Saturday, July 30, 2011

0 Admin: PSA To All Camp Other Google Account Users And Readers

A message from Camp Other to readers:

Keep your eyes on Google and how they treat your accounts - especially if you have and use a pseudonym online connected with Google+ accounts.


"When it comes to Google services, we support three types of use: unidentified, pseudonymous and identified. And each mode has its own particular user benefits.

Unidentified. Sometimes you want to use the web without having your online activity tied to your identity, or even a pseudonym—for example, when you’re researching a medical condition or searching for that perfect gift for a special someone. When you’re not logged into your Google Account (or if you never signed up for one), that’s how you’ll be using our services. While we need to keep information like IP addresses and cookies to provide the service, we don’t link that information to an individual account when you are logged out.

Pseudonymous. Using a pseudonym has been one of the great benefits of the Internet, because it has enabled people to express themselves freely—they may be in physical danger, looking for help, or have a condition they don’t want people to know about. People in these circumstances may need a consistent identity, but one that is not linked to their offline self. You can use pseudonyms to upload videos in YouTube or post to Blogger.

Identified. There are many times you want to share information with people and have them know who you really are. Some products such as Google Checkout rely on this type of identity assurance and require that you identify yourself to use the service. There may be other times when it’s more desirable to be identified than not, for example if you want to be part of a community action project you may ask, “How do I know these other people I see online really are community members?”

Well, this all sounded like a reasonable division to me, and that's worked fine for me for ages.


But during the past month, Google apparently began shutting people's Google accounts down across the board without warning - because users were using pseudonyms.

I only learned about this within the past 24 hours (I guess I've been too buried in research about antigenic variation and serology to notice the news lately) and was disturbed to hear about what happened to GrrlScientist and her accounts.

Apparently a lot of people's accounts were suspended without prior notice, and outrage over this spread across the blogosphere. Search online for "privacy, pseudonyms, and google accounts" and you are likely to find more information on this action from more than one web site.

At any rate, looking at the stream of events unfolding, I've had to wonder if Camp Other blog would be next. If so, I'll be posting an announcement on Lymenet Europe letting people know where the site would be getting moved - somewhere without a policy that discriminates against anonymity - and pseudonyms in particular.


But, it may be that my search for an ISP to host my blog would be premature, as I just came across an announcement from Bradley Horowitz on Google+ that came from a discussion between Robert Scoble of Rackspace and Vic Gundotra, Senior VP of Social at Google - the most important snippet posted below:

MYTH: Not abiding by the Google+ common name policy can lead to wholesale suspension of one’s entire Google account.

When an account is suspended for violating the Google+ common name standards, access to Gmail or other products that don’t require a Google+ profile are not removed. Please help get the word out: if your Google+ Profile is suspended for not using a common name, you won't be able to use Google services that require a Google+ Profile, but you'll still be able to use Gmail, Docs, Calendar, Blogger, and so on. (Of course there are other Google-wide policies (e.g. egregious spamming, illegal activity, etc) that do apply to all Google products, and violations of these policies could in fact lead to a Google-wide suspension.)

Camp Other doesn't use Google+ in the first place, so I am making the assumption based on the above that my blog will continue to operate on Blogger as it has been.

If something changes... well, you know where to find me. And if Lymenet Europe for some reason goes down, I'll post to CanLyme, and so on - to other Lyme disease related forums which have not unceremoniously banned me.


PS: Just in case you wondered, I make a regular backup of all the site entries. Reformatting the content and moving to another web site host may not be a trivial matter, though, so I don't want to do it unless there's a very compelling reason.

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Thursday, July 28, 2011

9 Borrelia Infection in Ticks in Norway

ScienceDaily (June 24, 2011) — The most common tick-borne disease in humans is Lyme borreliosis. Extensive field and laboratory tests have revealed that the Borrelia bacterium is present in a larger proportion of ticks than has been shown by earlier studies. Another finding is that migratory birds play an important role in the spreading of ticks and pathogenic agents borne by ticks.



The researcher working on this project, Vivian Kjelland, found a strong correlation between the spread of Borrelia bacteria and birds in Norway - and discovered a decline in the hare population had little to do with Borrelia infection.

Perhaps the most interesting or surprising part of her research is this: Kjelland's doctoral thesis indicates that there is a lower incidence of the Borrelia bacterium in ticks that have sucked blood from deer and moose than in ticks collected from the ground/vegetation.

One thing to keep in mind with research in Norway as well as other countries is that the shouts of "kill all the deer" in order to stop Lyme disease may not be the best decision, as ticks will colonize other animals and take blood meals from them instead. What happens all depends on the local ecology and which host animals are available.

We can't kill all the potential hosts for ticks. Other solutions to fighting Lyme disease and related tickborne illnesses need to be found.

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Saturday, July 23, 2011

7 NC Teen Develops Red Meat Allergy After Tick Bite

ELIZABETH CITY, N.C. (AP) — About a year ago, 15-year-old Andrew Treadway of Currituck got a tick bite while camping near Charlottesville, Va.

The bite did not appear serious. When he returned to his Moyock home, his mom looked for the tell-tale bulls-eye rash indicating Lyme disease and the flulike symptoms from Rocky Mountain spotted fever, but all appeared normal.

Little did they know that the tick bite would later trigger an allergy to red meat. Today, the Treadways want others to know about the newly discovered allergy that puzzled their family for months.

Making the connection between the tick bite and the allergy was not easy. Several months after the tick bite, the teenager began complaining of unexplained stomach aches and migraines. Ann Treadway said she was baffled by what was causing the problem.

The real alarm came a little later when the family went camping with friends...

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Thursday, July 21, 2011

2 Oh, Canada: Infected Ticks Found In Alberta

Just a quick FYI to my friends in Alberta, Canada: Be careful out there...

Alberta issues Lyme disease warning

Posted By: NCCID on July 21, 2011
Calgary Herald, July 20, 2011

Infected ticks turn up in city, Edmonton

As health authorities urge Albertans to guard against Lyme disease after five infected ticks were found so far this year, a Calgary mother says she's frustrated her sick daughter hasn't been tested for the illness despite repeated requests.

The pinhead-sized ticks carrying the Borrellia burgdorferi bacteria that cause Lyme disease were spotted recently on four dogs and a cat, through Alberta's surveillance system, said the province's chief medical officer of health, Dr. Andre Corriveau.

