Sunday, January 29, 2012

0 Poll: Cause Of Post Treatment Lyme Disease Symptoms

A couple months ago, a non-scientific poll was placed on the site which asked readers to select from a number of choices for what they think causes post treatment Lyme disease symptoms: persistent infection, an autoimmune disorder, b-cell dysfunction, all of the above, and none of the above.

During the two months the poll was open, only 18 votes were cast by readers who were given the option to select more than one response. 

This time, the poll will be open again with the same question - and in the interest of collecting more votes,  the poll will be open to voting for one year. Also, additional choices will be given (molecular mimicry, metabolic disorder, and immunosuppression) for readers to select. After the poll is closed, the results will be reported and further discussion of each of these choices will go on.

As it stands, of the 18 responses given in two months' time from the old poll, 10 responses stated that post treatment lyme disease symptoms are caused by a persistent infection, 3 stated that they are caused by an autoimmune disorder, one stated they are caused by a b-cell dysfunction, and 7 stated they are caused by all of the above.

We'll see what kind of responses are received on the new poll as time goes on...


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Friday, January 27, 2012

11 Rant: Why Dealing With Lyme Disease Drives Me Crazy. (Part 1)

Note: The content that follows is part one of a personal rant and is atypical of most content as well as context covered by this blog. 

I've been meaning to write this entry for a long time.

Many attempts have been made before this - many which have been scrapped because they neither met my general standards for publication nor managed to convey what I wanted to express.

 But I have to get it off my chest because face it, I've been dealing with this condition and its complications for years now and every so once in a while I've gotta just let it all rip, Camp Other style.

Why Dealing With Lyme Disease Drives Me Crazy

Where do I even begin?

Let's start with the more obvious, from a patient's perspective.

1) Because the lack of early diagnosis and treatment occurred for something which should have been obvious to not only the first family doctor who saw me - but the second one. 

I had a textbook case of Lyme disease: EM rash, history of a tick bite, and symptoms consistent with a Lyme disease diagnosis. I knew the geographic location in which the tick had bitten me because I found the tick within a day of hiking in an endemic area. The state health department and university researchers knew it was an endemic area.

The index of suspicion should have been high, but I was treated dismissively and told that Lyme disease doesn't happen in my state or the area in which I'd been bitten.

Admittedly, I myself did not know how endemic the area was for Lyme disease until after I received my bite and went to my first doctor's appointment. It's after that point when I decided to look it up, and discovered the doctor had made a mistake. People are human and doctors are human and make mistakes, but for me this has been a very costly one - the doctor I saw should have known more about surveillance and epidemiology in the area than I did.

The second doctor had an opportunity to see my larger than 5 cm expanding rash and still thought I just had a sinus infection. When I brought up that I thought I may have Lyme disease, the doctor ran an ELISA -  but this testing was too early to show an antibody response. What the hell, I already had an expanding EM rash - I was treatable on that count alone. Again, a sign of ignorance about the disease, even from a basic IDSA/CDC/State health department point of view.

After having read many other patients' stories about having had a similar experience, I can only suggest that doctors need more education about tickborne diseases and to be more vigilant about immediate treatment as the risks of early treatment are far less than managing complications that come from disseminated and late stage infection.

 2) Because of the lack of a timely and accurate diagnosis and treatment by a family doctor, I ended up seeing an LLMD for diagnosis and treatment.

After my initial research of Lyme disease, of course I came across information about the controversy in Lyme disease and both information singing the praises of LLMDs and how they saved patients' lives as well as information condemning them for their overpriced fees, lack of taking insurance, rude support staff, difficulty in getting appointments, and unproven protocols. I heard both sides from patients. I also got to hear criticisms about LLMDs from some science writers and medical professionals about how their diagnostic and treatment methods were not well supported by science and that LLMDs were only out there to take advantage of the gullible.

I got an earful early on, believe me. But despite hearing the negative reports, I still found myself in the position of having to make my own decision as what to do next and soon, because I was so sick.

I had to do something. I could barely think straight at the time. I was so ill I could barely follow someone else's conversation. I could only read in very short spurts. I was exhausted, in pain, could not work, and could barely take care of myself.

I had to network with people and figure out what I was willing to do. I had to rely on others' suggestions and concerns more than I usually would simply because I had trouble thinking straight. It was rough going.

In time, I realized not all LLMDs were cut from the same cloth and I already knew why I was sick - so controversy or not, I was going to go where I knew someone would help me. If an LLMD was going to treat my Lyme disease and the doctors I'd seen at my supposedly highly rated clinic weren't, I was going to see an LLMD. Simple as that.

At the time, I didn't want to get involved in the controversy at all - even as I felt sympathy for everyone dealing with long term symptoms. I thought that as long as I was treating this infection early that I would be one of the lucky ones - I would take antibiotics for 3-4 weeks and not have to face persisting symptoms.

However... I was wrong. Only I didn't know it at the time. My infection disseminated fairly quickly early on and I was already sicker than others who had acute Lyme disease and received treatment early. I developed symptoms of a coinfection later on that I would not have known to look for or even suspect. The LLMD did suspect this coinfection, then ran tests - for which I was positive - and as a result, I was treated for it and my symptoms improved.

I am still in less pain than I used to be and some of my symptoms completely disappeared from this treatment, so I think there were measurable gains and seeing an LLMD for treatment was the right thing to do when I did it. I genuinely had Lyme disease to begin with - and if two other doctors were not treating it - then someone else damn well was going to treat it.

My question is why did I have to see an LLMD for all of this when a well-trained family doctor should have known from day one what was wrong with me and treat it back then?

Maybe in my case, weeks or a few months of not having treatment or having inappropriate treatment made all the difference in the world for my outcome. The earlier the better, they say. And I could have had that and sidestepped this mess had the family doctors I'd seen earlier on knew what they were looking at and got right on top of it.

3) Because for some reason, having a Lyme disease history is either not calculated into any new symptoms I present to most doctors (both family practice and emergency medicine) and each symptom set I experience is either attributed to something entirely new and separate - or I am told that there is nothing the doctors can do for me (not even palliatively).

Again, I see this response as a lack of education of the doctors in question. I think that doctors have to take into account that even if they themselves do not believe in a chronic infection model of Lyme disease which the Lyme disease patient community supports - that they need to at least consider that the patient in front of them with a history of Lyme disease may be suffering complications related to having had the infection, and to consider the possibility of a coinfection or relapse of a coinfection where symptoms appear to overlap.

If Babesia is a growing problem in our national blood supply and has killed people through transfusions, it seems important to me to rule out Babesia in patients whether they have a mild presentation or a serious one. The risk to everyone's general health is involved.

