A new study may help us understand why some patients get better and other don’t. This topical study: Serum Inflammatory Mediators as Markers of Human Lyme Disease Activity, was published in PLOS one-- the lead authors are from Johns Hopkins University. All published Lyme studies have had problems with patient selection. Patient groups are selected because they are supposed to have the same thing. IDSA criteria are generally used. The group in this study had early Lyme associated with EM rash. As I have discussed previously, most patients with acute Lyme do not present with a rash; and more to the point, most patients with chronic Lyme are not diagnosed in a timely fashion. Nonetheless, this study conveys important information.
This study demonstrates the exist of two distinct patient populations who have very different immunological responses to infection with Borrelia burgdorferi (Lyme) – one group has a robust response based on measurements of cytokines and markers of inflammation; the other group has a minimal immunological reaction using the same indicators. The two groups have very different clinical outcomes.
I am pleased by a change in verbiage/terminology. In this study the authors use the words PTLDS, post-treatment Lyme disease syndrome, which replaces the old term PLDS, post-Lyme disease syndrome. This small change leaves the door open to the notion that Lyme organisms may persist after treatment. And here we are dealing with acute patients treated early in the course of the illness.
The study measures molecules which moderate immune responses. The immune system is tasked with finding offending invaders, like germs, and eradicating them by a host of complex mechanisms and devices. (Seek out and destroy) This study measures the messengers that help direct the traffic of the immune system – sending signals to an assortment of cells, telling them where to go and when.
The authors note the immune system alone is unable to eradicate Lyme infection and that late-stage arthritis develops in many patients. They describe a subset of patients who develop antibiotic refractory disease 12 months or more. The dogma that host immune responses is the major factor in such cases is discussed, but, from the mouse model -- another possibility is discussed. “Delays in the generation of long-lived plasma cells (the cells that make antibodies) and a weak, largely IgM response (sound familiar) may be part of a Lyme (Borrelia burdorferi) strategy to avoid clearance.”(Yet another mechanism of survival). The authors reflect that residual antigen or infection in some treated patient may explain the persistence of symptoms, in post-treatment Lyme disease, but state: “this is a very controversial area.”
The scientists measures many molecules that traffic immune cells, with names like: CCL1 9, CXCL 19, CXCL 10, CRP, SAA, IL-1a, IL-18, IL33, IL6, TNF alpha, and others.
Two distinct responses were identified. On groups showed high levels of these markers of immune response while the other showed low levels of these markers.
One particular mediator of inflammation, IL-6 remained elevated in patients with late stage Lyme which the authors found surprising. These patients with post-treatment, symptomatic Lyme disease showed immunological evidence of persistent inflammation – or infection.
The group of patient with a high level of reaction (cytokines, chemokines) had lower WBC counts, increased liver function counts and higher levels of markers of inflammation such as CRP. This group produced Lyme antibodies, or seroconverted. This group showed clinical remission. The group with low level reactions to the same molecules did not share these features: these patients had a tendency not to seroconvert. This group of patients was more likely to develop post treatment symptoms like chronic joint pain.
This study has clearly identified a subset patient who are more likely to develop chronic Lyme disease even after IDSA recommended treatment for stage one disease. This study sheds light on why many patients are seronegative (do not make antibodies) or have weak IgM responses as we commonly see. This study lays the foundation for the development of a test which helps us predict which patients need more help early on -- those who are at higher risk for developing chronic disease.
On another note…
Another scientist’s face is displayed in a Johns Hopkins University magazine in an article which states he has beliefs contrary to the IDSA and that he believes in Lyme persiters which might respond to a drug for tuberculosis. The article say that while these ideas would not be controversial regarding tuberculosis they are very controversial when mentioned in the context of Lyme disease.
Anyone else tired of hearing the phrase "antibiotic refractory?" How do they know it is? By treating a while, symptoms still there, no more treatment. Refractory or just needs more treatment?
When will they characterize patients who do respond to antibiotics but relapse off them. Treat again, withdraw meds, relapse again. This is the most common pattern. Why aren't they studying it?
Have you investigated the efficacy of low dose naltrexone for lyme? It looks good for an immune booster. But how does one tolerate the elimination of opioids to pursue this therapy?
Really interesting. Could you give the name Researcher of the publication information for the article?
The giant misconception is that Borrelia is driving the Lyme epidemic , It isn't, the real driving pathogen is Bartonella. This is because bartonella creates transgenic tumors that sequester the pathogens.
Perhaps one difference might be that the individual had lyme from birth, so the immune system has harder time recognizing it as a problem.
Looking forward to real evidence of persister cell to spirochete conversion from that guy on the cover of the magazine! He actually believes, given what he has seen in the lab, that there is persistent Lyme.
That JH microbiologist who believes in persistent infection just published a study with the JH head of infectious disease (a chronic Lyme denying IDSA spokesman) about testing 165 existing approved antibiotics against those persister cells (a.k.a. cysts, round bodies, L-forms, or cell wall deficient forms).
They discovered that the front line drugs for Lyme infection (Doxy & Amoxicillin) work poorly against these cells. Haven't LLMDs have known this clinically for a while? It certainly explains why established infections so often aren't resolved by these drugs. (And how did the IDSA conclude that 3 weeks of Doxy cured late stage infections? It seems unlikely to me that ANY late stage infection is cured with just that.)
Some older drugs worked great against the persisters, but they tended to work poorly against spirochetes.
The study acknowledges that we need more research, and that possibly a combined therapy will be more effective in treating Lyme and preventing PTLDS. That deserves a cheer!
I thought maybe this is a crack in the door to admitting persistent infection. After all, persister cells are blamed for infection relapses in other diseases. But then there's statements at the end saying it's unlikely that these persister cells constitute ongoing infection, that ongoing symptoms do not justify long term treatment, and that antibiotics should not be given to PTLDS sufferers.
Same old-same old. At least it's a step in the right direction.
It doesn't say if they've ever seen a persister cell revert into a spirochete. If they did, that would be the proof of ongoing infection that the IDSA has said we don't have. Let's just hope that with a microbiologist who believes in persistent infection, JH et.al. will not suppress such evidence.
Dr. Jaller, what's your opinion on pyrazinamide? There seems to be some hope that in conjunction with other antibiotics, this stuff can be very effective with longtime suffers.
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