan to get the FDA to approve the use of ceftiofur in human studies. That may take a long time to do….

3. Since I have retired from the NIH, I don’t know what their plans are for future research on Lyme disease. But, I can tell you that about 90% of the research that NIH supports is driven by proposals submitted as investigator initiated grant applications — the RO1 grants. 
So, if anyone has any good ideas, they are always welcome to submit a grant application, although competition for grants is very keen and only about 25% of all applications submitted are funded. One has to be persistent as most of my colleagues are to make it in science. 
Although I am not opposed to conducting another clinical trial, the odds for such a proposal getting funded are rather slim, especially since NIH has already supported 4 trials indicating that extended antibiotic therapy is not beneficial. 
Obviously, I would like to see more work done on whether the “persistors” Bockenstedt and Barthold noted in mice are infective and can cause disease, as well as whether they can stimulate a local inflammatory response. But, I think we would be making a big mistake by not considering other possibilities as I’ve mentioned in a recent article ( 
There are MANY people who believe that they have “chronic Lyme disease” with no evidence that they ever had Lyme disease in the first place. Some have been misdiagnosed and are being subjected to all sort of unproven therapy. Also, there are individuals who go from one doctor to another seeking a “cure” and who often are victims of “quack” remedies. 
One reason we had so much difficulty enrolling patients into the Klempner study was that only about 5-8% of those who presented themselves for enrollment had unequivocal evidence in their medical record of having been diagnosed correctly for Lyme disease in the first place. Obviously, one can not have a chronic infection without first having an active and correctly diagnosed infection in the first place. That was made a criterion for enrollment to ensure that we would have a cohort of patients with a reasonably high — though still not absolutely certain– probability of having a persistent infection — if one were present. I assure you, and you can ask Brian Fallon and Lauren Krupp, such people are NOT easy to find.
But, I have said enough. The biggest obstacle to making any progress is the lack of trust and the tendency to condemn anyone in the scientific community who disagrees with the unproven concept of others. Some simply have no understanding of evidence-based research and how it works, let alone things like the placebo effect. There is just too much misinformation being spread on the internet — and too many people gobbling it up as though it were fact. It’s an ideal environment for all the “quacks” to thrive — and they surely do. And that is what disturbs me the most………

So, there you have it - that's his response, and while I posted a response to the Wonk blog, because my response was too lengthy it has not been posted there. So I posted it to comments below, after an explanation of why my response was not posted there.

The moderator emailed me personally and said that I could post another 150 word comment of my choosing, but I have declined for now because I don't think what I can say in response to Dr. Baker is adequately summed up in 150 words.

There was a second comment with other content which I submitted that I later decided needed a serious rewrite before posting - I won't be posting that here now and am okay with the moderators not publishing it (good job, mods - thanks).

I just want to take a moment here to acknowledge those who left intelligent and insightful questions and comments on the Wonk blog - even when addressing someone with whom they vehemently disagree. I would like to see more dialog such as this, but even more so I would like to see more thorough education and outreach going on which deconstructs all the hypotheses behind why chronic Lyme disease patients have persisting symptoms and what research is required to resolve the debate over cause.

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Wednesday, February 22, 2012

1 Patent: Viral Genetics Chronic Lyme Disease Treatment

This post is related to an earlier post about Viral Genetics application for a pre-IND to begin clinical trials on their VGV-L product for the treatment of Chronic Lyme disease.


Apparently, I found Viral Genetics' current patent. And as I had previously speculated, I was correct that the treatment is going to modify B cells. I knew it! Buy me a drink, eh?

Here is a link to the patent online:


Inventors: Haig Keledjian (San Marino, CA, US) Michael Agadjanyan (Huntington Beach, CA, US) Martha Karen Newell (Colorado Springs, CO, US) Evan Newell (Menlo Park, CA, US)
IPC8 Class: AA61K3900FI
USPC Class: 4241851
Class name: Amino acid sequence disclosed in whole or in part; or conjugate, complex, or fusion protein or fusion polypeptide including the same
Publication date: 07/01/2010
Patent application number: 20100166789

And here are the excerpts on how the invention will be used to treat chronic Lyme disease (patent text slightly modified to correct spelling errors):

[0114] Lyme Disease is a tick-borne disease caused by bacteria belonging to the genus Borrelia. Borrelia burgdorferi is a predominant cause of Lyme disease in the US, whereas Borrelia afzelii and Borrelia garinii are implicated in some European countries. Early manifestations of infection may include fever, headache, fatigue, and a characteristic skin rash called erythema migrans. Long-term the disease involves malfunctions of the joints, heart, and nervous system. Currently the disease is treated with antibiotics. The antibiotics generally used for the treatment of the disease are doxycycline (in adults), amoxicillin (in children), and ceftriaxone. Late, delayed, or inadequate treatment can lead to late manifestations of Lyme disease which can be disabling and difficult to treat.

