Monday, August 4, 2014

Are staunch supporters of the IDSA admitting they might have been wrong all along?


A paper from the Department of Molecular Biology and Immunology from Johns Hopkins is quite remarkable, especially since Paul Auwaerter is one of the authors.  The paper presents ideas which are a complete turnaround from the previous orthodoxy promoted by this institution and this author in particular.  The entity in question is called PTLSD, post-treatment Lyme disease syndrome by the authors. The authors state they do not know the cause of the syndrome. They concede that up to 1/5 of the patients treated for Lyme disease by IDSA standards have persisting or lingering symptoms.
The authors state recruitment for clinical trials has been difficult. Why?  The only patients accepted into the studies were treated for early, classic Lyme and subsequently developed the famous 5/10 CDC IgG bands. Findings these patients is like finding a needle in a haystack.  Recent peer-reviewed literature suggests that patients with chronic symptoms tend to have poor IgM responses and never develop IgG responses. The patients we see in our clinical practices rarely have CDC positive IgG responses. Chronic Lyme studies recruit a small cohort of patients likely to be healthier than the vast majority of chronic patients.



Let me digress.  The IDSA and CDC keep insisting that patients with chronic Lyme develop 5/10 IgG bands in virtually every case. Repeating something over and over again does not make it true.

The 5/10 come from a paper written by Dressler in 1993, one year before the ill-fated Dearborn conference. This is the same Dressler that suggested IgM criteria should be 2/8 bands (sounds an awful lot like IgeneX criteria). The criteria was dismissed because Dressler’s research was based on the N40 strain of B. burgdorferi, not the B31 which has become the standard. Therefore, the “flawed” IgM standard was dismissed. Somehow, the “flawed” IgG criteria based on the same discarded strain of Lyme was allowed to become the standard and this has never changed.

The authors list possible causes of the syndrome:  autoimmune, persisting debris (dead germs) or persisting infection. Only the persistent infection hypothesis is called “controversial,” even though this is the only hypothesis backed by fact.

It is silly to have a discussion about whether animals have chronic Lyme symptoms. The authors state: “a number of prospective, randomized clinical studies demonstrated no significant beneficial effect of additional antibiotic therapy… and no evidence of presence of B. burgdorferi in patients with long-term symptoms.” 

How do they define “significant?”  Patients showed improvements in fatigue, pain and quality of life issues and Dr. Fallon the last author of the famous NIH sponsored studies believes that additional antibiotic therapy helps because there is persisting infection.  The authors claim there is no evidence of presence of B. Burdorferi. There certainly is no evidence that the spirochete is gone. The authors also note that some studies showed a decrease in fatigue. The authors seem to be arguing amongst themselves.

The authors are intrigued by the fact that one patient who had been treated for Lyme gave the germ to a tick allowed to feed on his blood.  This test seem just wrong to me.  Why wasn’t a PCR done of the patient’s blood at the same time? This procedure makes a lot more sense to me. Anyway, I am glad the authors are intrigued.

The authors concede that recent literature demonstrates the persistence of infection in mice.

This is where it gets weird. The authors talk about 3 morphological forms: spirochete, L-form, and cyst. I am I reading this right? This sounds like the ILADS’ pabulum which the same sources have spent a lot of resources on, even in recent months, discrediting.

Without this apparent change of face there would be reason to do this research or publish this paper.

These authors discuss two stages in the life cycle of Lyme: the rapid growth phase and the stationary phase. These authors commit blasphemy. The cross one more line and talk about “biofilm-like aggregates.”

In the test tube, the researchers found there are always persisters.

The purpose of the study was to show the researchers had developed a tool to help identify antimicrobials which may better able to eliminate persisters.

“Our findings may have implications for the development of a more effective treatment for Lyme disease and for the relief of long-term symptoms that afflict some Lyme disease patients.”

I am getting confused.  Was this study written by IDSA proponents or backers of the ILADS’ way of thinking?

Even in a test tube. No antimicrobial was found that could kill all the persisters.  That should be like “shooting fish in a barrel.”

In a real human being things are a bit more complex. The germs hide on the inside and outside of cells. The germs penetrate deep tissues like cartilage with minimal blood flow. The spirochetes invade a panoply of host tissues, all with different characteristics:  brain, nerves, joints, cartilage, tendon, heart, colon and numerous others.

Based on these few facts it seems outlandish to believe that a short course of IDSA sanctioned therapy is likely to eradicate all of the spirochetes.

Novel drugs like: clofazimine, daptomycin, cefoperazone, carbomycin are the best drugs for killing cysts.

Let’s not rush in – please.  Flagyl is said to have no anti-cyst activity, contradicting other work which proves the opposite. Most of these drugs are highly specialized, too potent and should likely not be used.

It seems that the science is catching up with ILADS, leaving the IDSA in it's wake.

13 comments:

Jimmy Branch said...

Very well stated, Dr J.

WLP Romania said...

can you please post the original link with the paper written by dr. Paul Auwaerter?

WLP Romania said...

http://www.nature.com/emi/journal/v3/n7/full/emi201453a.html

??

Kurt said...

I'm glad you commented on this paper. I look forward to the research from Kim Lewis's team at Northeastern, which is undertaking similar research:

http://www.northeastern.edu/news/2014/04/lewis-3qs/

Perhaps they can corroborate the effectivity of the drugs in the Johns Hopkins study.

Kenneth P. said...