Canada is increasingly becoming an area of Lyme disease activity. What actions are the provinces taking to address this issue and make sure people are diagnosed and treated early?
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Monday, July 18, 2011

13 Lyme Disease Western Blots And Antigen Presentation

I've been thinking of this particular passage on page 504 of the book, Borrelia: Molecular Biology, Host Interaction and Pathogenesis:

"The general picture to have emerged over the years is that IgG and IgM antibodies to the spirochaete develop slowly and are directed against an increasingly diverse array of proteins as infection progresses (Craft et al, 1986; Dressler et al, 1993; Nowalk et al 2006). The earliest responses are to flagellin B (FlaB) and p66, followed by OspC (25kDa) with responses to a number of additional antigens, such as VlsE, fibronectin-binding protein (BBK32), FlaA (37kDa), BmpA (39kDa), and decorin-binding protein A (DbpA) developing as B. burgdorferi disseminates (Coleman and Benach, 1987; Engstron et al, 1995; Bacon et al 2003; Aguero-Rosenfeld et al 2005; Wilske et al, 2007). This temporal pattern is consistent with the notion that the bacterium draws upon an expanding repertoire of differentially expressed proteins once within its vertebrate host, including phased expression of paralogous surface-exposed lipoproteins.
The clinical ramifications of these observations are significant. Because approximately half of patients with EM do not mount detectable antibody responses to the pathogen, lack of seroreactivity cannot be used to rule out the diagnosis of EM (Steere, 2001; Dananche and Nadelman, 2008). Seroreactivity increases substantially following therapy for EM (Vaz et al, 2001; Dandache and Nadelman, 2008), indicating that killing of the bacterium enhances processing of spirochaetal antigens."

Prior to the 2006 IDSA Lyme disease guidelines, the first set of Lyme disease guidelines which were written contained this specific remark on laboratory criteria for diagnosis:

"Significant change in IgM or IgG antibody response to B. burgdorferi in paired acute and convalescent phase serum samples"

It seems to me that this would still be an important guideline to follow, yet I am aware of a number of stories where patients stated their family doctors gave them an ELISA blood test early after infection, were told it was negative, and because of this, were not given further testing.

This is an inappropriate response, especially given what is known about antibody response in Borrelia burgdorferi infection over time, and given the lack of adequate antibody response early in infection.

Retesting using the western blot several weeks after the initial test - even if negative - makes sense. And if someone is displaying unusually long and moderate-severe flulike symptoms even if there is no EM present, confirmation testing is sensible.

Given this is a serologically progressive infection, why isn't it possible to determine how far long the infection is to some degree (under delayed acute care, at the very least) if the antigens present in a specific order over time? In later infection, it is harder to detect - but doesn't ospA present itself again in neurological infection? Something I have to look into...

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Wednesday, July 13, 2011

19 Chicago Tribune's Dubious Writer Is At It Again...

For those who were not here when this blog started,  a reminder:

This blog began because I wrote commentary in response to last December's Chicago Tribune article, "Chronic Lyme: a dubious diagnosis". I was not pleased with how the topic of Lyme disease was discussed in that article because it focused on doctors' disciplinary records and self-reported charlatans working in alternative medicine - and did not focus on science and clinical microbiology.

The best of my efforts to deconstruct that article is here:

Now, several months later, there is an article in the Chicago Tribune by one of the same authors of the original "Chronic Lyme" article - this time on one specific doctor who has a number of lawsuits and charges on his record.

This was posted early this morning:,0,3542528.story

Well Trine, you've done it again.

My issue with Trine Tsouderos' writing is that it is always written in such a way that the content emphasizes the most controversial topics that could possibly be related to chronic Lyme disease without actually discussing chronic Lyme disease itself.

It's sensationalism, and it is about getting the audience's outrage in print. It's an open invitation for the general public (who is fed up with mainstream medicine and bad doctors, and often rightly so) and skeptics (who do not think Lyme disease can be a persistent infection) to comment on how horrible Lyme literate doctors must be in general if someone specializing in the treatment of chronic Lyme disease has a background such as Dr. Piccirillo's.

Tsouderos' article written last December also focused on two doctors with disciplinary actions on their records. Never once did Trine mention that there are many doctors - both ILADS and non-ILADS doctors - who treat Lyme disease patients with longer than standard courses of antibiotics and help people get their lives back. These doctors have many years of experience treating patients and do not have the kind of disciplinary record which is on display here.

I have a major issue with Tsouderos' previous and current writing on chronic Lyme disease because it does not mention this nor does it mention any of the science and research behind Lyme disease and persistent symptoms.

As an investigative reporter, she could be putting her skills to use and advance science education for the general public if she wrote about research which demonstrates that Borrelia burgdorferi spirochetes can persist after antibiotic treatment and pointed out that researchers are not 100% certain of their significance. They argue over it, just as the IDSA and ILADS argue over it. It would also be beneficial if she mentioned the IDSA's position on supporting an autoimmune response and the molecular mimicry hypothesis as the cause for post-treatment Lyme disease symptoms - but she has never even gotten this far to explain why any researchers support a non-infectious model for persisting symptoms.

Reporting on these aspects of post treatment Lyme disease or what has been called chronic Lyme disease is what fair and balanced reporting would entail. Instead, what we get is pure and unmasked sensationalism geared to getting the most rise out of the audience.

All Trine seems to do is repeatedly point out a litany of bad medical decisions or charges related to a handful of doctors - and in the case of December's Chicago Tribune article - at least for one of those doctors, the charges were dropped.

There is no mention of the Lyme disease patient community's position that doctors who treat Lyme disease with more than the IDSA Lyme disease panel's guidelines recommended amount and duration of antibiotics are subject to being reported by insurance companies solely for that purpose. Nor is there mention of what evidence there is to support the patient community's statements on these reports. Instead, there is no mention of this at all - whether Trine thinks these reports are genuine or not.

Now, with what follows, I am probably going to receive some hate mail because of what I am about to say, but so be it. (I will create a special tab, "Hate mail" at the top of this page just for that purpose. If anyone writes in support of what I say, you too will get your comments on a separate page, "Love letters", or something like that.)

But anyway, I have to call it as I see it:

I have issues with Dr. Piccirillo's decision.

If Dr. Piccirillo was inspired to become an LLMD because he himself contracted Lyme disease and suffered due to it, I admire his desire to help others who have suffered a similar fate. But at the same time, was he hoping that his record would go unnoticed and he could start anew?

Dr. Piccirillo, you realize that doesn't happen when you enter the deep end of the pool in the Lyme disease controversy, don't you? Everyone and everything is scrutinized. To go into one of the most controversial jobs with a number of marks already on one's record adds to the existing public misconceptions and generalizations that are held about LLMDs.

Your decision to make this career move affects patients and reflects on everyone working in the field. If you were in fact by your own admission not the best surgeon and your record reflects charges of incompetence - then was picking a potentially high profile, high demand job such as an LLMD the way to go?

I appreciate your stated desire to do better and your own acknowledgment that you weren't cut out to be a surgeon. I take that with sincerity and at face value. And I understand that it's not your fault that Tsouderos wrote about you this way - through no fault of your own, your story and your past has been dragged out before the public for all to see.

Unfortunately, your past is exactly what they wanted to put on display and what many people would want to know about if you were to become their own doctor. As someone who has the lives of other people in your hands, you are going to be held accountable for what you do and do not do. It follows you; that's how it is.

But to be quite pointed about it, had you been the best doctor in the world and helped many people and harmed none - would Tsouderos have written about your work? Probably not. In terms of Lyme disease reporting, so far Tsouderos is a one trick pony.