[0115] A vaccine, called Lymerix, against a North American strain of the spirochetal bacteria was approved by the FDA and later removed from the market. It was based on the outer surface protein A (OspA) of B. burgdorferi. It was discovered that patients with the genetic allele HLA-DR4 were susceptible to T-cell cross-reactivity between epitopes of OspA and lymphocyte function-associated antigen in these patients causing an autoimmune reaction.

[0116] It is believed according to the invention that Borrelia burgdorferi also produces a Toll ligand for TLR2. Replacement of the CLIP on the surface of the B cell by treatment with a thymus derived peptide with high affinity for the MHC fingerprint of a particular individual, would result in activation of the important Tregs that can in turn cause reduction in antigen-non-specific B cells. Thus treatment with thymus derived peptides could reactivate specific Tregs and dampen the pathological inflammation that is required for the chronic inflammatory condition characteristic of Lyme Disease. With the appropriate MHC analysis of the subject, a specific thymus derived peptide can be synthesized to treat that subject. Thus individuals with all different types of MHC fingerprints could effectively be treated for Lyme disease.

[0117] Chronic Lyme disease is sometimes treated with a combination of a macrolide antibiotic such as clarithromycin (biaxin) with hydrochloroquine (plaquenil). It is thought that the hydroxychloroquine raises the pH of intracellular acidic vacuoles in which B. burgdorferi may reside; raising the pH is thought to activate the macrolide antibiotic, allowing it to inhibit protein synthesis by the spirochete.

Read more:

How will this theoretically stop inflammation present in chronic Lyme disease? What does the above all mean, in English? More details coming soon - for now I wanted to share this.

In the meantime, you might want to review this:

Image credit: Thymus by LearnAnatomy from Wikipedia under a CC 3.0 license.

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Tuesday, February 21, 2012

0 More On Lyme Disease In Australia On The Today Tonight Show

There's been increased interest from my readers in learning more about Lyme disease in Australia, so I decided I would offer an update on the situation for everyone including my northern hemisphere readers who are interested in new developments there.

Last week, the Australian television news show, Today Tonight, posted a segment on Lyme disease in Australia and how it has become a controversial issue as a number of Australians who have never left the country were bitten by ticks and developed symptoms very much like those of Lyme disease.

As far as it is known, the bacteria which causes Lyme disease has not been detected in ticks in Australia - unless the researchers mentioned in the previous episode of Today Tonight which was covered here have finally discovered it.  Without their official announcement, though, it has been the situation that cases of Lyme disease within the country which have been confirmed were attributed to infections acquired overseas. Any recent reports of Lyme disease contracted within Australia have become controversial.

This week, Today Tonight has posted another segment about a man, Robert Sotur, who became ill on the job after numerous tick bites and won a government workmans compensation case due to an infection with Lyme disease.

This is pretty notable because he received compensation for a disease that the Federal Government, the Australian Medical Association, and Australian State Governments all say doesn't exist in Australia.

View the video of the show and transcript here:

A lawyer, David Jones (yes, seriously, David Jones - wonder how much tiresome joking he gets about that name), who is working on behalf of over fifty patients who never left Australia yet have come down with Lyme disease-like symptoms in Australia made this statement to Today Tonight:

"There needs to be an acceptance that there are many people within our community that are having symptoms that are Lyme or Lyme-like, and Governments need to take these people seriously. They need to commission the research, and they need to determine whether or not this disease, or a disease like it, exists here in Australia.”

He's right. If one man has won a workmans compensation case within Australia for falling ill after tick bites, there will likely be others. More than fifty, judging from his caseload alone. But there will be far fewer cases if the research is done to find the causative agent of this disease and to treat people for it as soon as possible.

If it is a bacterial agent, then unlike Ross River Virus and other viral infections which are more well known throughout Australia - early treatment can prevent more serious symptoms and potential permanent damage, and in the worst case scenario - death, as in the case of Karl McManus.

Given the limited amount of recent surveillance and examination of ticks for an indigenous spirochete that could cause a condition similar to Lyme disease - if not the potential importation of Borrelia spirochetes from neighboring Asia - it is not clear what reality is. The last major study to discover if Australian ticks harbored a spirochete similar to one that causes Lyme disease was conducted over 15 years ago. The situation may be different now.

