Coming soon... ILADS 2012 Conference Remarks - watch this space.
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"These data, in conjunction with available clinical and epidemiologic evidence, show that repeat episodes of erythema migrans in appropriately treated patients were reinfections and not relapses."
"[...] some persons have attributed recurrent episodes of erythema migrans to relapses in patients treated with recommended courses of antibiotic therapy; they cited experiments in animals that showed persistence of B. burgdorferi despite antibiotic treatment."This was about as close as I could get to finding a statement in the study that chronic Lyme disease does not occur, as the majority of the content of the paper focuses on the fact that new erythema migrans are associated with new infections.
"Patients were treated with standard courses of antibiotics at each episode of erythema migrans, with subsequent resolution of the skin lesion or lesions."The key words to keep in mind here are: "erythema migrans" and "appropriately treated patients".
"Two genetically linked typing systems, one based on sequence variation of outer surface protein C (OspC) and the other on ribosomal RNA intergenic spacer type (RST), have been used to classify US B. burgdorferi strains.The above description of how OspC RST typing is taken from the paper, "Borrelia burgdorferi RST1 (OspC Type A) Genotype Is Associated with Greater Inflammation and More Severe Lyme Disease".
OspC typing divides B. burgdorferi strains into 21 genetically distinct types, 16 of which have been identified in the northeastern United States and RST divides B. burgdorferi into three groups.
RST1 corresponds to OspC genotypes A and B; RST2 corresponds to OspC types F, H, K, and N; and RST3 corresponds to the remaining 10 OspC types, including D, E, G, and I.
In the northeastern United States, infection with OspC type A (the most common RST1 strain) or OspC type K (the most common RST2 strain) accounts for approximately 60% of Lyme disease cases; and all of the OspC types within the RST1 and RST2 groups account for approximately 80% of cases. RST3, the least common type, is the most diverse, although infection with OspC type I accounts for approximately half of the RST3 cases.
Because RST typing of isolates may miss differences within groups and because OspC typing may lead to small groups, more information for clinical correlations can be obtained from the use of both typing systems."
"[...] However, when mice were infected by tick bite, as in the natural infection, RST 1 isolates displayed higher densities in blood, but the number of spirochetes in the heart or bladder was similar with either RST 1 or RST 3 strains (14). This suggests that in the natural infection, smaller numbers of RST 3 organisms, which may not be detectable in blood, are still able to spread to the joints and cause infection there. Consistent with this observation, the frequencies of B. burgdorferi genotypes in human patients in the current study were similar in EM skin lesions and in joints. Thus, it seems that all 3 RSTs have a similar predilection for dissemination, but larger numbers of RST 1 organisms are more often detectable in blood."[12 ]According to research to date, the B. burgdorferi RST1 (OspC type A) genotype - followed by the RST3 (OspC type I) genotype - cause greater inflammation and more severe disease than other genotypes, establishing a link between spirochetal virulence and host inflammation.[ 3]
"I’ve been following the issue of chronic Lyme disease closely for a number of reasons, and anecdote aside, think that the situation surrounding the diagnosis and treatment of Lyme disease and other tickborne diseases is more complex than most of the media has led the public to believe.
I hear that Lantos – like Dr. Lawrence Zemel of the Infectious Disease Society of America – has more or less stated that half of those patients who claim they have chronic Lyme disease have no evidence of having prior or active Lyme disease. Lantos stated, “Only 7–31% had active Lyme disease and 5–20% had previous Lyme disease,” he writes. “Among the remainder, 50–88% had no evidence of ever having had Lyme disease. Most of these patients had either an alternative medical diagnosis or a functional somatic syndrome such as chronic fatigue syndrome or fibromyalgia.”
If this is in fact the case, then we are still looking at up to 51% of the patient population in this group as either having had Lyme disease or currently having it – meaning that up to little more than half of patients’ persisting symptoms do correlate with evidence of having Lyme disease.
It is this population of which I am a part of, having had a textbook case of Lyme disease – known tickbite in endemic area, an EM rash, flu-like illness, severe joint pain and swollen lymph nodes – the whole nine yards – only to be followed by years of ongoing symptoms I did not have pre-infection.
So, when someone brings up the pseudoscience of “chronic Lyme disease”, understand that I might get a little testy because it seems almost inevitably, the cases which are highlighted in skeptical discussions are those Lantos states do not have evidence of Lyme disease. Whether that is accurate or not, what about the rest of us? (Side note: chronic fatigue syndrome and fibromyalgia are problematic diagnoses in their own way, too, as they are of unknown etiology.)
I want to know as much as the next person exactly what has led to persisting symptoms. After doing the research on my condition to the extent I have, I’m coming to the conclusion that more research is necessary. I am skeptical about their being “sides” to this debate in the first place and also think science has not come to a full understanding about the process behind why we have persisting symptoms.
Embers et al’s recent study on persistence of Borrelia burgdorferi after antibiotic treatment in Rhesus macaques brings up the question of persistent infection after antibiotic treatment. More research is required on this, and persistence studies such as an NIH-NIAID xenodiagnosis study where patients with chronic Lyme disease are bitten by lab-raised ticks in order to see if they pick up the infection are underway. On the autoimmune angle for finding cause, Bockenstedt recently published a paper showing gfp concentration of Borrelial antigens in tendon* tissue in mice, and the hypothesis is spirochetal antigens cause persisting symptoms long term. See this Research Blogging blog post for more info: http://spirochetesunwound.blogspot.com/2012/11/inflammatory-spirochete-debris-left.html
So one cannot avoid that persisting symptoms after initial infection and treatment or delayed treatment is an issue; the research is there and being conducted on it.