Everyone who has read this kind of article realizes that this isn't fair and this isn't balanced reporting. How do you change this situation?

If you want to see balance in the kind of press doctors have been getting, then the media has to provide more coverage for and emphasize doctors who are mainstream, take insurance or charge reasonable fees (e.g. Dr. Cathryn Harbor), are willing to treat patients longer term with antibiotics based on case studies and research, and monitor and care for patients diligently.

We need more experienced doctors to come forward and publish their case studies and conduct new research on longer term antibiotics and other treatments. We need to have the best doctors work on our problems from the beginning and give them more positive exposure, not less. Otherwise, the only kind of story people hear will be the syndicated one which is presented to them across the country in sound bites by Tsouderos and others.

As patients we have our own job to do: Those of us whose symptoms have improved from treatment should be informing people of the positive aspects of treatment and how it has improved our quality of life - and how it has helped many of us return to work and the active lives we had before getting bitten by ticks.

Emphasize the positive. Let people know how treatment has helped you and write and talk about the importance of more research and clinical trials on different treatments for post-treatment Lyme disease. Get the word out there and blog about it, and ask your doctor to work with others and publish research.

This controversy seems never ending and I want it to stop, but things won't change unless what we're doing changes.

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Monday, July 11, 2011

0 Blog Log: Retraction Watch

Readers might be interested in the blog, Retraction Watch (it's listed on my right sidebar, too, and not just in this entry).

Retraction Watch is a blog with two authors - namely Ivan Oransky, the executive editor for Reuters Health, and Adam Marcus, the managing editor for Anesthesiology News - who write about scientific papers which are fully or partially retracted from different journals.

Retraction - to those uninitiated into the ways of scientific publishing - means that the authors of the paper are either found to have faulty data and/or conclusions for their paper or report it themselves, and the paper is removed.

To give a more involved definition from Wikipedia:

"A retraction is a public statement, by the author of an earlier statement, that withdraws, cancels, refutes, diametrically reverses the original statement or ceases and desists from publishing the original statement. Retractions may or may not be accompanied by the author's further explanation as to how the original statement came to be made and/or what subsequent events, discoveries, or experiences led to the subsequent retraction. They are also in some cases accompanied by apologies for previous error and/or expressions of gratitude to persons who disclosed the error to the author."

So today's Retraction Watch entry, "So how often does medical consensus turn out to be wrong?", is of particular interest to those who question the utility and basis for medical and clinical treatment recommendations.

Here is an excerpt:
"In a quote that has become part of medical school orientations everywhere, David Sackett, often referred to as the “father of evidence-based medicine,” once famously said:

Half of what you’ll learn in medical school will be shown to be either dead wrong or out of date within five years of your graduation; the trouble is that nobody can tell you which half–so the most important thing to learn is how to learn on your own. 
Sackett, we are fairly sure, was making a wild estimate when he said ”half.” But a fascinating study out today in the Archives of Internal Medicine suggests that he may have been closer than any of us imagined."
With that, you know we're off to a good start...

Read more at Retraction Watch >>>

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Sunday, July 10, 2011

2 Looking At Camp Other Blog In A Different Way

I don't know how many of my readers are aware of this feature of  Blogger - not everyone's blog is set up this way, where you can change how you view the content.

Try this link out for fun:
(I don't know if it works on mobile; suspect it's web-only)

Note that you can change the format of the blog entries listed by using the pulldown menu in the upper right corner.

I think "flipcard" and "timeslide" are the two best formats, the other ones are not as interesting or useful.

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5 Google Trends On Lyme Disease

I have been having fun with this specialized search tool on Google called Trends, and also an advanced trend tool, Insights. You might want to give them a try here:

In particular, I've been looking up "Lyme disease" and "Borrelia burgdorferi" and breaking down the search into different data sets by region.

Check this out...

Between 2005 and 2010,  of all worldwide Google searches related to Lyme disease, these were the top keyword searches made:

Notice that most people worldwide have been interested in knowing about Lyme disease symptoms, ticks, and treatment - with tests weighing in at #9.  Some unfortunate people do not know how to spell  "Lyme disease" properly.

Now, take a look at this... Here is a list of the top ten worldwide keyword searches related to Lyme disease which are on the increase between 2005-2010:

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Wednesday, July 6, 2011

5 Fibroblasts And Lyme Disease: Sample Studies

One of the indications that Lyme disease may cause a persistent infection would be if it were intracellular and not just an extracellular obligate parasite. There are studies which show that Lyme disease spirochetes can be intracellular - at least in passing - in fibroblasts.

Fibroblasts are important cells to study in relation to Lyme disease and other diseases.

Mouse fibroblasts in cell culture
Fibroblasts are the most common cells of connective tissue in animals as well as humans. Tendons, blood, cartilage, bone, adipose tissue, and lymphatic tissue are all places where one will find fibroblasts and in many cases are  tissues where Borrelia burgdorferi likes to hang out.

Fibroblasts make collagens, glycosaminoglycans, reticular and elastic fibers, glycoproteins found in the extracellular matrix and the cytokine TSLP. On a more general note, they synthesize the extracellular matrix and collagen, the structural framework (stroma) for animal tissues, and play a critical role in wound healing.

To get a good idea of where fibroblasts are found in the human body, refer to this diagram:

In the above diagram:

epithelial cells = tissues which line the cavities and surfaces of structures throughout the body, and also form many glands. Functions of epithelial cells include secretion, selective absorption, protection, transcellular transport and detection of sensation.
basement membrane = a thin sheet of fibers that underlies the epithelium, which lines the cavities and surfaces of organs including skin, or the endothelium, which lines the interior surface of blood vessels.The primary function of the basement membrane is to anchor down the epithelium to its loose connective tissue underneath.
endothelium = the thin layer of cells that lines the interior surface of blood vessels.
interstitial matrix = a type of extracellular matrix found in interstitial connective tissue, characterized by the presence of fibronectins, proteoglycans, and different types of collagen.

A study from 2007, Fibroblasts as novel therapeutic targets in chronic inflammation,  has this to say about fibroblasts in its abstract:
"A characteristic feature of many chronic inflammatory diseases is their persistence and predilection for certain sites. The molecular basis for such tissue tropism and failure of the inflammatory response to resolve has until relative recently remained obscure. Recent studies have strongly implicated fibroblasts as cells which contribute to disease persistence and which help define anatomical location. Therefore fibroblasts make an attractive therapeutic target as they help orchestrate the inflammatory infiltrate. Current anti-inflammatory therapies target immune cells in an attempt to inhibit the production of pro-inflammatory mediators. However an equally important target is the active induction of pro-resolution programmes responsible for the resolution of inflammation. Fibroblasts are likely to be an important source of these anti-inflammatory mediators. Therapeutic manipulation of fibroblasts and their biologically active products is an emerging concept in treating cancer and is likely to provide a novel method to achieve improved control of chronic inflammatory disease." [1]
Fibroblasts are likely to be a source of anti-inflammatory mediators, but they could also be a home for invading pathogens.