Sometimes I think it is not just a lack of education which prevents family doctors from dealing with Lyme disease patients. Sometimes it's a matter of fear of not having enough expertise and making a mistake, and not knowing to whom one should refer a patient. If family doctors were better trained to begin with, though, then they could gain that expertise themselves and be the front line for diagnosis and treatment as most patients expect them to be.

Other times, I think part of the issue is that some doctors have decided to overgeneralize about what they read from various medical journals, letters, and reviews, wherein the author states that at least half of those patients claiming they have chronic Lyme disease never had Lyme disease in the first place. Once having digested that nugget, the doctor then may go on to think that a patient who tells them they either have or have had Lyme disease that because it's at least a 50/50 chance the patient never had it in the first place that it is data not worth considering.

Given the growing number of documented Lyme disease cases reported to the CDC annually, I'd like to suggest to these doctors that they nip that thought in the bud and just look at each patient as an individual and consider that their Lyme disease history may play a role in their current symptom set. They don't even have to enter into the controversy to go there.

4) Because of the changing face of the medical profession and doctor-patient relationship in an era of managed care, anyone with a chronic or hard-to-define illness is getting shortchanged these days - and sadly, at times readily receiving a mental illness diagnosis when the evidence for one is weak at best (or at least not the primary cause of their symptoms). 

After reading many different patient forums - not only for Lyme disease, but for conditions like fibromyalgia and CFS/ME or even rare, orphan illnesses which most people do not know anything about - I've seen this happen time and time again: Doctors trying to nail down a diagnosis for a patient within that 10-15 minute appointment window, and when there seems to be "too much going on" for the patient, the immediate suggestion by the doctor is that the patient's condition could be psychological.

Now, I acknowledge that a number of physical symptoms are related to depression and anxiety, as well as chronic stress. And if one is suffering from these conditions, they need to be recognized for what they are and receive proper care. However, I think some doctors are too quick to make this judgment and need more time to listen to patients and create a list of non-psychological physical, endocrinological, infectious, and/or immunological disorders and conditions to test for first before referring patients to a therapist.

Or if the person is obviously psychologically ill, to at least consider a biological basis for that illness or that it may be contributing to it. There is no reason not to run tests while referring one for therapy just to deal with the frustrations of being ill, either - and a caring, compassionate doctor will know how to finesse the situation so that both physical and mental bases are covered without being dismissive towards their patients.

For what it's worth, my family doctor has not diagnosed me with a mental illness. I myself have sought out therapy for depression while dealing with illness - and of the two therapists I have seen, both have told me to keep talking to doctors because it's their assessment I am physically ill and disabled and any depression I have stems from my health - not the other way around.

The biggest problem I have had with being told "it's all in your head" came from ER departments who could not figure out what was wrong with me in the handful of hours that I was there.

5) My treatment has not led to a full recovery or even closer to a life where my symptoms are stabilized.

Some patients within the Lyme disease community have gone off on me for what I'm about to say, but it's an honest assessment about where I am: I have come to accept that I may never regain my former health again and be 100% cured of the symptoms I'm having.

I don't have any expectations that I can return to my old life and do what I used to do and have the same amount of energy I once did. Even if I could be assured of being cured now, there may still be residual damage in my body - plus I am getting older and my body has been deconditioned by years of nearly total sedentary living.

At times I have felt like I've been fed a false hope that I could recover 100% from treatment, because I have certainly tried a lot, above and beyond what the original IDSA Lyme disease treatment guidelines stated. I have not fully recovered, and it's already been several years since I was first infected.

While I do what I can within my limits to try to stretch and improve my health to the degree that I can, I'm aware that there is so much that isn't known about or understood about my condition that it doesn't seem unreasonable to me that I may not get back to my previous state of health before the tick bite.

About the best thing that has helped me was Mepron for Babesia. It helped take care of a number of the most debilitating symptoms I've experienced. But everything else has either resulted in temporary gain or made me feel so much sicker for a longer period of time - that for months at a time, I actually feel much better doing nothing at all.

This is not to say I will never try anything again. It's to say that I want more evidence that the next thing I try is going to make a positive difference and have a good idea of why and how it is going to make a difference. But it seems to me that as time goes on, I still have bad days and less bad days and occasional good ones regardless of what medications or antibiotics I'm taking.

My experience leads me to believe that I either have permanent damage or long term damage that will take years to heal - or that the proper treatment for my condition has yet to be discovered. This is one key reason why I think more research - particularly treatment trials - is important.

6) Because there is a lack of societal and institutional support for someone suffering from my condition, as well as the lack of a streamlined process for acknowledging and supporting how my condition disables me - a condition which should receive official recognition as a disability.

Mainstream medicine has societies for cancer research - multiple societies including ones for specific cancers. It has workshops and support groups for cancer patients. It has programs on nutrition and cooking for cancer patients on site at hospitals and clinics. There are large scale races for the cure and other fundraisers. There are conferences on cancer which some patients are invited to - and some not. And there are many oncologists and oncology staff members and therapists who specialize in dealing with the issues cancer patients face. So on an institutional level, the need for support and education for cancer patients is recognized and accommodated.

When it comes to other doctors' attitudes about oncologists, they do not envy their jobs and have respect for the difficult job they have to do. Being a family doctor, you are more likely going to see minor problems you can fix and not have to watch someone die of cancer before your eyes.  So there is a certain amount of personal and professional respect from many doctors towards oncologists just because of what they have to deal with on a daily basis.

From the perspective of someone who has had post treatment persisting symptoms of Lyme disease (however you name or characterize my condition) I have felt marginalized and that the kind of support I could use has been lacking.

There is nowhere near the infrastructure available for someone with my condition that there is for someone with cancer. If it weren't for some online forums, a few LLMDs, and a few organizations that bend over backwards to recognize that my condition is debilitating - there would not be anyone at all to acknowledge and validate my disability.

I deal with a condition where the doctors - LLMDs - who try to treat patients like me do not receive respect from a number of other doctors, some researchers, and some members of the media. And as patients we will continue to see these doctors not because we are gullible - but because they are actually trying to help us.

If those whom disrespect them have an issue with this, then instead of knocking the doctors who see us and the treatment we undergo, they should make more of an effort to provide patients with a helpful option under their care. We will vote with our feet if you have anything better to offer. And believe me, we are all such big mouths in the Lyme disease community that we would let everyone know if others' approach and treatments really helped us. Even if only symptomatically. Even if it wasn't a cure.