Australian support groups for patients with tickborne illnesses have not only reported being bitten by ticks and falling ill afterwards - some have also reported infestations of bird mites preceding the onset of their symptoms. If this is the case, there may be more than one pathogen and more than one vector responsible for an overlapping set of symptoms in patients. Careful and thorough research is needed to sort it out.

My advice to any Australians reading this is whether or not the controversy of the existence of Lyme disease in your country is resolved soon that you do what you can to protect yourself from tick bites. Learn how to properly remove a tick to minimize the risk of infection, find a place to send your ticks for analysis, and educate yourself about the spectrum of symptoms which are related to ALL tickborne diseases and not just Lyme disease.

Tularemia was discovered in Tasmania last year and there is evidence beyond a doubt of its presence. Lyme disease now appears to be a possibility. And then there are those mosquito-borne and tickborne conditions of which many Australians are already familiar with such as Ross River Virus, Barmah Forest Virus, Tick Typhus, and Tick Paralysis - none of which you want if you can avoid them.

See a doctor if you suspect you have contracted a tickborne infection - remember, it may or may not be Lyme disease and treatment will be different for coinfections. But do go as soon as possible in order to prevent serious and potentially long-lasting complications.

And last but not least:

Petition your government, CSIRO, and local universities to do more research on tickborne illnesses including Lyme disease. Make sure you have your own homegrown research teams that will investigate the possibility of Lyme-like illnesses from pathogens transmitted by both bird mites and ticks. Ask Australian scientists to pave their own path and to not feel obliged to model all their investigations and guidelines for treatment based on those found in the northern hemisphere until it is more certain what is happening. In the meantime, treatment will probably be empiric and based on history, symptoms, and test results.

Here is a helpful link with short videos on the prevention of tick bites and safe removal of ticks:

Rather than just "Slip, Slap, Slop", learn to "Cover, Check, Clasp"?:

Fine-nosed tweezers are your friends, and not flame throwers and lighters...

Links to Australian tick bite related posts on this site:

About the first Today Tonight show this year on Lyme disease:

On the outbreak of Tularemia in Tasmania late last year:

On the use of marsupial cathelicidin peptides to fight infection:

On Australian research on the relationship between tick bites and red meat allergies:

On Google search trends, and how Australians rank in the search for information on Lyme disease using Google:

Links to Australian resources on Lyme disease outside of this blog:

CSIRO Public Health Advice on Ticks:

The Karl McManus Foundation:

Lyme Disease Association of Australia:

Lyme Green Australia blog:

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Friday, February 17, 2012

6 Paper On Borrelia burgdorferi, RpoS, And Formation of Round Bodies or "Cysts"

Dr. MacDonald just posted information on Lymenet Europe concerning a new paper by Dunham-Emsl et al about the round body aka "cyst" form of Borrelia burgdorferi as part of the Lyme disease life cycle within the tick.

The indication here is that Borrelia burgdorferi assumes a round body form within the tick in order to survive until circumstances for transmission to the host are present. There is no confirmation here, however, of its formation in vivo within a host mammal...

Full Text Source:

Borrelia burgdorferi Requires the Alternative Sigma Factor RpoS for Dissemination within the Vector during Tick-to-Mammal Transmission

Star M. Dunham-Ems, Melissa J. Caimano, Christian H. Eggers, Justin D. Radolf


While the roles of rpoSBb and RpoS-dependent genes have been studied extensively within the mammal, the contribution of the RpoS regulon to the tick-phase of the Borrelia burgdorferi enzootic cycle has not been examined. Herein, we demonstrate that RpoS-dependent gene expression is prerequisite for the transmission of spirochetes by feeding nymphs. RpoS-deficient organisms are confined to the midgut lumen where they transform into an unusual morphotype (round bodies) during the later stages of the blood meal. We show that round body formation is rapidly reversible, and in vitro appears to be attributable, in part, to reduced levels of Coenzyme A disulfide reductase, which among other functions, provides NAD+ for glycolysis. Our data suggest that spirochetes default to an RpoS-independent program for round body formation upon sensing that the energetics for transmission are unfavorable.

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0 Phage-holder

Rather than use the term "placeholder" I decided to use "phage-holder" because this post is going to be all about bacteriophage and phage therapy.

First, I came across this Nature blog post from Jim Caryl from last April - "No action today, no antibiotics tomorrow..." It outlines the serious problem of growing antibiotic resistance to infection and proposes different technological solutions for combatting resistance.

