CO Comments on "The Pseudoscience of Chronic Lyme"

During the weekend, Ed Yong, who writes for Discover magazine's Not Exactly Rocket Science blog, of alerted me on Twitter to Cassandra Willyard's blog post on The Last Word on Nothing blog - "The Pseudoscience of Chronic Lyme". Not wanting to pass up the opportunity to comment on some journalists' bungling of how to interpret the significance of the New England Journal of Medicine (NEJM) published study, Differentiation of Reinfection from Relapse in Recurrent Lyme Disease, I decided to stop by and read what Cassandra and others had to say and leave a few comments.

So far, commenters are asking good questions and pointing out some logical oversights in what we have read, which is constructive.

I don't know that I recommend it for casual reading for a number of chronic Lyme disease patients, though - particularly if you are in a headspace where you are currently very angry about your condition being treated dismissively and can't hold up to reading anything which is skeptical about the existence of chronic Lyme disease. But I will say that if you can handle it, it might be worth it to stop by and periodically read the comments.

So far, I've left two comments on Cassandra's blog in response to her original post and another commenter:

"I’ve been following the issue of chronic Lyme disease closely for a number of reasons, and anecdote aside, think that the situation surrounding the diagnosis and treatment of Lyme disease and other tickborne diseases is more complex than most of the media has led the public to believe.

I hear that Lantos – like Dr. Lawrence Zemel of the Infectious Disease Society of America – has more or less stated that half of those patients who claim they have chronic Lyme disease have no evidence of having prior or active Lyme disease. Lantos stated, “Only 7–31% had active Lyme disease and 5–20% had previous Lyme disease,” he writes. “Among the remainder, 50–88% had no evidence of ever having had Lyme disease. Most of these patients had either an alternative medical diagnosis or a functional somatic syndrome such as chronic fatigue syndrome or fibromyalgia.”

If this is in fact the case, then we are still looking at up to 51% of the patient population in this group as either having had Lyme disease or currently having it – meaning that up to little more than half of patients’ persisting symptoms do correlate with evidence of having Lyme disease.

It is this population of which I am a part of, having had a textbook case of Lyme disease – known tickbite in endemic area, an EM rash, flu-like illness, severe joint pain and swollen lymph nodes – the whole nine yards – only to be followed by years of ongoing symptoms I did not have pre-infection.

So, when someone brings up the pseudoscience of “chronic Lyme disease”, understand that I might get a little testy because it seems almost inevitably, the cases which are highlighted in skeptical discussions are those Lantos states do not have evidence of Lyme disease. Whether that is accurate or not, what about the rest of us? (Side note: chronic fatigue syndrome and fibromyalgia are problematic diagnoses in their own way, too, as they are of unknown etiology.)

I want to know as much as the next person exactly what has led to persisting symptoms. After doing the research on my condition to the extent I have, I’m coming to the conclusion that more research is necessary. I am skeptical about their being “sides” to this debate in the first place and also think science has not come to a full understanding about the process behind why we have persisting symptoms.

Embers et al’s recent study on persistence of Borrelia burgdorferi after antibiotic treatment in Rhesus macaques brings up the question of persistent infection after antibiotic treatment. More research is required on this, and persistence studies such as an NIH-NIAID xenodiagnosis study where patients with chronic Lyme disease are bitten by lab-raised ticks in order to see if they pick up the infection are underway. On the autoimmune angle for finding cause, Bockenstedt recently published a paper showing gfp concentration of Borrelial antigens in tendon* tissue in mice, and the hypothesis is spirochetal antigens cause persisting symptoms long term. See this Research Blogging blog post for more info: http://spirochetesunwound.blogspot.com/2012/11/inflammatory-spirochete-debris-left.html

So one cannot avoid that persisting symptoms after initial infection and treatment or delayed treatment is an issue; the research is there and being conducted on it.

But in the meantime, people are suffering, and voting with their feet: The vast majority of patients in my situation think there is something to the persisting infection hypothesis, and treat with long term antibiotics. A number of them recover and report improvement in symptoms while on treatment.

Yes, it is anecdotal – true. And it doesn’t support the outcomes of some of those small clinical trials which were conducted. But perhaps instead of dismissing them, someone could step in and collect the data on these patients (with their consent, of course) based on how they are currently being treated, what the patient base is and common factors of different subpopulations, and so on – and see if any commonalities float to the top? This could be informative, to study patients who have made the decision to accept this treatment and see how they fare."

And the second comment:

While I have not read the full text of the study yet, I agree that your logic path is one I traveled as well. An EM or “bull’s eye” rash is a key part of the case definition for acute Lyme disease – however, it’s not always present with infection, nor do all EM rashes signal the presence of infection.

Much of the media’s write-up on this study has conflated the existence of reinfection with the nonexistence of a chronic condition connected with Lyme disease – but it has also left out a huge chunk of the story about the significance of EM rashes in Lyme disease infection.

Dr. Jorge Benach of Stonybrook University has stated that if multiple “satellite” rashes show up weeks to months after initial infection, that the bacteria has disseminated. This may mean the patient needs a different course of treatment at this stage, so new rashes in this situation are important to separate from new EMs from a new infection.

Dr. Benjamin Luft has been doing extensive mapping of the genetics of different strains of Borrelia burgdorferi and has discovered some strains create a rash but no infection, some create a rash and infection, and some create no rash and infection. These strains can have varying targets within the body; varying levels of virulence.

And not long ago, Horizon Press published a book, “Borrelia: Molecular Biology, Host Infection, and Pathogenesis”, and it mentions big gaps in patient management around EM rashes: Some people who were screened to be subjects in studies were seropositive for Lyme but have never had ANY symptoms – whereas others went on to develop a case of late stage Lyme disease. (See pp. 501-502)

This is problematic for patients and doctors alike, who may have difficulty diagnosing the cause for the patients’ symptoms with no prior history/evidence of Lyme disease.
(Serology might help – but you have to suspect Lyme disease first.)

(As an aside, you might want to check out this discussion on Lymenet Europe: http://www.lymeneteurope.org/forum/viewtopic.php?f=6&t=3856 – if only because of the references offered.)

So, I am concerned about the emphasis on rashes and think either one has to suspect Lyme disease based on other symptoms and potential exposure to ticks – or we need better testing… Solid direct detection tests would be great, but we don’t have one yet. I’m waiting to see what GMU does with its nanotrapping test development… It’s antigen based; hopefully superior to existing serological tests. But again: First one must suspect Lyme, and if there is no EM rash present, where do you begin?

* That should have been "joint" tissue, not "tendon".

When I wrote these comments for their intended audience, my goal was to focus on what by their standards would currently count as evidence they relied on in order to focus on the relevance of erythema rashes in infection. I avoided discussion of other issues I could have gotten into - such as the accuracy of early serological testing and differences in antibody response during infection - because my focused comment was already long and thought these topics were not as closely related.

One thing that has changed between the time I posted these comments and now: I now have a copy of the full text of the NEJM reinfection paper. So I am in the process of reading it, examining the data, and seeing how the authors correlate their findings with chronic Lyme disease. More later...

Edited to Add: When I talk about being skeptical about there being "sides" to the debate, what I am really meaning to say is that while two sides have developed over time, the only side that really matters is the truth.