Now, admittedly, there are fewer people who suffer from my condition than who suffer from cancer. But even so, it seems that no matter how many or how few people suffer from a medical condition and/or disability, that there should be a certain baseline recognition, acceptance, and accommodation for that condition or disability. Not just from patient organizations that patients have had to put together from scratch - but from medical institutions, doctors associations, societies, and research groups.

There is something, though, that has troubled me about what makes post treatment Lyme disease (or as the IDSA puts it, "Post Lyme Disease Syndrome") different from other conditions (orphan, or of unknown etiology) that has made me wonder how it has come to be treated as it has been, historically:

Unlike other conditions where the cause is unknown and speculated about, mine does have the distinguishing characteristic of having been triggered by Lyme disease in some way. There is a clear issue of cause and effect here; of some sort of relationship which has already been defined in medical literature.

But people in my situation don't even have the benefit of having the label of "Post Lyme Disease Syndrome" holding significant meaning for them when they apply for disability - even though a number of us suffering with persisting symptoms would be considered to have this condition by some medical professionals.

In the Klempner trial, it was noticed that those most severely affected by this condition had a quality of life and functionality similar to patients with congestive heart failure. This statement was not made by an LLMD (for those whom have issues with an LLMD and may be dismissive about such statements) - this was a statement made by an academic researcher who studied patients suffering with my condition, whatever label you want to apply to it.

Somehow, it seems that whatever I have should be taken more seriously, and there should be more institutional and societal support for it. It shouldn't be a backbreaking effort to explain what ails me - with my medical history, test results, and clinical diagnosis, it should just be accepted as part of my reality and worked with, rather than denied and shrugged off.

Note: Minor edits for style made to this text January 28-29, 2011.

This marks the end of part one of my rant, Why Dealing With Lyme Disease Drives Me Crazy. Continue on to part 2 HERE.


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Thursday, January 26, 2012

5 Two New Hypotheses For Chronic Lyme Disease Symptoms?

There have been a few hypotheses as to why some people experience persisting symptoms after antibiotic treatment for Lyme disease.

The predominant hypothesis supported by most of the Lyme disease patient community is that a chronic and persisting infection is caused by spirochetes sequestered in immune privileged sites - possibly dormant at stages - and difficult to beat without long term high doses of antibiotics. The predominant hypothesis supported by the IDSA Lyme disease guidelines panel appears to be divided between one where patients with persisting symptoms have some condition completely unrelated to Lyme disease - or patients have an autoimmune disorder triggered by Lyme disease.

There have been other hypotheses as to the cause on the table by various parties which are mostly immune-related, such as immune dysregulation and Pam3Cys/OspA immunosuppression. But now there may be two new hypotheses to add to the stack which might apply to some patients with chronic Lyme disease.

(Note that I say "might" and "some" in the previous statement. I have no means for testing these hypotheses, but it is something interesting to speculate about and discuss.)

Hypothesis #1: Chronic Lyme disease could be a metabolic disorder.

In a paper published in December in The Quarterly Review of Biology, one researcher argues that multiple sclerosis (MS) is not an autoimmune disorder as many have thought. She proposes that MS is actually a metabolic disorder.

To quote from Medscape:
"Corthals believes that the primary cause of MS can be traced to transcription factors in cell nuclei that control the uptake, breakdown, and release of lipids (fats and similar compounds) throughout the body. Disruption of these proteins, known as peroxisome proliferator-activated receptors (PPARs), causes a toxic byproduct of "bad" cholesterol called oxidized LDL to form plaques on the affected tissue. The accumulation of plaque in turn triggers an immune response, which ultimately leads to scarring. This is essentially the same mechanism involved in atherosclerosis, in which PPAR failure causes plaque accumulation, immune response, and scarring in coronary arteries."
What if infection with Lyme disease (and possibly coinfections) leads to disruption of PPARs and ultimately, tissue damage? What if at least some portion of patients with chronic Lyme disease are suffering from a metabolic disorder instead of a chronic infection?

What can patients do to treat and prevent this? It appears diet does play some role in developing MS - people with a Vitamin D deficiency and a high fat, high carbohydrate diet were more likely to develop MS than those who did not have a deficiency and such a diet. MS patients have said that taking more Vitamin D and switching to a low fat, low carbohydrate healthy diet has helped with their symptoms.

Other risk factors for developing MS include specific genetic backgrounds, pathogens (infections), and major cellular trauma. The same kind of factors may be relevant for Lyme disease patients who develop chronic symptoms.

Read more for food for thought:

http://www.medicalnewstoday.com/releases/239651.php 

Angelique Corthals, "Multiple Sclerosis (MS) is not a disease of the immune system," The Quarterly Review of Biology 86:4 (December 2011)

Hypothesis #2: Chronic Lyme disease could be a neurological/neurosensory disorder.

Lymenet Europe has been a wealth of scientific information over the years, and recent postings are no exception.

Recently, a thread on sympathetic neural hyperalgesia edema syndrome was posted, mentioning that its symptoms overlap many of those found in Lyme disease. Conditions and symptoms which relate to this syndrome are pelvic pain, abdominal pain, interstitial cystitis, backache, headache, arthritis, fibromyalgia, and mastalgia. This disorder may also manifest as unexplained weight gain, urticaria, chronic fatigue, and vasomotor symptoms unresponsive to estrogen, and a pseudohypothyroid state, according to the research cited on this thread (DOI: 10.1002/ibd.21269).

The proposed treatment for this condition? Dexedrine. That's right, good old dextroamphetamine sulfate, which is an amphetamine used to treat ADHD in adults and children.

While patients receiving this treatment achieved marked improvement in pain and relief from symptoms, I would be concerned about the long term potential for addiction and for side effects in people with certain preexisting conditions. On the other hand, if it is a drug which helps people with their symptoms and improves their quality of life, I think it might be a good idea for doctors to consider trying it on a case by case basis after giving patients an education about its benefits and drawbacks. Patients need to make a decision after being fully informed about its risks in particular.

Caution would also be warranted for patients who wished to try it alongside other supplements, medications, and antibiotics, given that some antibiotics (such as macrolides), medications, and supplements can affect heart rhythms and blood pressure - doubling up on this effect by using Dexedrine as well could have a serious impact on one's health.

This is one reason why I want more research: to know how often chronic infection plays a role in persisting symptoms and how often other conditions may be responsible for these symptoms - either concurrently or alone. Also, I'd want more specific treatments which are either curative and/or supportive for chronic Lyme disease to be investigated through clinical trials. It would be good to know how different potentially curative and supportive treatments could be helpful and harmful to a large body of patients and not just rely on the anecdotes and case studies of only a few.