Jim advocates the revamping of our current drug manufacturing system to produce new antimicrobial therapies based on new targets as well as remodeling old antibiotics with high toxicity so that they are less toxic. He is not as enthusiastic about the application of phage therapy, citing a need for more efficacy testing and double blind random control trials. Those who commented on his blog, though, are strongly in support of phage therapy and think it has much promise.

 If you are a Lyme disease patient (or care about someone who is) then his fourth item on his anti-microbials-of-the-future list may interest you - if the data is there to support persister cells as part of Borrelia burgdorferi's pathogenesis:
"The current model for drug discovery is towards drugs that interfere with actively growing bacteria, however, bacteria aren't always actively growing. I've written before about how being in a different growth-phase can render a bacterial cell resistant to antibiotics. This can lead to repeated flare-ups of the infection until, eventually, true genetic resistance evolves that allows the bacteria to survive, and continue growing in the presence of the antibiotic. Thus there is the proposal that as part of enhanced efforts in drug discovery, that a platform for developing drugs at slow- or non-growing bacteria be practised."
Check out Jim's well-written post, and check out the comments.

Second, I periodically see what's new in terms of phage therapy education and outreach in the United States - and in particular, drop by Evergreen State College's (ESC - Olympia, WA) pages on bacteriophage research.

If you take an interest in learning more about phage therapy, this is a good place to start for an English-language based repository. On ESC's web site you can learn about phage research around the world, including at the well-known Eliava Institute in Tblisi, Georgia - and there are interesting links such as one to a new journal, Bacteriophage, the first international, peer-reviewed journal dedicated to all aspects of bacteriophage research, ranging from basic phage biology and taxonomy to advanced bacteriophage-host cell interactions and various practical applications of bacteriophages.

If this is really your thing, you might want to prepare for the next International Phage Biology Meeting in 2013, with more details  about this meeting to be announced here in the future:

Third, little late to the game on this one - but I have news on the business side of phage therapy in the United States. I discovered the web site of this company, Amliphi Biosciences Corporation, which states "AmpliPhi Biosciences is the first company to demonstrate the clinical efficacy of phage technology in a controlled, regulated, human clinical trial."

While their focus is on researching bacteriophage therapy for resistant Gram-negative bacterial infections, there is currently no development underway for Borrelia burgdorferi infections (which if you'll recall is not exactly Gram-negative bacteria anyway). But the research they are doing may improve and save the lives of many people struggling with resistant bacterial infections such as children suffering from chronic ear infections and adults suffering from cystic fibrosis. In fact, AmpliPhi is receiving initial funding support from Cystic Fibrosis Foundation Therapeutics, Inc. (a nonprofit affiliate of the Cystic Fibrosis Foundation).

Check out their product pipeline page to learn more about the clinical trials they have been conducting on phage therapy for helping people with these conditions as well as for other purposes.

Last but not least, I wanted to announce that one of my own pages on bacteriophage will soon be updated due to a major oversight that was called to my attention through my recent exchanges with Dr. Alan MacDonald on Lymenet Europe. He posted some images of Dr. Alan Barbour's early research on Borrelia burgdorferi where a B-3-like phage was found on and in spirochetes (Why are there so many Allens or Alans doing research in this field?). This is research that definitely should have been included in this page and I am very remiss in not including it.

I also realize that part of it needs rewriting in general because a few basic concepts about how phage therapy works need to be included - including the fact that each phage is often very strain specific. My current writing suggests to the reader that one phage will handily kill all Borrelia burgdorferi when that is not so - though a genetically modified virus which attacks Borrelia might be altered in such a way as to inject different Borrelia with something that is disruptive to a common Borrelia target. Phages "in the wild" do not operate in this fashion - they are found and they evolve on their own and are strain specific. So expect this page to be updated to include this information soon.

One may wonder why Camp Other is so interested in bacteriophage therapy. The reason is simple: There may be some way in the future to detect which strains of Borrelia someone has been infected with at the site of a tick bite and develop a phage-based ointment that will prevent infection from disseminating. It will do so without the problem of antibiotic resistance cropping up and without all the horrible side effects that antibiotics can bring including the risk of contracting C. difficile.

So I would very much like to see this be made possible, though there are inherent difficulties in finding lytic phages for Borrelia and the issue that "handedness" ("male"/"female") of the bacteria is related to finding effective phages, much like the "handedness" of sugars has different effects in the human body.