Things are changing my friends. This paper coauthored by Dr. Paul Autwater basically.confirms the existence of persistent (chronic) lyme and acknowledges that current abx protocols are unable to irradicate the various forms of lyme.

It's interesting that they refer to one of the forms of lyme as the coconut form.. Now think of how hard the coconut shell is to break. I don't believe that they just pick the names they give these bacteria randomly. Is it coincidence that they named the form of the bacteria that builds a cyst around it a coconut? I think not

http://www.nature.com/emi/journal/v3/n7/full/emi201453a.html

WillowWii said...

Flagyl definitely breaks cysts. I don't think it kills Lyme but it releases it from the cysts. This is how I finally got my CDC/NYS positive test result after ten years of misdiagnosis. I took two weeks of flagyl then six weeks later tested. All my previous tests showed no lyme antibodies at all. This positive test had all IgM antibodies to the newly released bacteria. Was bit and hd the bite sight rash but my MD told me it couldn't possibly be lyme and didn't test me. I had the tick in hand. It was a dog tick.

lymie said...

This had multiple authors on the article and it seems they all added their own pieces without trying to fix the contradictions. So, I think we should not expect Auwaeter to be recanting any time soon. He wrote the negative doubting pieces, some one else wrote the other more honest stuff.

People like A. never admit to being wrong. They just get left in the dust over time looking like fools. But it takes a very long time, and in the meantime a lot of harm is done to innocent patients.

Christian said...

Much more research is needed. If you look at the history of Borrelial research papers you will find a lot of suceptibility testing done heralding some random antibiotic as extremely effective for Lyme. Yet patients are having only moderate successes. In vitro studies are not in vivo ones. Many studies in vitro say that macrolides are effective antibiotics for Lyme but in vivo, a lot of people are reporting little to no progress with macrolides. Vitro says nothing about drug dispersion into various tissues and compartments.
The authors need to present the entire list of antibiotics tested. They also need to start testing on different strains with various laboratory animals to even start making real progress into changing recommendations.

The original recommendations are still effective albeit, as with other antibiotics, they don't provide a cure. Penicillin-G, IV Cephalosporins and tetracyclines still continue to be very effective in vivo.

Nickname said...

Isn't it amazing that after all this time and money spent on Lyme research, no scientist ever bothered to put some Borrelia in a dish, wait a week, dose it with doxycycline, the IDSA recommended antibiotic that is supposedly curative in the "vast majority" of patients, and wait another week, and see what happens?

Clearly if persisters were left in the petri dish, in a human this is even more likely. I can't believe its taken all this time for the CDC/IDSA to check their work and see if doxycycline is actually curing the infection or just making sure its permanent. Incredible! How can they have been so certain of a quick cure from doxycycline when someone hadn't even done the simplest, most obvious experiment with it?

James Carl said...

Could you write an update as to how your patients have responded to mild hyper treatment. I believe you have been using this for quite some time now and it would be good information.

Paula Kozinn said...

So happy to see posts like this. We are long overdue for a bit of reality regarding Lyme diagnosis and treatment. Big changes are coming, my friends!

I cannot underestimate the value of hope.

We cannot be a strong country and society with 300,000+ new sick people a year. We need to start acting like a first world country, again.

Brian White said...

I think the weight of the obvious has become too great. Peter Kemp in England has been culturing his own Lyme for several years and he recently started doing tests of other people who had long term antibiotic treatment. He uses a high powered but vintage microscope and watches the spirochetes and string of pearls in red blood cells and in media. He has successfully cultured borellia from blood that tests negative too.

Claus-Peter Kessler MD said...

Mercury and Chronic Lyme
Patients with Lyme disease: most therapies just focus on the symptoms and fight the spirochetes without involving the order of the system of your body.
The order of the system of a mercury-sensitve person (ApoE4), what most chronic Lyme patients are, is disturbed by chronic, daily exposure with traces of mercury by ingestion, inhalation and skin penetration. The infection with Borrelia can not be correctly counteracted and faught by the disturbed immunesystem, and the burden of the Borrelia infection and the unknowing new daily exposure of mercury weakens the body even further.
Medicine wants to add information antibiotics, supplements etc., find pathological, biochemical changes of the disorder , but the information is not carried to the place where it is needed, because the body is in a dysautonomic state, is out of order, and even more highly weakened by those invaders (they even have electromicroscopic pictures of). It is like: You want to put tiles on a wall (treat Lyme) and someone is using a sledgehammer (mercury exposure) next door. It makes no sense in adding more and stronger glue (antibiotics, supplements); you have to stop the vibration of the sledgehammer first to be able to work in a field, which then is not disturbed.
The flair ups of the disease can only be explained by the incidence and level of new mercury exposure, because the level of borrelia is not changed from one hour to the next, like the symptoms change. All patients feel better with chelation, as long as the chelator doesn't contain traces of mercury, and if the exposure is stopped or drastically reduced. For possible sources of mercury read my notes.
See also:
http://lymetolimeade.blogspot.com/2011/05/general-notes-from-dr-klinghardt.html?spref=fb
Herxheimer reaction is a dysautonomic reaction to acute mercury exposure (inhalation, ingestion or transdermal), it has nothing to do with release of toxins from killed spirochetes. This is a postulate by Dr Herxheimer, not a proven fact, everyone takes for granted.
If a factory is not organized and controlled, it doesn't work.
Bring your system back in order, so that it helps to fight the disease.
That is why I teach my patients how to test for the ingredients, they are sensitive to, in each article they like to ingest, inhale or put on their skin.