But in the meantime, people are suffering, and voting with their feet: The vast majority of patients in my situation think there is something to the persisting infection hypothesis, and treat with long term antibiotics. A number of them recover and report improvement in symptoms while on treatment.
Yes, it is anecdotal – true. And it doesn’t support the outcomes of some of those small clinical trials which were conducted. But perhaps instead of dismissing them, someone could step in and collect the data on these patients (with their consent, of course) based on how they are currently being treated, what the patient base is and common factors of different subpopulations, and so on – and see if any commonalities float to the top? This could be informative, to study patients who have made the decision to accept this treatment and see how they fare."
While I have not read the full text of the study yet, I agree that your logic path is one I traveled as well. An EM or “bull’s eye” rash is a key part of the case definition for acute Lyme disease – however, it’s not always present with infection, nor do all EM rashes signal the presence of infection.
Much of the media’s write-up on this study has conflated the existence of reinfection with the nonexistence of a chronic condition connected with Lyme disease – but it has also left out a huge chunk of the story about the significance of EM rashes in Lyme disease infection.
Dr. Jorge Benach of Stonybrook University has stated that if multiple “satellite” rashes show up weeks to months after initial infection, that the bacteria has disseminated. This may mean the patient needs a different course of treatment at this stage, so new rashes in this situation are important to separate from new EMs from a new infection.
Dr. Benjamin Luft has been doing extensive mapping of the genetics of different strains of Borrelia burgdorferi and has discovered some strains create a rash but no infection, some create a rash and infection, and some create no rash and infection. These strains can have varying targets within the body; varying levels of virulence.
And not long ago, Horizon Press published a book, “Borrelia: Molecular Biology, Host Infection, and Pathogenesis”, and it mentions big gaps in patient management around EM rashes: Some people who were screened to be subjects in studies were seropositive for Lyme but have never had ANY symptoms – whereas others went on to develop a case of late stage Lyme disease. (See pp. 501-502)
This is problematic for patients and doctors alike, who may have difficulty diagnosing the cause for the patients’ symptoms with no prior history/evidence of Lyme disease.
(Serology might help – but you have to suspect Lyme disease first.)
(As an aside, you might want to check out this discussion on Lymenet Europe: http://www.lymeneteurope.org/forum/viewtopic.php?f=6&t=3856 – if only because of the references offered.)
So, I am concerned about the emphasis on rashes and think either one has to suspect Lyme disease based on other symptoms and potential exposure to ticks – or we need better testing… Solid direct detection tests would be great, but we don’t have one yet. I’m waiting to see what GMU does with its nanotrapping test development… It’s antigen based; hopefully superior to existing serological tests. But again: First one must suspect Lyme, and if there is no EM rash present, where do you begin?
"This is one of several articles I have seen which conflates this study on new rashes and new infection with the issue of chronic Lyme disease or persisting post-treatment symptoms - when the two issues are distinctly separate ones.
Even if one does not believe that Lyme disease can be a chronic infection (which in the scientific world it continues to be a matter of debate if a study like Dr. Embers' Persistence of Borrelia Burgdorferi after antibiotic treatment in Rhesus Macaques has been published recently and the NIH-NIAID is funding a xenodiagnosis study to see if human hosts with chronic Lyme disease can pass their infection onto lab-raised ticks - hardly a sign the debate has been resolved), the IDSA itself recognizes that a percentage of patients who were treated for Lyme disease go on to have persisting symptoms for months to even years after initial infection. Their organization thinks it is possibly autoimmune and call it Post-Lyme disease syndrome; there are now proteomics studies that have been done which provide markers for this condition.
Whichever model of persisting symptoms you support, it is incorrect to associate this one study with disproving the existence of either a chronic infection or post-infection autoimmune condition in patients with ongoing disease and disability since contracting Lyme disease.
I think that one also has to be careful about the utility of the EM or bulls' eye rash in proper diagnosis of Lyme disease in general: According to Dr. Jorge Benach of Stonybrook University, if more satellite rashes erupt after the initial rash (usually within weeks to months) the infection has disseminated. Also, not all cases of Lyme disease present with an EM rash, and research by Dr. Benjamin Luft has shown that some strains of Borrelia which disseminate with a rash do not cause disease and some without rashes do cause disease.
One study like this is not enough to set the course for Lyme disease, which is an emerging infectious disease which requires more research."
"ILADS has submitted four objectives addressing chronic manifestations of Lyme disease to the U.S. Department of Health and Human Services (HHS) for inclusion in their Healthy People 2020. Healthy People 2020 is an ambitious, yet achievable, 10-year agenda that could improve the Nation’s health for individuals with Lyme disease. It is important that your voice be heard.
ILADS Lyme Disease Objectives:
1. Increase the proportion of persons with acute disease who are timely and accurately diagnosed.
2. Decrease the proportion of persons with chronic manifestations of Lyme disease.
3. Increase the proportion of persons with chronic manifestations of LD who are timely and accurately diagnosed.
4. Reduce the number of persons with a history of Lyme disease with subjective symptoms severe enough to result in a substantial reduction in previous levels of occupational, educational, social, or personal activities."