In yesterday's paper outline, Interaction of of Borrelia burgdorferi in coculture with human fibroblasts, the results stated:
"Electron micrographs showed borreliae which were able to attach to the fibroblast membrane through protein bridges. Single spirochetes seemed to pervade fibroblast cytoplasm by invagination surrounded by an intact fibroblast membrane."
This recent research indicates that Borrelia burgdorferi (and afzelii) spirochetes attach to fibroblasts and individual spirochetes enter the cytoplasm by invagination while the fibroblast membrane remains intact.

Here, invagination means just what you imagine it would be: A single spirochete can enter the wall of the fibroblast without disrupting its integrity and happily live within its cytoplasm.

The conclusion reflects this statement:
"The interaction of B.b.s.s. and B. afzelii with human fibroblasts was verified by electron microscopy. Fibroblast integrity was not disturbed by borreliae. Intracellular accumulation of spirochetes was not detectable." [2]
So according to this research, single spirochetes enter fibroblasts without disturbing the fibroblasts, and there was no evidence that more than one spirochete was found within the fibroblasts. I'm taking this to mean that spirochetes neither entered fibroblasts en masse nor did they find any reproducing spirochetes inside fibroblasts. It doesn't mean that isn't what might happen, but such behavior was not observed.

Another study was conducted in the same year, in Poland, in 2010, Interactions between Borrelia burgdorferi and Mouse Fibroblasts, and this study states more happens within those fibroblasts:
"Electron microscopic studies reveal consecutive stages of B. burgdorferi spirochetes penetration to mouse fibroblasts in vitro. It has been observed, as a first step attachment and engulfment of spirochetes followed by formation of vacuoles. After 48 hours of infection, vacuoles of fibroblastic cells have been seen full of B. burgdorferi bacteria and latter they have been released from infected cells to extracellular space. It can be the evidence that B. burgdorferi multiply intracellulary."[3]
Here the authors have stated that vacuoles within fibroblasts were full of Borrelia burgdorferi, and that was evidence that Borrelia burgdorferi multiplies within fibroblasts.

What portion of their lives Borrelia burgdorferi spends within fibroblasts remains to be seen, but if they spend any amount of time as intracellular obligate parasites and not just extracellular ones, this could explain why infection may be persistent.

Earlier studies on Borrelia burgdorferi in relation to fibroblasts have been completed, some of which indicate that perhaps Borrelia burgdorferi does not survive inside fibroblasts very long and instead destroys them. A 2001 study,  Insights from a novel three-dimensional in vitro model of lyme arthritis - Standardized analysis of cellular and molecular interactions between Borrelia burgdorferi and synovial explants and fibroblasts, states the following in its paper:
"Results: Both culture systems proved to be stable and reproducible. The host cells and spirochetes showed high levels of viability and maintained their physiologic shape for > 3 weeks, Bb invaded the synovial tissue and the artificial matrix in a time-dependent manner. Host cells were activated by Bb, as indicated by the induction of interleukin-1 beta and tumor necrosis factor alpha. Electron microscopic analysis revealed Bb intracellularly within macrophages as well as synovial fibroblasts, suggesting that not only professional phagocytes, but also resident synovial cells are capable of phagocytosing Bb. Most interestingly, the uptake of the spirochetes appeared to cause severe damage of the synovial fibroblasts, since the majority of these cells displayed ultrastructural features of disintegration.

Conclusion: A novel 3-D in vitro model has been established that allows the study of distinct aspects of Lyme arthritis under conditions that resemble the pathologic condition in humans. This reproducible, standardized model supplements animal studies and conventional 2-D cultures. The disintegration of synovial fibroblasts containing Bb or Bb fragments challenges the concept of an intracellular persistence of Bb and may instead reflect a mechanism that contributes to the inflammatory processes characteristic of Lyme arthritis."
Is this a reasonable conclusion to draw, based on this in vitro study? What other studies challenge the concept of intracellular persistence of Bb?  What about findings from other studies including Klempner's earlier study on not only fibroblasts, but Borrelia burgdorferi's intracellular relationship to other cells?

In a 1992 study, Fibroblasts Protect the Lyme Disease Spirochete, Borrelia burgdorferi, from Ceftriaxone In Vitro, stated this in its abstract:
"... The ability of the organism to survive in the presence of fibroblasts was not related to its infectivity. Fibroblasts protected B. burgdorferi for at least 14 days of exposure to ceftriaxone. Mouse keratinocytes, HEp-2 cells, and Vero cells but not Caco-2 cells showed the same protective effect. Thus several eurkaryotic cell types provide the Lyme disease spirochete with a protective environment contributing to its long-term survival."
Later on, within the study, the following statements are made:
"One of the regimens most commonly used clinically for treatment of Lyme disease is administration of ceftriaxone for 14 days. Our time course experiments showed that human skin fibroblasts can protect B. burgdorferi from ceftriaxone for 14 days. It will be of interest to examine the maximum duration of this protective effect."
"It has been previously demonstrated that B. burgdorferi penetrates endothelial cell monolayers and can be observed inside and between these cells; however, the viability of those potentially intra- and intercellular spirochetes was not assessed."
How many studies have been conducted since this study to see if spirochetes survive inside fibroblasts while exposed to more than 14 days of ceftriaxone? 28 days? 42 days?

Has anyone completed repeat studies which show Borreliae spirochetes surviving and replicating inside of other cell types?

How many intra- and intercellular spirochete studies have been completed, and what were the results?

A later, 1993 study by Klempner had this to say in its abstract:
"The ability of Borrelia burgdorferi to attach to and invade human fibroblasts was investigated by scanning electron and confocal microscopy. By scanning electron microscopy, B. burgdorferi were tightly adherent to fibroblast monolayers after 24-48 h but were eliminated from the cell surface by treatment with ceftriaxone (1 μg/mL) for 5 days. Despite the absence of visible spirochetes on the cell surface after antibiotic treatment, viable B. burgdorferi were isolated from lysates of the fibroblast monolayers. B. burgdorferi were observed in the perinuclear region within human fibroblasts by laser scanning confocal microscopy. Intracellular spirochetes specifically labeled with monoclonal anti-flagellin antibody were also identified by fluorescent laser scanning confocal microscopy. These observations suggest that B. burgdorferi can adhere to, penetrate, and invade human fibroblasts in organisms that remain viable."[6]
What do all the studies on Borrelia's interaction with fibroblasts to date suggest about its intracellular behavior? Is it possible that this is a major cause of some patients' persistent symptoms - even after antibiotic treatment?

This is only a sampling of studies on Borrelia burgdorferi and fibroblasts - what is needed is a meta analysis of the data on this phenomenon and further studies to confirm Borrelia burgdorferi's intracellular nature.

With confirmation of Borrelia burgdorferi's intracellular nature and its proclivity for fibroblasts, new treatments could be developed that help patients more effectively fight off infection.