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Monday, February 13, 2012

2 Lyme Disease In Australia On Today Tomorrow Show

Last night the Australian television news show, Today Tonight, aired a segment on Lyme disease in Australia. While the dramatic reporting in this segment is not to my taste, I took special note of the research starting at roughly the 6:28 mark [11 minute video below may not work on all mobile devices]:
Excerpt from the transcript:
Inside a laboratory at Newcastle University a dedicated team, including Professor Tim Roberts, is toiling away on a fresh independent study - a collaboration with Sydney University - to determine whether Lyme disease is carried by Australian ticks. 
Professor Roberts thinks that Lyme Disease is in Australia. Thousands of ticks are being collected, and already he disputes long held theories that Australian sufferers only contract the disease after visiting Europe or America. 
“What we say and conclude is there is an organism here which is very similar to those two infected organisms, the one in Europe and the one in America,” he said. 
Some believe it got to Australia from migratory birds that fly all the way from Siberia and nest on our beaches. Then there's another school of thought that it's actually an indigenous strain, and it's always been in our country.
Professor Roberts believes that many people carry Lyme disease and don't even know. “A whole lot of people could, certainly absolutely, in the group with chronic fatigue syndrome,” he said.
It should be noted, however, that not everyone agrees with Professor Roberts - here is one person who disagrees:
“The opinion is that there is no good evidence that Lyme disease is acquired in Australia at the moment,” Dr Jeremy McAnulty from New South Wales Health and Protection said. 
“The other important information is that ticks that carry Lyme disease overseas aren't present in Australia, so we don't seem to have the right ticks for Lyme disease in Australia,” he added.
So no matter where one is in the world, Lyme disease generates controversy.

I want to know more about what Professor Roberts has found regarding finding an organism similar to the Borrelia that is in the US and Europe. This video is short on details in this regard.

I've found some mention of previous attempts to find the causative agent of this Borreliosis-like illlness from research done over 15 years ago - but nothing definitive.

What was said back then could well apply today:
Dr Bernie Hudson, a microbiologist who runs a clinic for Lyme disease sufferers at Royal North Shore Hospital, said it was better to treat those with symptoms of the disease as if they had it, rather than waiting years to have its existence in Australia accepted by other scientists, he said. 
Westmead entomologist Dr Richard Russell said his group had been "painted as baddies" but he would like to see the Newcastle team "get some money to do a definitive study and find out if it does exist".
Over fifteen years ago... is this Newcastle team which is doing research now related to those who had done the research in the past?

In the meantime, I hope those patients who were interviewed get the help they need and get better.

The transcript for the above video can be found here:

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Friday, February 10, 2012

2 More Thoughts On Birds, Cool Shirts, And My Evil Twin?

More On Ticks And The Atlantic Flyway:

I continue to think about the role of birds carrying ticks to different regions and how Lyme disease (and other tickborne infections) could be spread that way. But much as I found the overlay map I posted earlier this week to be intriguing, I don't think that tracking infected ticks on birds is as simple as following major and principal flyways - even though that could be a reasonable point to start an investigation.

Yale has already done some work in this area, and I have no idea whether or not they've factored the results of this publication, "Do birds affect Lyme disease risk? Range expansion of the vector-borne pathogen Borrelia burgdorferi", into their recently published Lyme disease risk map.

It's important not to discount the role of birds here:
"Although the role of birds in B burgdorferi transmission dynamics is often discounted, data compiled from published studies indicate that the majority (58.6%) of bird species that have been evaluated are capable of infecting larval I scapularis with B burgdorferi. We estimated – for two bird species – that the number of individual birds required to produce one infected I scapularis larva is as low as three, and we conclude that bird-mediated tick movement is an important factor in the range expansion of both I scapularis and B burgdorferi."
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There are certain behaviors birds engage in and seasonal activities which would lead to a higher likelihood of birds contributing to the spread of Lyme disease on the ground. Specific kinds of birds would be more likely to contribute to infection spread than others - for example, I suspect birds which build their nests on the ground and are ground-based hunters are more likely to contribute to infected tick populations than birds which build their nests in trees. Also, some birds feast on ticks (such as guinea fowl) and they will lower local tick populations.

These are just a few examples - there are many more. I imagine there is no simple algorithm for determining the role for birds in spreading infection. I don't know what all the factors are which would contribute to the spread of Lyme disease via birds, and it's something I continue to look into because it does play an important role in surveillance and determining how infection could spread through different vectors.

