There is some heated discussion going on at CALDA's web site regarding Embers et al study, "Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection (2012)".
I wrote about this study last month and commented on some of the findings and the need for further research and confirmation of the findings in this study. (I recommend reviewing that post and comments made on it.)
CALDA's Lorraine Johnson has questioned Dr. Phillip Baker, who was Program Officer for the NIH's Lyme disease research division at the time the Embers study began (then known as Mario Phillip's study; Baker retired from NIH in 2007 and is now in charge at the ALDF), over the 12 year delay of Embers et al publishing the results of this study.
Dr. Baker himself decided to respond to Lorraine's questions and respond to a number of the comments and questions patients and advocates shared on CALDA's Lyme Policy Wonk blog.
Interestingly, a number of people have discussed this study on Lymenet Europe - with one member, Henry, questioning the use of ceftiofur when Embers study was supposed to emulate Klempner's chronic Lyme study. This issue happens to be one of of main issues Dr. Baker also raises on the Wonk blog about the Embers study. (Warning: There are seven pages of spirited discussion on this topic at LNE thus far - some of which may raise blood pressure in readers.)
To follow the discussion and see an example of different points of view over the issue of chronic Lyme disease, read here: http://lymedisease.org/news/lymepolicywonk/lymepolicywonk-was-this-important-lyme-study-hidden-for-12-years.html
In the meantime, I have submitted my own questions and comments to CALDA's web site for Dr. Baker. As of this writing, my post has just cleared moderation and I await a response from Dr. Baker.
I want some answers. Not just about oversight for how the study was designed but about the lack of treatment studies for chronic Lyme disease patients.
Even if your position is that chronic Lyme disease is not caused by a persisting Borrelia infection, there is no reason why more research cannot be completed to provide evidence that this is or is not the case in some circumstances. And even if your position is that chronic Lyme disease's persisting symptoms may be caused by other factors, there is no reason why more treatment research cannot be completed to provide evidence either for or against these factors playing a role...
First of all, I want to thank you for being here and presenting your view in the presence of Lyme disease patients who have different points of view than your own and who are at a minimum questioning your opinion about Lyme disease and at a maximum - quite angry.
This isn't an easy thing to do. I recognize that. But this is a necessary thing to do, and I wish that more dialog occurred between people with differing views even at the risk of it becoming contentious. It is often the only way opinions get aired and heard and questions get answered - even if we don't like the answers we hear.
I have a few questions for you, and hope I did not miss the boat on getting a response from you at this late hour:
1) Just so the storyline is clear: Who determined that ceftiofur should have been used in Embers et al study on NHP and is this decision something that NIH would have had to give approval - or is this a decision that would have been made at the individual level of the PI/researcher and not require any approval from the NIH? Would any independent governing scientific board outside the NIH been expected to approve of the study design including methods and materials? It seems that in order to emulate the Klempner study, the antibiotic chosen should either be the same as used in the original study or have, as you've stated, PK and PD that are pretty much indistinguishable from ceftriaxone.
2) In your opinion - and in the opinion of others at the ALDF - would you have to see studies separately completed on ceftiofur that provide you with evidence that its PK and PD in NHP are functionally equivalent to the use of ceftriaxone in humans? If these studies are conducted and they are found to be equivalent, then would you say that the results of the Embers et al study are valid? (Even if - according to your position - they don't yet prove a persistent infection/persister cells are the cause of patients' symptoms.)
3) The central point on which a lot of this debate hinges is whether or not spirochetes which remain after antibiotic treatment are viable and infectious. I've never gotten the impression that the majority of researchers out there have debated the existence of spirochetes after abx treatment - the impression I've had is that they either didn't think they were the cause of persisting symptoms in patients or did not know one way or the other if they were the case of persisting symptoms.
Parallel to demonstrated survival of some spirochetes after abx treatment, some research has indicated that a combination of Borrelial strain, host genetics, immune system response, and in some cases, molecular mimicry - may be causative factors for persisting symptoms. I myself think that based on evidence I've read to date, both persisting spirochetes and immune system changes can lead to persisting symptoms. I am particularly intrigued by HLA-DRs and variable immune response in this regard (see "HLA-DR alleles determine responsiveness to Borrelia burgdoferi antigens" by Bettina Panagiota Iliopoulou, Mireia Guerau-de-Arellano, and Brigitte T. Huber. Arthritis Rheum. 2009 December; 60(12): 3831–3840.).
My questions are:
When is the NIH-NIAID going to conduct more studies aimed towards this end? And also, if you and others are convinced that chronic Lyme disease patients are not suffering from persisting infections - why hasn't more treatment research been conducted that supports your point of view of what is or what are the causative factors for such symptoms?
Why are patients, advocates, and Lyme disease advocacy organizations having to donate money to Dr. Karen Newell Rogers and Viral Genetics to find alternative treatments to long-term antibiotics - why isn't the NIH-NIAID pursuing these alternative approaches now, if the argument is that long term antibiotics do not work and you consider them unsafe (Which in my opinion debatable in my eyes - I have personally benefited from more than the guidelines recommend - and I do not think the use for or against more abx is applicable to everyone because this is a heterogenous patient population. The patients need to be characterized into subgroups first rather than boxed into meeting CDC specific requirements before designing new trials.)?
I have been offended with the letter to the Lancet about Lyme disease patients and advocates supporting pseudoscience when so many of us have wanted to fund more research and get answers. When a number of our friends and families have donated their money to research even when they have already paid so much for treatment.
Some of the answers are already there. If more than one hypothesis is solid enough for testing, I'm for it. Test different combinations of antibiotics. Create drugs which have the anti-inflammatory properties of these antibiotics and use them as a control against combinations of antibiotics. Use higher doses of orals, if the fear of line sepsis freaks you out (it does me, and I have not had a PICC line by choice). Try testing thymus peptides and altering the distribution of B cells to see if that helps patients.
What I see as an observer is that Lyme disease treatment research has been shut down unless it's for acute Lyme disease. We need more late stage untreated Lyme disease research, and I'm with Fallon on this one - more specific neuroborreliosis research. His suggestions for those trials seem worthwhile.
But for God's sake, something has to be done. Some people are seriously impaired. I am doing somewhat better now and have my mind back to a large degree and don't need a wheelchair. But I am not yet well enough to work due to pain and fatigue with normal amounts of exertion. Something is broken there.
Dr. Baker's response to me:
So, there you have it - that's his response, and while I posted a response to the Wonk blog, because my response was too lengthy it has not been posted there. So I posted it to comments below, after an explanation of why my response was not posted there.
The moderator emailed me personally and said that I could post another 150 word comment of my choosing, but I have declined for now because I don't think what I can say in response to Dr. Baker is adequately summed up in 150 words.
There was a second comment with other content which I submitted that I later decided needed a serious rewrite before posting - I won't be posting that here now and am okay with the moderators not publishing it (good job, mods - thanks).
I just want to take a moment here to acknowledge those who left intelligent and insightful questions and comments on the Wonk blog - even when addressing someone with whom they vehemently disagree. I would like to see more dialog such as this, but even more so I would like to see more thorough education and outreach going on which deconstructs all the hypotheses behind why chronic Lyme disease patients have persisting symptoms and what research is required to resolve the debate over cause.
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