[1] SJ Flavell, TZ Hou, S Lax, AD Filer, M Salmon, and CD Buckley. Fibroblasts as novel therapeutic targets in chronic inflammation. British Journal of Pharmacology. 153(S1): S241–S246.March 2008.
[2] Interaction of of Borrelia burgdorferi in coculture with human fibroblasts. International Conference of Lyme Borreliosis and Other Tick-borne Diseases. 2010.
[3] Chmielewski T, Tylewska-Wierzbanowska S. Interactions between Borrelia burgdorferi and Mouse Fibroblasts. Polish Journal Of Microbiology. Volume: 59 Issue: 3 Pages: 157-160. 2010.
[4] Franz JK, Fritze O, Rittig M, Keysser G, Priem S, Zacher J, Burmester GR, Krause A. Insights from a novel three-dimensional in vitro model of lyme arthritis - Standardized analysis of cellular and molecular interactions between Borrelia burgdorferi and synovial explants and fibroblasts. Arthritis and Rheumatism. Volume:44 Issue:1 Pages: 151-162 Jan. 2001
[5] Kostis Georgilis, Monica Peacocke, and Mark S. Klempner. Fibroblasts Protect the Lyme Disease Spirochete, Borrelia burgdorferi, from Ceftriaxone In Vitro. Journal of Infectious Diseases. Vol. 166, pp. 440-444. 1992.
[6] Mark S. Klempner, Richard Noring and Rick A. Rogers. Invasion of Human Skin Fibroblasts by the Lyme Disease Spirochete, Borrelia burgdorferi. The Journal of Infectious Diseases. Vol. 167, No. 5 pp. 1074-1081.  May 1993.

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Monday, July 4, 2011

0 Abstract: Interaction of Borrelia burgdorferi in coculture with human fibroblasts

I haven't seen this paper mentioned elsewhere - this is from a conference held last year. Need to find full text - not available on ASM or Scholar...

Interaction of Borrelia burgdorferi in coculture with human fibroblasts 
Daniel Wilfinger, Gerd Leitinger, Anna Maria Pabst, Helmut Schaider, Elisabeth Aberer

Kurzfassung/Background: B. burgdorferi (B.b.) can be recovered long after initial infection from antibiotic-treated patients; a protective effect of fibroblasts was assumed. Outcome of previous studies differ whether spirochetes are able to invade fibroblasts. Skin fibrosis has repeatedly been observed in European chronic Lyme borreliosis. So the aim of our study was to examine the interaction of B.b. with fibroblasts in coculture ultrastructually and to investigate key factors for fibrosis such as transforming growth factor ß (TGF-ß) and the production of type I collagen.

Materials and Methods: Human skin fibroblasts were propagated in Dulbeccos’s modified medium at 37°C and 5% CO2 up to 10 5 cells per culture. Bb sensu stricto and B. afzelii were cultured at 34°C in BSK-H medium up to 10 8 cells per culture. Borreliae and fibroblasts were then coincubated in RPMI medium at 37°C for 14 days. Cocultures and fibroblasts only were harvested between 2 and 14 days 3-4 times, fixed in glutaraldehyde and prepared for electon microscopy analysis. Supernatants were investigated for TGF-ß by ELISA. mRNA levels for type I collagen were measured by real time PCR.

Results: Electron micrographs showed borreliae which were able to attach to the fibroblast membrane through protein bridges. Single spirochetes seemed to pervade fibroblast cytoplasm by invagination surrounded by an intact fibroblast membrane. Structural changes of extracellular borreliae due to the adverse culture condition were observed. Shedding of outer membrane blebs forming granules and tubules were seen as well as cystic degeneration of borreliae.

After 2 days of coculture with B.b.s.s. the total amount of TGF-ß in the supernatants was approximately the same as in fibroblast-cultures, after 14 days of coculture production of TGF-ß was decreasing in cocultures with B.b.s.s.. In supernatants of cocultures with B. afzelii TGF-ß was not detectable at any time.

The mRNA-levels for type I collagen were elevated after 2 days of coculture with B.b.s.s. as well as in cocultures with B. afzelii in comparison to fibroblast-cultures. After 7 days the mRNA-levels for type I collagen were decreasing in cocultures in comparison to fibroblast-cultures, a stronger decrease was observed in cocultures with B. afzelii.

Conclusions: The interaction of B.b.s.s. and B. afzelii with human fibroblasts was verified by electron microscopy. Fibroblast integrity was not disturbed by borreliae. Intracellular accumulation of spirochetes was not detectable.

We demonstrated differences in the two species B.b.s.s. and B. afzelii concerning production of type I collagen and TGF-ß. In contrast to cocultures with B.b.s.s. TGF-ß was not detectable in cocultures with B. afzelii at any time. In line with these findings in cocultures with B. afzelii a stronger decrease of collagen production was observed in comparison to cocultures with B.b.s.s. after 7 days of coculture. The elevation of mRNA-levels for type I collagen in cocultures after 2 days is confirmed by literature: Scleroderma-fibroblasts also show an increase in collagen production after 2 days of culture.

Schlagwörter/Keywords : Borrelia, B. burgdorferi sensu stricto, B. afzelii, electronmicroscopy, morphology, TGF-ß, mRNA collagen, morphea, fibrosis, ACA
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Sunday, July 3, 2011

0 Blog Log: Spirochetes Unwound on Lymph Nodes and B cells

Quickly posting this fascinating entry on Spirochetes Unwound that you might want to read:

Does Borrelia burgdorferi cause an inadequate antibody response by altering B cell activation in the lymph node?

One of the characteristic features of Lyme disease is lymphadenopathy or swollen lymph nodes. It's not too surprising when a lymph node draining a site of infection swells. However when investigators looked at the lymph node draining the inoculation site of Borrelia burgdorferi in mice, they found that the spirochete had somehow altered the course of activation of B cells producing the antibodies that targeted the spirochete.

Read more at the below link:
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Friday, July 1, 2011

19 Admin Update: Holiday break & Request For Topics

I've been pounding the keys pretty heavily in the past couple days on commentary, and after taking a break for a few days, I would like to get back to discussing more of the science of Lyme disease.

I have some topics in the pipeline I can write about, but I'm putting out a request for feedback here:

What Lyme disease and other tickborne infection topics would you like to know more about?

Please leave your topics in comments - your top three choices if you have them, but one is okay, too.


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9 Recap Of Dr. Zemel and Dr. Cameron Chat

I'm going to be posting comments here during the course of the chat, then offer additional feedback here afterwards.

So far, this is off to a slow start. I don't know if it's the live chat software or if the servers are flooded with Lyme disease patients, but it's 10 minutes in and we barely have introductions. Dr. Cameron apparently wasn't logged in or having trouble logging in.

Okay, now things are moving along, and questions about testing are being posted by the audience. Questions on how to test for Lyme disease and on seronegative Lyme disease.