Photo credit: Andreas Trepte,

Cool Lyme Disease T-shirts:

While doing a general search for Lyme disease related news the other day, I came across these shirts on Cafe Press:

I think they must have had me in mind as a target demographic, because it's the first Lyme disease related t-shirt that  I've seen which appealed to my appreciation of the TV show, "The Big Bang Theory", and also appealed to my appreciation on word play while mentioning Lyme disease research. It says "More nervous tics than a Lyme disease research facility"- playing on the word "tics" or "ticks".

There are a number of products for sale with this slogan on it (not just t-shirts) at Cafe Press  -  I don't know who is selling them and if they're another Lyme disease patient or not - the product page did not display this information. Check it out if you think it's something you'd like, too.

My Evil Twin?

It's been pointed out to me that I have a doppelganger online named Tom Carolan. He has Lyme disease blog, Tick Borne Diseases Radio, with entries in it which upon reading looked strikingly similar to my own blog at first glance. However, after more examination,  it's clear Tom's blog contains different content and his own unique commentary on the same topics which have grabbed my attention.

(Just so everyone knows, I have no problem with anyone passing on the content I write here as long as you give this blog credit and link to it. That's why I have a Creative Commons license posted at the bottom of each entry - so you know I support a more open source approach to copyright.)

Tom also has a podcast on iTunes on Tick Borne Diseases:

How about going over there to Tom's site and giving it a good read, and encouraging him to continue to post more podcasts and blog entries? It looks like he has a good thing going on and more content like his would be welcome - particularly more podcasts.

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Wednesday, February 8, 2012

7 The New Tick Map Vs. The Atlantic Flyway: Things That Make You Go Hmm.

[Ed. - Overlay map revised Feb. 9, 2012.]

Well, I guess everyone has seen this map from Yale University by now...

Yes, it is a map of Lyme disease risk areas based on tick flagging from 2004-2007 in the above regions, followed by an analysis of those ticks. No matter where one looked, the odds of a tick carrying Borrelia burgdorferi were 1 in 5 everywhere... So be careful out there, huh?

While it's good to let people know there are transition areas where Lyme disease is up and coming, it's good not to be too complacent if you fall into a green zone. Today's low risk zone can be tomorrow's transitional area, and these maps must be accurately updated in order to reflect reality.

Thing is, I haven't been thinking of this map as regards tick distribution and Lyme disease so much as I've been thinking about this map:

Because there is evidence that ticks' distribution is spread not only by mammals which hug the ground - but can also be spread geographically by birds. 

So look at the above two maps. Now look at this, after I scale and resize them to overlap (somewhat off-bias, but best I could get with different projections):

Questions for my readers:
  • For those of you along the southern principal flyway, how many of you received an infected tick bite near that flyway, either to its north or south?
  • For those of you in northeastern and north central Florida, how many of you received an infected tick bite near that flyway passing over your state?
  • For those of you in eastern Canada, can you tell me if you received an infected tick bite near that flyway by the Great Lakes?

I'm looking at this and wondering a few other things, too, like I think these flyways would end up moving a little further north as global warming progresses - so I would expect a greater distribution of infected ticks further north as time goes on. Is there any way to confirm this is what is happening?

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1 Memo: Borrelia Are NOT Gram-Negative Bacteria, And Might Become Resistant

For years, Borrelia have been thought to be Gram-negative because of their diderm and structural appearance upon staining. Borrelia - including Borrelia burgdorferi - are not Gram-negative bacteria, though - even though many people are still referring to them as such. They belong in their own category.

As I was telling Dr. MacDonald this week:
I found information confirming the fact that Borrelia is not Gram-negative or Gram-positive. It's its own special thing:

"Borrelia were thought to be Gram negative because of their double membrane structure, but genetic analysis places them - along with other spirochetes - into a separate eubacterial phylum. Ultrastructural molecular and biochemical studies have emphasized the wide taxonomic gap between spirochetes and Gram-negative bacteria."

- From "The Genus Borrelia" by Melissa Caimano. Prokaryotes (2006) 7:235-293.

"Although Borrelia spirochetes are often, but mistakenly described as Gram-negative bacteria due to their diderm, i.e. double-membrane envelopes, a closer examination reveals significant differences in composition and architecture. Probably most striking is the lack of LPS, the presence of major surface lipoproteins at the host-pathogen interface during transmission, persistence and ensuing pathogenic processes and the additional function of periplasmic flagella in defining cell shape. While surface lipoproteins such as the Osps interact with a variety of ligands in different organ tissues, they are also targets of the immune response and several have emerged as vaccine candidates."

