Saturday, February 5, 2011

23 What's In A Name: Is Chronic Lyme Real?

"Anyone who has a lot of information, thinks a lot, and by thinking increases his understanding of a situation, will have not less, but more trouble coming to a clear decision. To the ignorant, the world looks simple. ...Once we gather a little information, however, we run into trouble. We ... become more acutely aware [of] what we don’t know. This probably explains why we find so few scientists and scholars among politicians. It probably also explains why organizations tend to separate their information -gathering and decision -making branches. ... to provide decision-makers with only the bare outlines of all the available information so that they will not be hobbled by excessive detail when they are obliged to render decisions."

Dietrich Dorner,
The Logic of Failure, 1988

A few weeks ago I was reviewing my stat logs for web traffic and looked at the list of common web searches that people used and ended up finding this blog.

One string of keywords popped out to me and it was simply this: "is chronic lyme real".

Of course, I don't know who they were or where they came from, or what their story is. I wonder if they are another human being suffering with symptoms making their life miserable and asking, "Is this it? Could this be my problem?" or if they were perfectly healthy and stumbled upon some article about chronic Lyme Disease that cast doubt on its existence.

I'll probably never know who it was or their reason for being here. But the question is a good one, and surprisingly not a simple one.

Over the course of time I intend to examine the issue of persistence in Lyme Disease - which is directly tied to this question. But to draw on the quote at top, it's not an easy question to answer in some ways.

I know there are likely to be people reading this at this very moment about ready to throw something at the screen because I wrote that. I can hear you all the way over here, through that mass of Cat-5 cables and 3G networks, saying, "What? What do you mean, 'it's not an easy question to answer'? Of course it is - I'm sick with chronic Lyme disease, you ass, so of course it's real!"

And on the flip side, I can also hear the rare, passing IDSA-guidelines-believer almost audibly shrugging and saying, "Heh. That's easy. Of course chronic Lyme is not real... What was that link I was really looking for? Ah, yes... there is that abstract on Ebola vaccine development..." and moving on.

Now that the initial reaction has passed, though, I'll explain where I was going with my statement if you're still sticking around.

You are? Okay. Then read on, and be prepared for some TLAs (Three Letter Acronyms).

Problems with Naming Conventions 

On the one hand, Chronic Lyme Disease (CLD)* is defined by the Lyme patient community as having chronic and persisting Borrelia bacterial infection. That is a simple baseline definition of CLD.

On the other hand, the Infectious Disease Society of America (IDSA) has been the primary institution in the US (and to some extent, the world) which has set the standard for infectious disease definitions and treatment guidelines for some time.

For the subgroup of the IDSA which set the definition of Lyme Disease and guidelines for its treatment, their current opinion is that Chronic Lyme Disease does not exist, yet they have used the term one way in the past and have defined it differently now.

They believe that people with self-reported symptoms matching those of Lyme Disease are mostly sick with something else other than Lyme Disease, and that a small subset of patients who have had Lyme Disease and are experiencing Lyme-like symptoms after three weeks of antibiotic treatment have a condition known as Post Lyme Disease Syndrome (PLDS).

To use myself as an example, I am what the IDSA (and the cited NEJM article) would consider a "Category 4 Chronic Lyme Disease patient".

According to the IDSA, this means:
"Category 4: Symptoms of unknown cause after antibiotic therapy and resolution of an objective manifestation of Lyme disease. 
Only patients with category 4 disease have post-Lyme disease symptoms. Data from three double-blind, randomized, placebo-controlled trials have shown that there is substantial risk, with little or no benefit, associated with additional antibiotic treatment.  
Most patients presumed to have chronic Lyme are in category 1 or 2; antibiotic therapy in these patients is not warranted."
The IDSA has also given the following definitions to describe those who have Post-Lyme Disease Symptoms/Syndrome and those who have CLD:
"post-Lyme disease symptoms: fatigue, musculoskeletal pain, difficulties with concentration or short-term memory, or all of these symptoms when experienced by patients despite resolution of the objective manifestations of infection by Borrelia burgdorferi after antibiotic treatment. Seen in a minority of patients.
 post-Lyme disease syndrome: symptoms above lasting longer than six months. 
 chronic Lyme disease: The term has been applied to patients in a variety of contexts, including those with objective late manifestations (such as arthritis) and those with purely subjective complaints after antibiotic therapy. It is also applied to those with unexplained subjective symptoms without credible laboratory evidence for Borrelia burgdorferi infection irrespective of exposure to an endemic area. The term has also been applied to patients with other identifiable conditions such as multiple sclerosis."
So to make matters all the more confusing to the random passerby, the term "Chronic Lyme Disease" as currently used by the IDSA does not match the term "Chronic Lyme Disease" as it is used by the Lyme patient community.