(I think that the servers are really busy - huge lag time on my end. I emailed my questions in advance, and I don't know if they are taking a combination of emailed questions or live - what is the deal here?)

Not that Milton! We said
Milton Carrero!
Milton Carrero, live chat moderator just wrote, "Because the questions are so many, and often similar I'm trying address the most prevalent topics associated with Lyme disease" - I suspect only a small fraction of questions and comments that got emailed or posted are showing up here and they may not ever pick mine. Or yours.

Okay, now we're getting a mix of questions and answers on different topics, some personal and some general. One man asks about the relationship between lipogranuloma cysts and late stage Lyme disease, a good question about the existence of chronic Lyme disease being investigated by an NIH study, the ineffectiveness of oral antibiotics for neurological Lyme disease, one mother's question about the relationship between her daughter's symptoms of anxiety and depression after Lyme disease...

Is Lyme disease underreported, why not continue to treat the patient if he is suffering, what is the role of coinfections, treatment approach by each organization, question about neurological testing... It's hard to keep up now, and the questions and answers are a jumble.

Okay, it looks like it's wrapping up now... Dr. Zemel has to leave even though Milton said an extra 15 minutes could be extended for the live chat.

My questions never made it into the chat - did any of yours?

In case you're wondering, here is a copy of what I sent out:

Mr. Carrero, I'd like to ask the following questions of Dr. Zemel and Dr. Cameron for Friday, July 1, chat on Lyme disease:

For Dr. Zemel, I have the following questions:

1) Since there is evidence that Borrelia burgdorferi can be intracellular and studies indicate a small number of spirochetes can survive antibiotic treatment, what further studies can be conducted to provide evidence of persistent post-antibiotic infection in human hosts? Are there any currently being done which address these issues?

2) What mechanisms does Borrelia burgdorferi use which lead to immune dysregulation in the human host, and what research do you know of being conducted now that could determine how to prevent immune dysregulation in the infected human host?

For Dr. Cameron, I have the following questions:

1) Do you and other members of ILADS compare case studies and have you been working on conducting your own clinical trials based on those case studies? Lyme patients are sorely in need of more research for effective treatment and hopefully shorter term treatment.

2) Have you and other members of ILADS considered writing a detailed, scientific book with citations that explains for both public and medical professionals why your treatment guidelines are more in line with the state of the science on Lyme disease? If not, would you? It would be great to have a better understanding why long-term treatment is an effective approach for a number of patients beyond their own success stories.

Thank you,

Camp Other

My general thoughts about the chat:

I think that a live, in-person presentation of the material would be more effective than the live chat presentation. One thing which kept happening is that even with leaving audience participation limited, questions and answers to those questions were being posted out of sync and hard to follow.

The answer to a previous question asked minutes ago would show up directly after a question which was just posted, making it difficult for the audience to line up questions and answers.
In a real time, in-person presentation, an answer would immediately follow a question. I would have preferred something along the lines of streaming video with a split screen that looked like a Presidential debate if I have to watch something like this again.

It's not clear to me from where Milton was drawing his questions at all times. Sometimes they seemed to be taken from email, and at other times from the live chat box. I wish that the Morning Call could put together a page showing all of the questions they'd been asked because I (and I'm sure others) are curious about what they are - and perhaps leave it up to Dr. Zemel and Dr. Cameron to address them in writing at a later time either for the Morning Call or elsewhere.

At any rate, my questions did not get asked. I'm wondering how much success I would have if I wrote the doctors directly.

Okay, comments on what was said:

"Dr. Lawrence Zemel: Approximately 10 percent of people who have had Lyme Disease will develop persistant symptoms following appropriate treatment. Most of these patients are no longer considered infected. Previous research has shown that at least 50 percent of people with "chronic Lyme Disease" never had Lyme Disease in the first place. We as physicians are obligated to treat these patients in the most humane and safe way possible."

Dr. Zemel, please provide references and citations for your statements. Up to 10 percent of early cases of infection have resulted in treatment failure and by extension, persisting symptoms. In a number of studies, the authors retreated individual patients - in some cases, with IV antibiotics when the study was based on oral antibiotics. They went on to improve, when they hadn't improved earlier. Do you call this a discrepancy, or is this a case where a garden variety Lyme disease infection became neuroborreliosis and researchers decided to give the patient additional treatment? Consider the real life scenario of a patient who fails early oral antibiotic treatment and does not go on to receive additional treatment when symptomatic. How do you differentiate between an individual case which requires more treatment versus one which has immediately become an autoimmune case?

Can you please cite evidence and research on how many patients with Chronic Lyme disease never had Lyme disease to begin with? I'd like to know more about that research.

It seems to me that between the IDSA Lyme disease guidelines panel's article in the NEJM and your comments that you tend to focus on this group of patients who never had Lyme disease in the first place. I know nothing about this group. Please focus on those of us who have had it and conduct more research for effective treatment for us. We deserve humane, safe, and effective treatment.

"Dr. Lawrence Zemel: Dr Cameron is correct: early treatment with antibiotics may blunt an antibody response, but at that point, no further treatment is needed."

But what about early treatment which is inadequate? Dr. Zemel, you're making an assumption that everyone who gets treated early has had enough antibiotics for a long enough duration of time. If a patient only receives 10 days of doxycycline - which is what some patients receive from their doctors (and not 21-28 days of oral antibiotics) is that enough? What if the patient has neuroborreliosis and they only receive a short course of doxycycline? What if they are allergic to doxycycline - could they have treatment failure from having had a shorter course of a third line choice which was not the most effective antibiotic to use for Borrelia burgdorferi?

A patient, Steve Hollingworth, had this to say:

"The NIH's study brief at actually says "It is currently unknown why some patients continue to have symptoms. One possibility is that the antibiotics have not successfully gotten rid of all of the bacteria. Current tests for Lyme disease cannot tell whether the bacteria have been successfully eliminated from the body." Care to comment on that government statement?"


"In particular, how does the doctor expect an infection in the brain by the Lyme spirochete to be eradicated by oral antibiotics, when no appropriate oral antibiotic is capable of crossing the blood-brain barrier?"

Go Steve! Please keep asking these kinds of questions! This is the line of questioning which is sorely needed in these discussions.

Sadly, they never did answer your question about the NIH, did they? But you got this response from Dr. Zemel on your second one:

"Dr. Lawrence Zemel: Steve, CNS infections are treated with intravenous antibiotics. Thank you for sharing the other information."

Steve, I take it that this answer was inadequate for you? It was for me. While Dr. Zemel is technically correct, he is answering the letter of the question and not the spirit of it. His response didn't address my concern that a number of cases of neuroborreliosis are missed in diagnosis and not treated adequately. Dr. Brian Fallon has cited research which shows a relationship between neuroborreliosis and the development of chronic, persisting symptoms. Diagnosing and treating neuroborreliosis early on seems key to me in preventing persisting symptoms.

Backtracking a bit, I'd like to make a comparison here on the responses both doctors gave:

"Dr. Lawrence Zemel: There are at least 3 studies that demonstrated the lack of benefit from the use of long-term antibiotics, suggesting that persistent symptoms are no longer antibiotic sensitive.

