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.
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