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Monday, January 23, 2012

0 Paper: Vector Competence of the Tick Ixodes ricinus for Transmission of Bartonella birtlesii

This paper's abstract was recently posted to Lymenet Europe. For those not familiar with one of the debates over the issue of tickborne coinfections, for some time some researchers have claimed that Bartonella can not be transmitted by ticks - while others claim it can be.

Up to this point, Bartonella DNA has been found in ticks, there have been positive PCR results in questing ticks which indicate that the bacterium (or at least its DNA) can survive in the tick through the molt from one life stage to another - and there has been evidence that people who have had tick bites have produced antibodies for both Lyme disease and Bartonella concurrently. But his was not taken as evidence that the tick was the vector responsible for transmission of Bartonella.

As it's been said many times before: Correlation is not causation. There needed to be evidence that Bartonella from ticks carrying the pathogenic organism could be directly transmitted to its host.

In light of the research cited below, it appears this evidence has been found: An Ixodes tick has been shown to be a vector for Bartonella in vivo.

My practical response to this one way or the other has been that regardless of source - fleas from one's cat or dog, or tick - that if one has symptoms of Bartonella and positive test results that they definitely should be treated for Bartonella.

Treat first, and let researchers sort out the source over time...

Reis C, Cote M, Le Rhun D, Lecuelle B, Levin ML, Vayssier-Taussat M, Bonnet SI. Vector Competence of the Tick Ixodes ricinus for Transmission of Bartonella birtlesii. PLoS Negl Trop Dis. 2011;5(5):e1186.

Source:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104967/?tool=pubmed

Abstract

Bartonella spp. are facultative intracellular vector-borne bacteria associated with several emerging diseases in humans and animals all over the world. The potential for involvement of ticks in transmission of Bartonella spp. has been heartily debated for many years. However, most of the data supporting bartonellae transmission by ticks come from molecular and serological epidemiological surveys in humans and animals providing only indirect evidences without a direct proof of tick vector competence for transmission of bartonellae. We used a murine model to assess the vector competence of Ixodes ricinus for Bartonella birtlesii.

Larval and nymphal I. ricinus were fed on a B. birtlesii-infected mouse. The nymphs successfully transmitted B. birtlesii to naïve mice as bacteria were recovered from both the mouse blood and liver at seven and 16 days after tick bites. The female adults successfully emitted the bacteria into uninfected blood after three or more days of tick attachment, when fed via membrane feeding system. Histochemical staining showed the presence of bacteria in salivary glands and muscle tissues of partially engorged adult ticks, which had molted from the infected nymphs. These results confirm the vector competence of I. ricinus for B. birtlesii and represent the first in vivo demonstration of a Bartonella sp. transmission by ticks. Consequently, bartonelloses should be now included in the differential diagnosis for patients exposed to tick bites.




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Sunday, January 22, 2012

0 US HR Bill 3699 Would Put Tax Payer Funded Science Behind Pay Walls

US HR Bill 3699: I have a stake in this one. Many people have a stake in this one. I think that tax payer funded scientific research should be open access and published online as it has been in PLoS ONE and PubMed.

I value high quality peer-reviewed research. It's important. And peer-reviewed journals with high standards and ethics are necessary.

Given the amount of work involved, I think it's okay for privately funded research to be behind a pay wall for certain period of time - publishers need to recoup their money for editing and publishing journals which include not only research papers but articles, letters, and reviews.

Once more knowledge milestones are met and that privately funded research becomes effectively dated then it would best be released into the wild where the general public and students at community colleges and high schools could access it for free.

But this bill? This bill would ensure charging access to tax payer funded research.

An excerpt from the Doing Good Science blog on Scientific American web site pretty much sums up my own thoughts about it:
"The public is all too willing already to see public money spent funding scientific research as money wasted. If members of the public have to pay again to access research their tax dollars already paid for, they are likely to be peeved. They would not be wrong to feel like the scientific community had weaseled out of fulfilling its obligation to share the knowledge it builds for the good of the public. (Neither would they be wrong to feel like their government had fallen down on an ethical obligation to the public here, but whose expectations of their government aren’t painfully low at the moment?) A rightfully angry public could mean less public funding for scientific research — which means that there are pragmatic, as well as ethical, reasons for scientists to oppose the Research Works Act."
Read more commentary about this at the Doing Good Science blog on the Scientific American web site:
http://blogs.scientificamerican.com/doing-good-science/2012/01/06/the-research-works-act-asking-the-public-to-pay-twice-for-scientific-knowledge/

The original text of US HR Bill 3699:
http://thomas.loc.gov/cgi-bin/query/z?c112:H.R.3699:


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Wednesday, January 18, 2012

2 Blog Post: A Letter To A Patient With Chronic Disease

This blog post from Dr. Rob Lambert got passed on to me by a friend.

Although the blog post is from 2010, the advice given of how to approach a doctor when you have a chronic illness is good advice any time.

And with over 250 comments, those who posted and exchanged comments with the good doctor had their own advice and concerns to share.

 I highly recommend checking out Dr. Rob's post in Musings Of A Distractible Mind blog:

A Letter To A Patient With Chronic Disease:
http://distractible.org/?p=3912

You also might want to check out Dr. Rob's new blog, too:

More Musings (Of A Distractible Mind):
http://more-distractible.org/


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Monday, January 16, 2012

0 Dr. Alan MacDonald Discussing Spirochetal Biofilms on LNE

There are a series of discussions going on right now on Lymenet Europe I want to point out.

It looks like Dr. Alan Macdonald is having an involved exchange about biofilms in different spirochetes with someone (Henry) who has identified as a microbiologist in previous entries.

You might want to check out this thread now:

Biofilms of still yet spirochetal type - Treponema:
http://www.lymeneteurope.org/forum/viewtopic.php?f=5&t=3607

Also follow the following related threads:

Structure of Biofilms of Borrelia Lecture link:
http://www.lymeneteurope.org/forum/viewtopic.php?f=5&t=3602

Biofilms of yet another spirochetal species - Leptospira:
http://www.lymeneteurope.org/forum/viewtopic.php?f=5&t=3606

I would like to see more doctors and microbiologists engage in discussion about Borrelia and other spirochetes more often - especially if the implications have an impact on translational medicine and clinical outcome. Obviously some of this discussion is going to be purely speculative, but it is interesting to hear different points of view.

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Sunday, January 15, 2012

4 Admin Update: Comments on Embers Research; Site Changes Coming

Quick update here from Camp Other:

First, I've finally written some comments on select excerpts from Embers et al's most recent publication, Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection.