Daniel Cameron: Dattwyler published several papers on Late Lyme disease with success. Donta also described successes, The original Logigian papers on neurologic LD also described successes. The Krupp clincal trial supported treatment."

Dr. Cameron, you get points for citing names for research. Dr. Zemel, given my knowledge and experience in the Lyme world, I know which studies you are likely to be referring to - but for the sake of the audience, please give names and citations for your studies.

I often wonder why in mentioning any studies on long-term antibiotic use, most of the media does not mention Dattwyler's research - given he is a member of the IDSA and has done a lot of Lyme research. Same goes for Logigian, who has cowritten work with Dr. Steere.

Biostatisticians such as Alison Delong have analyzed the raw data and data reporting on the clinical trials and studies related to the 2006 Lyme disease guidelines and came to the conclusion that while the studies were well designed, the data could be finessed in different ways and extended antibiotic treatment did, in fact, help a sub-population of the groups studied.Her team concluded that more research is necessary - something I've been saying all along.

Further discussion by both of you about the data on this sub-population would be very insightful for us all.

"Daniel Cameron: The three trials -Klemner's and Fallon describe patients ill an average of 4.7 to 9 years after treatment failures. Patients this severe for this long need much more support and treatment than was offered in the trials."

Dr. Cameron, where are these patients now? How are they doing? Were they on any treatment after the trials? Has anyone followed up on them?

Time for another comparison, this time on the issue of if Lyme disease is underreported:

"Dr. Lawrence Zemel: Most likely under reported. Estimates are that Lyme Disease may be two to three times more prevalent than the CDC data

Daniel Cameron: There are at least 10 time more cases than the 30,000 cases reported to the CDC per epidemiologist projections. The chief epidemiologist in Connecticut estimate in testimony there are 24 times the numbers in their state."

So, guys, you both agree on something: Lyme disease IS underreported, anywhere from 2 times the reported number of cases are out there on upwards of 10 times. What about the citation by the CDC of there being 6-12 times the number of reported cases in highly endemic areas?

Could we please hire more epidemiologists and expand surveillance? I noticed it's getting the lowest amount of funding from the NIH. Can you shift funding from another area even if funding isn't increased for 2012? I'd like to aim for a more accurate estimate here if nothing else.

"Dr. Lawrence Zemel: Dr Cameron's data is pure speculation. Current testing for the Lyme bacteria picks up all spirochetes in North America, at all commercial labs. One lab in California has not been shown to produce reliable results."

Dr. Zemel, please provide citations and research to support your claims. Last I checked, research indicated that Borrelia lonestari is not picked up by standardized lab tests for Lyme disease, and according to Durland Fish, neither is Borrelia miyamotoi. There may be other strains which have yet to be discovered which are not picked up.

I'm hoping that Dr. Ben Luft's research will lead to better testing in the future.

"Dr. Lawrence Zemel: Chris: Persistent symptoms may represent earlier tissue damage even though the bacteria is gone. Futher more, antibodies to the Lyme bacteria may be toxic. Persistent symptoms do not necessarily mean ongoing infection."

Dr. Zemel, can you explain how to detect evidence a patient has tissue damage, persistent infection, or a combination of both?

In stating that "antibodies to the Lyme bacteria may be toxic", could you explain more to me and everyone else reading along? This sort of statement requires clarification and sounds off a cause for concern in everyone not knowing what you mean.

"Daniel Cameron: Many of these chronically ill patients remain sick. Symptomatic treatment with pain medication, Lyrica, Neurontic etc often fail. Antibiotics have helped many of these patients."

Dr. Cameron, do you have a record of case studies on these patients? Have you conducted any larger scale studies on the treatment of post-treatment Lyme disease patients (to use Dr. Maloney's term, which is growing on me) which show which patients receive benefit from pain medication and which fail?

I'd be curious to know, because some subset of patients I know of have received some relief from pain medication while others have not. Do they have different conditions? I have also found some people have had abdominal pain and other pain is relieved by use of small doses of specific antidepressants and tranquilizing medications such as Ativan. Any comments on this?

"Daniel Cameron:
Krause first introduced the concept that Babesia and Lyme together can lead to a severe presentation."

True. Krause also wrote the Babesiosis treatment guidelines for 2006, if I recall correctly, and acknowledges that Babesia can relapse and may need additional treatment - especially in immunocompromised patients.

"Dr. Lawrence Zemel: Coinfections do not interfere with diagnostic testing. If patients have high fever and other flu like symptoms, then tests for anaplasma and Babesia are indicated."

You know what? This is a good response. But time and again, what I have noticed is that the reasonable response the ID doctor gives is not what is happening with people who are showing up to their primary care physician or urgent care clinic. Based on patients' own self reporting, what I hear about are people who were not accurately diagnosed early on by their family doctor and went on to develop more severe symptoms

If the agreed upon mantra between ILADS and IDSA doctors is "early treatment usually leads to success", Dr. Zemel, what is your organization doing to ensure patients get diagnosed and treated early on for both coinfections and Lyme disease, since coinfections can increase the severity and duration of symptoms?

"Dr. Lawrence Zemel: IDSA recommends oral antibiotics for 10-21 days for early Lyme Disease, one month for Lyme arthritis, and intravenous antibiotics for CNS disease or persistent arthritis."

Dr. Zemel, why is the treatment range such a wide number of days? How does a clinician make the decision to use 10 days versus 21 days? What if 10 days doesn't work - is retreatment advisable then?

If someone takes the recommended 2 tabs of doxycycline after a tick bite as prophylaxis, does that prevent a seropositive test from developing later if the prophylactic treatment fails and the patient goes on to develop Lyme disease later? This is important to know, and to let doctors know not to rely to heavily on tests and look at the clinical picture.

"Dr. Lawrence Zemel: Dr Cameron, while physicians have a right to treat with antibiotics, they have a responsibility to practice medicine in the safest way possible, following established scientific principles. Avoiding science is not in society's best interest."

I agree with this statement on face value. But I don't always agree with the implied statement behind it, which is, "long-term antibiotic treatment is not safe and is not scientifically supported".

I think that more research is required on this issue, in terms of efficacy, and I think that long-term antibiotic use confers the same kinds of risks for many different kinds of infections. One has to weigh the risks and benefits in any medical treatment, and recognize there will always be risks. For example, I had to get a colonoscopy and sign a paper before the exam, a paper telling me there was a small chance I could die from the procedure - miniscule - but the benefits outweigh the risk. Do you make sure you don't have colon cancer or do you avoid the small chance of death? Most people would go for the colonoscopy. (No cancer was found, thankfully!)

"Dr. Lawrence Zemel: Medicine should be practiced by physicians and not by politicians. Physicians should engage in a dialogue with their patients."

Microbiologists and molecular biologists will hopefully split the difference for you all.