- From Borrelia: Molecular Biology, Host Interaction and Pathogenesis. Edited by D. Scott Samuels and Justin D. Radolf. (2010)

So one could say they are Gram-negative-"like" - but strictly speaking, Borrelia is not Gram-negative bacteria."
He accepted this response, and is now stating that Borrelia burgdorferi is Gram-indeterminate.

There is additional information from the second source cited which indicates that Borrelia spirochetes are different from other bacteria, summarized here:
"Some of the identified periplasmic lipoproteins, i.e. the OppAs, are components of substrate transport complexes. Investigations into integral membrane proteins led to the identification of several Borrelia porins: P13, whose structure and function is unknown, DipA, which is specific for dicarboxylates and P66 (Oms66), which has a dual role as a pore-forming outer membrane protein with an extremely high single channel conductance and an adhesin for β3-integrin. The recently identified Tol homologs BesA, -B and -C appear to form a Type I 'channel' to export exogenous toxic agents such as antibiotics and to maintain infectivity by an unknown mechanism. Initial studies on envelope biogenesis pathways based on diderm proteobacterial model organisms already revealed significant deviations from the norm. This further bolsters the unique status of Borrelia among microbial pathogens."
Damn Borrelia... Why do you have to be such a deviant? Why can't you just conform?

Anyway, the Type I 'channel' they're talking about above which exports or removes antibiotics and helps maintain infectivity is said here to do so using an unknown mechanism. Judging from research out there, this channel relates to transmembrane proteins which span the outer and inner membranes of the bacteria - and it appears to function like an efflux pump (in this case, a resistance-nodulation-division-like pump) which removes antibiotics and is involved in antibiotic resistance. Check out this paper (full text at link):


An RND-Type Efflux System in Borrelia burgdorferi Is Involved in Virulence and Resistance to Antimicrobial Compounds

Ignas Bunikis1, Katrin Denker, Yngve Östberg1, Christian Andersen, Roland Benz, Sven Bergström. PLoS Pathog. 2008 Feb 29;4(2):e1000009.


Borrelia burgdorferi is remarkable for its ability to thrive in widely different environments due to its ability to infect various organisms. In comparison to enteric Gram-negative bacteria, these spirochetes have only a few transmembrane proteins some of which are thought to play a role in solute and nutrient uptake and excretion of toxic substances. Here, we have identified an outer membrane protein, BesC, which is part of a putative export system comprising the components BesA, BesB and BesC. We show that BesC, a TolC homolog, forms channels in planar lipid bilayers and is involved in antibiotic resistance. A besC knockout was unable to establish infection in mice, signifying the importance of this outer membrane channel in the mammalian host. The biophysical properties of BesC could be explained by a model based on the channel-tunnel structure. We have also generated a structural model of the efflux apparatus showing the putative spatial orientation of BesC with respect to the AcrAB homologs BesAB. We believe that our findings will be helpful in unraveling the pathogenic mechanisms of borreliae as well as in developing novel therapeutic agents aiming to block the function of this secretion apparatus.

Obviously, more research in this direction is necessary.

So when people ask, "Camp, why are you so interested in learning about something like TolC? Why don't you want to learn about different kinds of treatment and how they've helped patients?" my answer for them is this:

I do want to learn about different kinds of treatment - it is in my best interest to do so, given I have been dealing with Lyme-related health problems for years. And I make my own decisions about treatment which are largely personal to my situation.

But learning this stuff - these details tucked away in what must appear to most people to be obscure publications in little-known journals outside of researchers within the field? To me, this stuff is what may get us all closer to better treatment for many people.

Do I know this for sure? No. No one does. But with some of the specifics under my belt, I can then at least petition the science world and advocate for the funding to do research on some very particular subjects to get very specific knowledge. Knowledge which may give us a solid idea as to how to treat chronic Lyme disease so that it doesn't become chronic.

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Monday, February 6, 2012

6 Viral Genetics Issues Latest Report On Chronic Lyme Clinical Trials Status

Recently, Viral Genetics posted an update on its move towards testing its product, VGV-L, for treating chronic Lyme disease.

Research for this product was funded by two Lyme disease advocacy organizations, Time For Lyme, Inc. and the Turn The Corner Foundation.

You might be familiar with the project lead, Dr. Karen Newell Rogers, whose research was mentioned at the LDA-Columbia University Lyme 2011 Lyme and TBD Conference.