Read more here: http://campother.blogspot.com/2012/01/paper-persistence-of-borrelia.html

Second, I'm looking to overhaul the site in the coming days. So expect some changes - possibly major changes - as I want to streamline Camp Other blog. Comments are welcome on the process as it unfolds.

Over and out...

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Thursday, January 12, 2012

9 Paper: Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection

Lymenet Europe scooped this first, and it's important enough that I had to share it here...

Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection (2012)

Monica E. Embers, Stephen W. Barthold, Juan T. Borda, Lisa Bowers, Lara Doyle, Emir Hodzic, Mary B. Jacobs, Nicole R. Hasenkampf, Dale S. Martin, Sukanya Narasimhan, Kathrine M. Phillippi-Falkenstein, Jeanette E. Purcell, Marion S. Ratterree, Mario T. Philipp


Source Links:
http://www.plosone.org/article/fetchArticle?articleURI=info%3Adoi%2F10.1371%2Fjournal.pone.0029914


PLoS ONE 7(1): e29914. doi:10.1371/journal.pone.0029914

Abstract

The persistence of symptoms in Lyme disease patients following antibiotic therapy, and their causes, continue to be a matter of intense controversy. The studies presented here explore antibiotic efficacy using nonhuman primates.

Rhesus macaques were infected with B. burgdorferi and a portion received aggressive antibiotic therapy 4–6 months later.

Multiple methods were utilized for detection of residual organisms, including the feeding of lab-reared ticks on monkeys (xenodiagnosis), culture, immunofluorescence and PCR.

Antibody responses to the B. burgdorferi-specific C6 diagnostic peptide were measured longitudinally and declined in all treated animals.

B. burgdorferi antigen, DNA and RNA were detected in the tissues of treated animals.

Finally, small numbers of intact spirochetes were recovered by xenodiagnosis from treated monkeys.

These results demonstrate that B. burgdorferi can withstand antibiotic treatment, administered post-dissemination, in a primate host.

Though B. burgdorferi is not known to possess resistance mechanisms and is susceptible to the standard antibiotics (doxycycline, ceftriaxone) in vitro, it appears to become tolerant post-dissemination in the primate host. This finding raises important questions about the pathogenicity of antibiotic-tolerant persisters and whether or not they can contribute to symptoms post-treatment.



Comments:

A number of Lyme disease patients who initially read this abstract went wild over it, thinking, "Here is the Holy Grail - here is the research that firmly establishes that anyone with post-treatment persisting symptoms is suffering from a chronic bacterial infection".

While this paper is an important piece of research, it is not the final word that clinches chronic infection as the cause of post-treatment symptoms. It does lay the groundwork for specific research that will bring us closer to an understanding of what happens with Borrelia burgdorferi in vivo.

Taking a closer look, the following passages of the full text caught my attention:

This is just a small thing, but I like that the three primary hypotheses for persisting symptoms are mentioned in the introduction section:
"Signs and symptoms of putative failure of antibiotic treatment in late disease or ineffectiveness of repeated treatment in patients with PTLDS may be formally attributed to several causes, including: 1) spirochetes that persist in the tissues, likely in small numbers, inaccessible or impervious to antibiotic; 2) inflammatory responses to residual antigens from dead organisms; or 3) autoimmune responses, possibly elicited by antigenic mimicry [10]."
It's important to note these three hypotheses when reading the text to follow because the authors indicate how findings may relate to them.
"In the assessment of gross pathology, histology, and immunofluorescence, no gross lesions were observed in any of the animals. Fragments of heart and meninges were collected postmortem, and fixed, sectioned and stained for histology and immunofluorescence. Three animals, all of them treated, had moderate to severe inflammatory lesions in the heart."
Post treatment animals showed signs of moderate to severe lesions in the heart. At what rate would it take for these lesions to heal and how much they would affect the animals over time?
Does comparable damage occur in humans after the same antibiotic treatment?
"At 7 and 11 months PI, all monkeys were fed upon by Ixodes scapularis nymphs for the uptake of persisting spirochetes by xenodiagnosis. The number of nymphs that fed to repletion varied considerably between animals. For the first round, a total of 7, 8, and 11 ticks, respectively, fed on the treated animals, whereas only 5 ticks fed on each of the untreated animals (Table S2). Tick midguts were split into 3 parts for culture, direct fluorescence and for DNA extraction. The probability of recovering spirochetes would be higher from animals upon which more ticks feed. As such, intact spirochetes were detected from the cultured midgut contents (Figure 5A) or directly from tick midgut smears (Figure 5B) of two animals at 7 months PI, both of which had been treated. These animals (GB56 and GA59) also had the most xenodiagnostic ticks feed (Table S2)."

The use of xenodiagnosis in this situation can be used to support Koch's first and second postulates, but Koch's third and fourth postulates require more evidence. Intact spirochetes were found in ticks which had fed on antibiotic treated animals. In order to meet Koch's third and fourth postulates, another experiment would need to be conducted where the ticks feed on uninfected animals and disseminated spirochetes would have to be found in tissues in the newly infected animals.

(Additional postulates can be tested for on a molecular level. See Molecular Koch's Postulates. The below excerpt relates to this with evidence of transcription of a lp28-1 gene in a treated animal.)

"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 2009 paper, Antibiotic Treatment of Animals Infected with Borrelia burgdorferi, Gary Wormser asked, "What are causes of the attenuation of the spirochetes that persist posttreatment? Are they in the process of dying? Are they producing mRNA, and if so, which mRNA? Are they motile? Can they replicate? Are they genetically altered? Can they regain pathogenicity?"

In his own conclusion, he states, "The biological nature of these spirochetes is unclear," along with some caveats about the likelihood of their being pathogenic.

Now here we have evidence that points to Borrelia spirochetes which are metabolically active and transcribing OspA and an lp28-1 gene in antibiotic treated animals. So at least part of Wormser's questions are answered. But not all.