I'm really tired of your infighting. Jane! Stop this crazy thing! I want to get off!

"Daniel Cameron: We need many more physicians to diagnosed and treat chronic Lyme disease. We will have less chronic LD if they are recognized early. Finally, more physcians will offer more options for patient within HMO's"

Dr. Cameron, I'm going to emphasize this bit: We need many more physicians to diagnose and treat Lyme disease, period. Early on, along with coinfections, so that people can avoid persistent symptoms.

Saying that more physicians and HMOs should be participating in increased early diagnosis and treatment is a positive statement on your end for both patients and for how it reflects on ILADS, because critics have stated that as long as ILADS stands to profit from their position there is no reason for the current situation to change.

"Dr. Lawrence Zemel: Insurance companies respond to evidence based medicine. Since there is no evidence, that IV therapy beyond 4-6 weeks is effective, they should rightfully deny coverage."

Dr. Zemel, what do you do about insurance companies denying patients access to any IV therapy to begin with? Let alone beyond 6 weeks?

"Dr. Lawrence Zemel: A small vocal group of constituents should not be dictating medical care."

Oh, I agree. But what does science have to say about this? If all we have is a hypothesis and not a proven and accepted theory, is it ethical to base treatment guidelines on a hypothesis or is more research required?

"Daniel Cameron: We need more dialogue among physicians to come to common ground for the increasing number of patient who fail treatment."

Yes, I agree here, too. But first and foremost, we need more research, more meticulously reported case studies, and clinical trials using antibiotic and non-antibiotic treatments. If you've got a hypothesis you want to provide evidence for, I'd like to see both sides actually do something about it to help patients.

More treatment studies, please? And more scientific research on Bb pathogenesis, please?

Are you familiar with William Burgdorfer's "thirty years quote"? I want to hear Dr. Zemel's response to it.

"Dr. Lawrence Zemel: Lois: Most physicians are now testing for Lyme Disease if there is a reasonable likelihood that Lyme disease is present. It is probably not accurate to say that Lyme Disease is still underdiagnosed in most Lyme areas."

Do you have references and evidence to support your statements? What about patients in the southeast US? The midwest? The west coast? Canada? There are many reports patients have given of being told by doctors that Lyme disease is rare and not in their area when according to what limited epidemiological data is on record and their state health departments, Lyme disease is not rare. How do you recommend closing this gap between doctors' knowledge and knowledge of other institutions?

More Q & A:

"[Comment From Dedee]
Is it common for scientific principles to not be challenged? New discoveries cannot be made without challenging science."

"Dr. Lawrence Zemel: Dedee: I entirely agree with you. This is why scientific guidelines are continually updated. The problem occurs when the public and wayward physicians ignore the science."

It's a good question, Dedee. And Dr. Zemel, it's a good answer.

The problem is, I think treatment and diagnosis is lagging behind the science at the moment, and that right now, not enough is understood about chronic Lyme disease and Lyme disease's pathogenesis to effectively treat everyone in a timely fashion.

When one makes the statement, "We don't know what causes persisting symptoms", what that should mean is "We don't know what causes persisting symptoms". Period. The rest is speculation, and what the cause is may not be a uniform, one-size-fits-all answer. This is why I ask for more research, and I want to see more independent research from parties not invested in either "side", if there have to be sides at all.

Ah, look! This sounds like consensus. Sorta...

"[Comment From Ellen] My insurance will not cover the antibiotics my doctor prescribes and I can not afford them out of pocket. What are your thoughts on homeopathic and herbal treatments?"

"Dr. Lawrence Zemel: Ellen: I'm not aware of evidence to support alternative treatments in place of antibiotics. Can you please educate me?"

"Daniel Cameron:
Many of my patients with chronic issued try many different alternative medications. We need more research on new strategies."

I initially found it amusing that Dr. Zemel is asking for a patient to educate him on the use of alternative treatment. But then I got pissed off. As someone who is supposed to be upholding his own guidelines, if that patient needs antibiotics, he could be providing advice as to how to get authorization for antibiotics if they are medically necessary and/or advise further testing to substantiate her diagnosis for treatment. Instead, he is humoring her.

But in the end, the message I'm getting out of this: Alternative treatments are currently not evidence-based treatments for Lyme disease. Sure, people try them, and some may help with some symptoms - but we need more research on them.

"Daniel Cameron: ILADS published an evidence based guideline in 2004 reviewing the evidence. See our website at ILADS .org. We expect a new guideline soon. Many of our members are now publishing. The publication should help the dialogue."

I hope that you are providing more peer-reviewed-from-established-journal citations and references to support your guideline, and that we get to see it soon. I eagerly await the outcome of all this work you've been doing.

"Dr. Lawrence Zemel: The ILADS guidelines were reviewed by the British Health Agency and found to lack scientific credibility. Most major specialty organizations in North America and Europe have endorsed the IDSA guidelines."

Dr. Cameron, there's a reason why I said what I did above.

Interesting, Dr. Zemel. Could you please explain why each of these countries overseas have adopted IDSA's guidelines and not written their own, given that they have historically had somewhat different diseases and disease presentations? (This is becoming less the case with bird migration affecting infection distribution and rate.)

And then there are these differences in approach. Why is it in much of Europe doctors are trained to look for more cases of neuroborreliosis and treat them earlier on, whereas in the US they aren't? Recent evidence from EUCALB and your not-cited organizations state that the percentage of American-based Bb infected patients in Europe show a percentage of neurological symptoms equal to those found in European-based Bb infected patients. (It's in that recent Institute of Medicine report that was posted in April.)

Another patient weighs in...

[Comment From Julia Wagner]
Actually - while a dialogue will help, it is not uncommon in medicine to have multiple schools of thought that inform a physician, who can make the call that is best for that patient - the same approach should be used with Lyme - and physcians need to be educated that 2 schools of thought. Any scientist who vociferously opposes other thinking, is limited the potential for progress in medicine - we need to follow the science as it emerges, and not ignore or disparage this. The science just evolving last year was significant in explaining "chronic lyme" from the 13 subtrains genotyped by Dr. Luft with some having serious neuro sx and others a more limited easy to cure disease, to lymphadenopathy study finding spirochetes hiding in the lymphs as another means to evade the immune system. I so no reason why the IDSA should fight other points of view - physicians should be informed about emerging science period, and treat their patients to get them well. Chalking up all remaining symptons to "aches and pains of daily living" is not acceptable when other viable options have not been explored."

I've bolded what I particularly would want to emphasize of your good points - thank you for contributing to this discussion. We need more people to ask questions referring to the science related to Lyme disease.

PS Julia: Please have someone proofread your question or type it into Word or some other text editor to run it through spell check first. I know you didn't mean to post typos, but it makes it harder to read.

So after this, Milton asked questions about vaccines, but they went unanswered as the chat was shut down at 1 pm EST.

This is all I have to say on this for now.

What are your thoughts about it?

Refer to the original chat transcript here:,0,4675217.htmlstory

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The Camp Other Song Of The Month

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