I previously wrote about Dr. Newell Rogers research, and highlighted the following excerpt from a summary report on her conference presentation:
"Dr. Karen Newell Rogers presented a talk about novel ways to target chronic inflammation and chronic immune activation among patients with chronic Lyme disease. 
She pointed out: 
"[...]Some researchers would argue that chronic inflammation requires the continuous presence of bacteria, whereas others would suggest that continuous presence of bacteria does not always result in inflammation and that exacerbations of chronic symptoms could result from infection with a different organism--or that chronic symptoms could re-cur from unrelated pro-inflammatory events. Potentially reconciling these seemingly conflicting perspectives on the mechanism of Lyme disease may be the effect of Borrelia burgdoreri’s bacterial by-products on Toll Like Receptors, (TLR)-mediated immune activation. 
TLR appear to be the “gate-keepers” of an inflammatory response. Bacteria, including Borrelia, produce products that, by binding to TLRs on the cell surface, promote leukocyte activation, cytokine production, and acute inflammation. In some genetic backgrounds of mice, acute inflammation is sufficient to fight off infection and resolve disease. In other mouse strains, the pathogens, or in this case the bacteria, get past TLR-induced inflammation and remain symptomatically undetectable in cells and tissues (Barthold, etc); Barthold et al. have found that no matter how severe or mild the disease in any of the genetically inbred strains of mice, there was no more inflammatory disease when the bacteria were eliminated."
So what is VGV-L, and what does this soon-to-be-tested product supposedly do? It would seem to fall more in line with Dr. Newell Rogers' research addressing chronic inflammation than addressing chronic infection, based on what I've read thus far.

According to Viral Genetics' web site, VGV-L seems to be related to Targeted Peptide Therapy (TPT), a therapy which uses synthetic peptides to "trick" cells that may be responsible for harmful symptoms and makes these cells vulnerable to the body's natural immune response mechanism.

What exactly are targeted peptides? According to Viral Genetics (VG), targeted peptides are custom-designed protein fragments that work to modify certain immune system reactions that they believe cause or worsen some inflammatory diseases.

More about Targeted Peptide Therapy is found on its own VG page:
 "Autoimmune diseases occur when the body reacts to itself or self-tissues. In some cases, an external threat from disease-causing organisms activates too many of certain types of immune cells which in turn cause damage the body. A physical trait of those cells also makes them impervious to the body's natural defense system that would ordinarily limit their numbers.  
TPT works by tricking those impervious cells into dropping their defenses. They can be fooled into releasing their protective shields, swapping the shield for a synthetic TPT-polypeptide instead. Those peptides, created by our research team, have been engineered to make the cell susceptible to the body's natural defenses. We expect our TPT drug compounds to enable the body to destroy the cells that help trigger the symptoms of autoimmune diseases." 
 So what this sounds like is it a treatment for chronic Lyme disease which lessens inflammation by modifying the immune system in some way.

And judging from the content above, I am wondering if the "certain types of immune cells" of which there are too many could be referring to the overabundant low quality plasma cells that were found in lymph nodes in Tunev and Barthold's study, "Lymphadenopathy during Lyme borreliosis is caused by spirochete migration-induced specific B cell activation."?

So what is the status of getting VGV-L's TPT to the clinical trial stage?

Excerpts from its letter to shareholders indicated that due to the time required for coordinating schedules, screening clinicians, and presenting the data, that it was only "recently that we neared finalization of securing a clinician to act as lead on this program. We expect to be able to discuss this in much more detail very soon, but I am very confident that we will be filing our pre-IND for our Lyme disease candidate this year."

 For those who are reading along who do not know what a pre-IND is, "IND" stands for Investigational New Drug, and any clinician who wishes to begin clinical trials to test a new drug must file for approval from the FDA.

From the FDA's own site:
"During a new drug's early preclinical development, the sponsor's primary goal is to determine if the product is reasonably safe for initial use in humans, and if the compound exhibits pharmacological activity that justifies commercial development. When a product is identified as a viable candidate for further development, the sponsor then focuses on collecting the data and information necessary to establish that the product will not expose humans to unreasonable risks when used in limited, early-stage clinical studies.

FDA's role in the development of a new drug begins when the drug's sponsor (usually the manufacturer or potential marketer) having screened the new molecule for pharmacological activity and acute toxicity potential in animals, wants to test its diagnostic or therapeutic potential in humans. At that point, the molecule changes in legal status under the Federal Food, Drug, and Cosmetic Act and becomes a new drug subject to specific requirements of the drug regulatory system."
(For more specifics, see:

I am finding this all very interesting and will continue to watch Viral Genetics as they move towards the trial phase.

I wonder what requirements will need to be met for study participants - and how many chronic Lyme disease patients would be willing to sign up?

Would you?

Additional Information:

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The Camp Other Song Of The Month

Why is this posted? Just for fun!

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