Now we examine the discussion portion of the paper...
"Our results indicate that disseminated spirochetes of two different B. burgdorferi strains can persist in the primate host following high dose, or long-lasting antibiotic therapy."
Many patients have made note of this particular passage, with the concern that surviving spirochetes are the source of persisting symptoms after high dose or long-lasting antibiotic therapy. A number of people have stated that this finding justifies the use of long-term high dose antibiotic therapy. However, it's not over from the researchers' perspective. Their work is still cut out for them - they still have to do additional research that links the presence of metabolically active spirochetes with reproduction and symptoms in the host.
"At the molecular level, B. burgdorferi DNA would indicate the presence of organisms, live or dead. The detection of RNA, however, should indicate that those present are metabolically active and thus alive. In Experiment 1, spirochetal DNA and RNA were detected in the tissues of a few animals, independent of treatment. This may reflect a low spirochetal burden, lack of flaB transcription [37], and/or seclusion in untested tissues."
This is probably one of the most important passages in the full text. While spirochetal RNA
was present in antibiotic treated animals and spirochetes were alive, the signficance of their presence has to be clearly determined. The worthwhile thing to note at this stage is that the spirochetes were metabolically active and alive after long-term high dose antibiotic therapy.
"[...] few slow-growing organisms were recovered by culture from each animal. We detected the ospA transcript in culture pellets from tissues of four animals and directly from at least one tissue from each animal. We chose ospA because this gene has been shown to be transcribed by host-adapted B. burgdorferi [38], in disseminated infection [39], and because of the induction of an anti-OspA response in patients [40] post-dissemination."
So much discussion in various publications has been leveled at the presence of anti-OspA response in patients and host animals, with the correlation being made between anti-OspA and the inflammatory response rather than the presence of continued infection. What if both are present? Given Barthold's studies on the immune system's response to Borrelia burgdorferi in lymph nodes, would a combination of infection and inflammatory response after antibiotic treatment be likely in treated human hosts?
"It has been postulated that the joint tissues provide a protective niche during antibiotic treatment [41]. Our studies and others [37], [42], however, have not demonstrated a specific predilection for spirochete presence in joints of treated animals."
Pointing this out for all Lyme disease patients: While Lyme arthritis is a well-known manifestation of Lyme disease, Borrelia spirochetes do not seem to congregate in joints on a massive scale.

(Personally, I have suspected nerve and tendon involvement all along, based on my own symptoms.)
"A “persister” phenotype may possibly be responsible for the recalcitrance of persisting spirochetes made evident by previous studies in mice and dogs [37], [42], [45], and by those presented in this report. Perhaps incomplete clearance of bacteria following antibiotic treatment is not a phenomenon unique to B. burgdorferi, but one that occurs with other bacterial infections as well. In this case, xenodiagnosis enables detection of otherwise inconspicuous live organisms through acquisition by the natural vector."
This is speculative, but something worth following up on in future studies: Is there a persister phenotype of Bb that survives high dose antibiotic treatment? Does this mean that Borrelia is antibiotic resistant - or more precisely, antibiotic tolerant? If so, how will long-term high dose antibiotic treatment kill these remaining spirochetes if it hasn't happened after the dosages and durations stated?
"Also, the C6 titers declined in some untreated animals over a long period of time, but not in others, though presence of spirochetes was indicated in C6-negative untreated animals by IFA or PCR/RT-PCR. This is likely due in part to genetic differences in outbred animals."
How do these data apply to untreated human hosts? Do people have different genetic backgrounds which can lead to negative tests even when spirochetes are present?

Let's read on...
"Possible explanations for the lack of correlation between C6 response and presence of spirochetes include: (1) the anti-C6 titer is an indicator of treatment efficacy and the infection is cleared despite the presence of spirochetal genetic material/antigen; (2) organisms persist and the anti-C6 titer does not reflect their presence, perhaps due to loss of plasmid lp28-1 (which encodes VlsE, the parent molecule of C6); or (3) anti-C6 titer declines with a significant reduction in spirochetal burden, but a low number of organisms reside in the host; if these organisms are dormant, then transcription of vlsE also may be negligible, minimizing re-stimulation with antigen.

The detection of intact organisms ruled out the first explanation and detection of transcript (bbf26) from lp28-1 disproves that explanation #2 may be operating exclusively. We therefore favor explanation #3 and seek to determine the level of transcriptional/metabolic activity, and pathogenicity of persistent organisms. If, for example, spirochetes that are recovered by xenodiagnosis from treated animals turned out to be non-pathogenic, this would validate the decline in C6 titer as a measure of successful treatment outcome."
Based on the above, the researchers have stated that:
  • Metabolically active and live spirochetes have been found in primates which were treated with long-term high dose antibiotics.
  • Whether or not these spirochetes can reproduce has not yet been established.
  • Whether or not these spirochetes are infectious has not yet been established.
"Due to the relatively small quantities of bacteria over a large amount of tissue, we were unable to reliably quantify DNA or transcript levels in nonhuman primates. Similarly, the recovery of few spirochetes by tissue culture is aptly a reflection of the rhesus model and not necessarily the treatment [48]."
This indicates that the authors of the paper are giving word of caution that the presence of a few spirochetes in non-human primates may be due to their being non-human primates and not because of the antibiotic treatment they received.
"The most pressing question in terms of human disease is whether or not spirochetes remain pathogenic after antimicrobial therapy. Similarly, do spirochetes persist long-term, or are they eventually cleared by the host? Clearly, the phenotype of persistent organisms needs to be elucidated. These studies support the use of the C6 test for diagnosis and measurement post-treatment; however, the absolute quantification of antibody levels may be essential in determining treatment efficacy for PTLDS patients, as low levels (yet above baseline) may indicate presence of residual spirochetes or antigen."
Yep, see my earlier bullet points.
"Finally, the use of variable and pulse-dosing regimens of antibiotics may improve efficacy [43] and this warrants testing in an appropriate model."
Now this is interesting... The suggestion is that pulsing antibiotics may work better as a treatment model for Borrelia/Lyme disease infection.
"Finally, in these studies we used an artificial mode of inoculation and spirochetal dose. The experimental results must be confirmed with tick-mediated infection, which is our intent. Our studies do however offer proof of the principle that intact spirochetes can persist in an incidental host comparable to humans, following antibiotic therapy. Additionally, our experiments uncover residual antigen associated with inflammatory foci. Whether persistent spirochetes or spirochetal antigen can cause PTLDS remains unanswered."
There you have it. This paper is a stepping stone to more research that will characterize the nature of Borrelia spirochetes after long term high dose antibiotic treatment. Research that I hope is coming soon.

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Saturday, January 7, 2012

8 What I'd Like To See The IDSA Do For Lyme Patients In 2012

Since Camp Other is not on Facebook and has only had the link and comments list (including deleted comments) passed along, I've decided to post here what my answer is to the IDSA's question, "What would you like to see from your society in the coming year?"

