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.