I realized in reviewing all the comments I've seen to date that some people are thinking along similar lines as I am. But anyway, here's my proposal:

I would like to see the IDSA publish a paper which characterizes all the data on those patients who have stated they have been diagnosed with chronic Lyme disease and/or Post-Lyme Disease Syndrome. What are the similarities both in terms of empirical testing (not just ELISA C6 and WB, but immunological as well), history, presence of coinfections, genetic profiles, preexisting conditions, and symptom presentation in this patient group? It'd be good to see aggregation and see if there are specific subgroups of all these patients - rather than just see and know about patients who met CDC surveillance criteria who could participate in clinical trials. Those who are living with CLD/PLDS may not be those who end up participating in clinical trials. Let's see a characterization of the data first, much like what the Norwegians did this past summer in an NIH study, "The Phenomenon of "Chronic Lyme"; an Observational Study"(of which I am still waiting for the results).

I would like to see the IDSA publish a detailed web site which explains their own hypothesis or hypotheses for autoimmunity giving rise to persisting symptoms after antibiotic treatment for Lyme disease. There is little detailed information available online all in one place on how autoimmunity hypotheses came to be adopted after persisting infection models were considered - even though there are plenty of research papers where the purpose was to determine any autoimmune factors in infection. The information is not laid out in one logical coherent piece displaying all the building blocks of findings for others to see. If the IDSA thinks they have a strong argument in favor of autoimmunity and many people fail to agree with it, it seems to me they have failed to support it.

I would like to see the IDSA also include on that web site what the evidence is for persistent infection after antibiotic treatment, and a detailed explanation on why they think an infection cannot persist beyond 2-3 weeks of antibiotic treatment in any patient, and a list of criteria which would need to be met in order to determine that Borrelia does and can persist in its host. (Something specific about #2 on this page, and more detailed.)

I would like to see an extension of the proteomics research which distinguished the CSF proteins of Chronic Lyme Disease/Post-Lyme patients from the CSF proteins of CFS/ME patients. In particular, see a comparison between acute Lyme disease, late stage Lyme disease, and chronic Lyme disease protein distributions. Are they the same? Are they different? Can we use this knowledge to learn more about disease progression?

I would like to see some more research done on how different genospecies of Borrelia register on different serological tests for Lyme disease. It might not even be fair to continue using tests for "Lyme disease" - what might be a more accurate test panel would be one for Borreliosis, which covers all Borrelia including relapsing fever Borrelia and forms of Borrelia which do not always present with the tell-tale EM rash (hardly tell-tale under those circumstances). I'd also like to see related research on how repeat panel testing catches more disseminated infection which was not caught earlier. (The issue here being that early suspicion of disease must be present - ethically if you suspect and do not treat, this creates problems when one is found serologically positive.)

I would like to see some more research done on how different antibiotics affect different kinds of Borrelia. The fact that some patients do experience treatment failure even in early Lyme disease - up to 10% of all acute patients - may be due to the efficacy of their initial treatment. Refer to this:
"In Vitro Susceptibility Testing of Four Antibiotics against Borrelia burgdorferi: a Comparison of Results for the Three Genospecies Borrelia afzelii, Borrelia garinii, and Borrelia burgdorferi Sensu Stricto."

"In 7 out of 12 comparative evaluations (P > 0.05), MBCs were significantly different among the three genospecies. B. garinii seemed to be especially susceptible to azithromycin, while amoxicillin had a significantly greater effect on B. burgdorferi sensu stricto compared to the other genospecies. Ceftriaxone had the lowest MBC with B. afzelii and increasingly higher MBCs with B. garinii and B. burgdorferi sensu stricto. Doxycycline did not show any remarkable differences in its effects on the three genospecies."
Most of all, I would like to see the IDSA have a heart, and for dismissive opinions such as "In many patients, posttreatment symptoms appear to be more related to the aches and pains of daily living rather than to either Lyme disease or a tickborne coinfection," to not be included in official professional medical guidelines for the treatment of Lyme disease. Any opinion such as this must be rigorously backed by fact and not by comparison to the population at large. Any condition which involves pain as a symptom could be compared to pain in the population at large. This should not distract one from the fact that certain medical conditions involve pain as a symptom. The controversy in Lyme disease may not end any time soon, but if patients were taken at their word for describing the serious limitations and degree of pain that they experience on a daily basis, that would go a long way towards a first step at healing the anger so many of us have.

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Friday, January 6, 2012

0 IDSA Requesting Feedback On Facebook

Well, the past 24 hours in Facebook Lymeland have certainly been interesting...

The Infectious Disease Society of America (IDSA), of whom a subset are authors of the 2000 and 2006 Lyme Disease Treatment Guidelines, decided to solicit comments from their readers on Facebook at the below link:

https://www.facebook.com/IDSociety/posts/357764004239867

The question they posed was simply this:

"What would you like to see from your society in the coming year?"



And with that question, the floodgates opened, and a rush of disgruntled sick Lyme disease patients, chronic Lyme disease patients, caretakers of patients, patient advocates, physicians who were not LLMDs but were on long term treatment, and those questioning chronic Lyme disease's causes and wanting answers responded at length.

At some point, responders complained both on and off Facebook that whoever moderates the Facebook IDSA page was deleting their comments - even if the contents were not abusive, insulting, or engaging in ad hominem attacks. I don't know the full story there, having only caught a portion of the accusations about deletions.

But I will say that whether one agrees with the content in total or not: over 1500 comments in so short a period of time is notable.

What would you like to see the IDSA do in the coming year?

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Wednesday, January 4, 2012

0 Camp Other Blog: 2011 In Review

A little over a year ago, I set out to write about the Chicago Tribune's article, "Chronic Lyme: A Dubious Diagnosis". My analysis of that article formed the basis for this blog, and from there, I hit the ground running.

I didn't know how long I'd write here or how often. Or know whether or not wrestling with chronic illness would interfere with writing. Sometimes it has. Sometimes it hasn't.

One year later, and I'm still here. Perhaps a bit battered around the edges. Tired. Exhausted. Overwhelmed, even. Disappointed with the lack of more treatment research for myself and my fellow sufferers. But also more knowledgeable, less naive, and more curious than when I began. Open to more new ideas. Questioning.

I'm somewhat amused this blog gets as much traffic as it has during the past year and it has only increased as time went on. I never expected it to be The Popular Blog Online, given the somewhat esoteric subject matter at times - but perhaps these stats mean something?

January 2011: 1,379 page views
March 2011: 2,539 page views
June 2011: 3,957 page views
November 2011: 5,579 page views

And for the most part, this trend in traffic increase continues. It only tends to dip down when I don't write something for a long time.

There were over 40,000 visits to this site during 2011 from over 114 countries - with the top ten countries' visitors coming from the United States, Canada, Russia, Slovenia, Germany, United Kingdom, Ukraine, Netherlands, India, and France. And there are over 104 more, from Australia to Algeria. This blog has had an ongoing international audience since it began.

Where Camp Other Is Read: Around The World
On average, about half my visitors are people who return to read something new on my blog. Some are repeat checkers who must hit refresh for the homepage daily or something. Sometimes they are deliberately looking in my archives. (I don't know why - hey, you're reading - perhaps you can tell me why?) The other half of my visitors are people using google and other search engines for specific research, possibly for university papers or their own personal education. Their keyword searches are often incredibly specific; with a keyword choice like "Borrelia burgdorferi + bacteriophage" they often end up here.

I didn't know who would be interested in reading along. Or how many people would want to scour Lyme disease related research and publications with me. But it seems like quite a number of you are interested because you keep coming back.

To you, I say thank you. Even if you have never commented on this blog, if you have been getting something positive out of being here and learned something new, that makes it worth it to write. It inspires me to keep going even when the going is tough.

(And I will say that my underwhelming publishing schedule in December was not only the result of holiday insanity/busyness my family participates in - it was also the result of life and my health being tough.)

(And it still is. I can't guarantee any sort of content/timeline/publishing schedule right now.)

But I made it this far, so I'd like to share some of the highlights of this blog from 2011:

In January, the blog looked at polymicrobial infections - also known as Lyme disease coinfections. How common are coinfections? What is the most recent body of literature on coinfections? What kind and severity of symptoms do patients with coinfections have? We took a preliminary look at these questions.

In February, we examined the different uses of the term, "chronic Lyme disease", and I wrote about how the IDSA Lyme disease guidelines group would label my condition - versus how patient advocates would label my condition. This link has been very popular during the past year up to now: http://campother.blogspot.com/2011/02/is-chronic-lyme-real.html

In addition to wrangling with disease definitions, in February there was much buzz about an old patent that I decided to comment on (including for its use of the above terminology), the VlsE sequence in Borrelia burgdorferi (as discussed at the 2010 Institute of Medicine workshop on tickborne diseases), and the interesting package insert from the Athena Multi-Lyte Borrelia VlsE Test, which states, "Lyme disease occurs in stages, often with intervening latent periods and with different clinical manifestations," and "Also, early antibiotic therapy after EM may diminish or abrogate good antibody response. Some patients may never generate detectable antibody levels." Yes, Virginia, there can be seronegative Lyme disease.

In March, the blog reviewed the 1993 U.S. Congressional Senate Testimony On Lyme Disease in two parts, including questions and commentary on various sections. We also discovered the value of anecdotal evidence, and offered links to online video tutorials on the immune system for beginners.

In April, we introduced readers to a blog about spirochete microbiology, Spirochetes Unwound. We also reviewed an outline of the book, "Borrelia: Molecular Biology, Host Interaction and Pathogenesis", and listed many definitions and terms used in Borrelia microbiology. Two other popular articles or series were published during this month - a two-part series on phage therapy: "One Way To Treat Borrelia Naturally?" and "Phage Therapy and Borrelia burgdorferi". We also shared a two-part series on neuroborreliosis based on the Institute of Medicine's 2010 tickborne disease workshop notes, and shared the news that a serious allergy to red meat can develop in some people who have had a tick bite.

In May, Camp Other blog contributed a series of posts at The Daily Kos in observance of Lyme Disease Awareness Month, and reposts of these posts can be found in May 2011 archives. Of the lot, I think "Lyme Disease Rant: The Wall Of Polarization" is particularly important for those engaged in discussing both sides of the Lyme disease controversy online. We also looked at someone's thesis, "Environmental Stress in Borrelia burgdorferi", and some initial late stage Lyme disease study outcomes from the 2000 Lyme disease guidelines.

In June, the blog took a preliminary look at the 2006 Lyme disease guidelines, examined the paper - "Borrelia burgdorferi RST1 (OspC Type A) Genotype Is Associated with Greater Inflammation and More Severe Lyme Disease" - on the growing evidence of differential pathogenicity among Borrelia burgdorferi genotypes in the United States, shared Dr. Elizabeth Maloney's critique of the IDSA Lyme disease guidelines, and wrote a critique of a (which has yet to be confirmed as official) letter from the CDC to a Lyme disease patient who had written looking for more information on Lyme disease.

In July, we referred to our favorite spirochete blog, Spirochetes Unwound, to learn more about Barthold's study on how Lyme disease affects the immune system in lymph nodes, asking the question: "Does Borrelia burgdorferi cause an inadequate antibody response by altering B cell activation in the lymph node?" We shared an overview of Lyme disease in vitro studies showing intracellular behavior, examined how Google can aggregate data sets for Lyme disease using Google Trends, and broadcast the news that a teen from North Carolina developed a serious allergic reaction to meat after a tick bite.

In August, the blog discussed the publication of a paper on the link of antibodies to long term symptoms related to Lyme disease infection, introduced readers to a new patient blog: Lyme Jello, and examined whether or not there is a connection between different genetic haplotypes (HLA-DR#) and Lyme disease in two related posts. I think, though, that the most profoundly compelling post of August (and related to the previous two) was this one: "Immune + Infection = HLA-DR alleles determine responsiveness to Borrelia burgdoferi."

In September, the blog looked at the development of new Lyme disease detection tests for patients, published two articles on the recognition that Borrelia miyamotoi can cause infection in patients in the United States, speculation about Borrelial blebbing and camouflage, and speculation on the role of cholesterol in Borrelia burgdorferi.

In October, the blog speculated what kind of new Lyme disease research may be useful, we learned that a Chacolithic iceman from 5,000 years ago had Lyme disease, we looked at a new molecular test which may be able to detect early Lyme disease, and reviewed the Stony Brook Young Investigators Series On Lyme Disease.

In November, the official final report of the Institute of Medicine workshop was published on Pubmed: "Critical Needs and Gaps in Understanding: Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases: The Short-Term and Long-Term Outcomes," a Tularemia outbreak hit Australia, and there were two notable articles published on long-term outcomes of antibiotic use as well as using cathelicidins as an alternative to antibiotic use. Perhaps one of my favorite links for November was about a series of articles by Slate on the use (and drawbacks) of the murine (mouse) model for researching human models of disease.

In December, the blog shared an outline and separate discussion on presentation summaries from the 2011 Lyme and Tick-Borne Diseases National Conference held in October 2011. The news of a new strain of Ehrlichiosis that is causing disease in Sweden was reported, and we took a look at concerns over a Canadian freedom of information request and response over patient advocacy and supportive treatment of Lyme disease at a new Vancouver Complex Chronic Disease Clinic.

So, those are the highlights of the past year in review.

What will 2012's blog posts have in store for you? Stay tuned...


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