The Lyme patient community, as you'll recall, states that CLD is caused by a persistent Borrelia infection. 

To further add to the confusion, the IDSA guidelines group used to define and use the term CLD the same way that Lyme patients currently do, and they still might in certain documents.

But now IDSA's current definition of CLD above is so broad as to be almost completely meaningless. It can be about objective late stage Lyme symptoms - but it is also stating that CLD is not related to Borrelia infection at all - especially if the patient lacks "credible laboratory evidence" for it (which is another issue - if that means serological testing, it is not always an accurate indicator for the presence of Lyme Disease - the most recent European study I posted bears this out) or perhaps it  isn't even Lyme Disease at all and it is MS.

This is unusually inconsistent with how one would determine definitions in many scientific realms. Consistency and specificity in language are important - especially in science. Words mean something.

Defining "Chronic Lyme Disease" in this manner, the IDSA might as well call it a dessert topping, floor wax, and a whole bass while they're at it.

My Diagnosis of Different Names

Today, for a more complete diagnosis, the IDSA would consider me a "Category 4 patient who has Post Lyme Disease Syndrome (PLDS)".

This would be based on case definitions, clinical diagnosis, and my patient history:

Several years ago I got bit by a tick and got a textbook case of Lyme Disease, and since then, I have not seen the same level of health I had before the bite and infection occurred. I suffer from fatigue, musculoskeletal pain, difficulties with memory and concentration, and a few other symptoms.

My original diagnosis for Lyme Disease was met on these points:
  • I was bitten by a tick in an endemic area.
  • I had an expanding erythema migrans (EM) rash around my tick bite.
  • The rash continued to expand and within ten days I began to show full-blown signs of a flu-like illness matching symptoms of Lyme Disease.
  • I have had positive serology for Lyme including a CDC positive Western Blot.
Anyway, I say all this to substantiate that in my case, that even by the IDSA's definition I have had Lyme Disease.

Not that this does me any good, to be believed by the IDSA on this point - identification under any of the above categories does nothing to help the Lyme patient receive effective treatment from IDSA doctors once the patient has received the standard treatment described in their guidelines.

Only LLMDs and alternative practitioners are trying to treat these groups at present.
What becomes an issue and is a big part of where the "Lyme controversy" comes from this:  
Whether or not the symptoms I had for weeks after treatment up through now are the result of continuing to be infected by Borrelia bacteria that are hard to kill off, or - by the current IDSA guidelines group's line of thinking - if some post-infectious process is taking place in my body which is producing my symptoms.
Once I went online seeking out information about Lyme Disease, it became clear that Lyme patient support groups and a number of doctors believed that Lyme Disease could be chronic in nature.

Other patients and some doctors have called my condition "Chronic Lyme Disease with coinfections".

And it was only later on that I began to dig more into research online to find out what different parties and institutions were finding and saying.

Most recently, Dr. Benjamin Luft spoke at an Institute of Medicine workshop in October 2010 and called my condition a sort of "Lyme Borrelia Complex". In so many cases, he knew ticks and patients were simultaneously infected with Borrelia and at least one coinfection, so this term may be more applicable than Lyme Disease to begin with.*

Documenting Chronic And Persistent Infection

While there is plenty of evidence that Borrelia spirochetes do persist in the host after antibiotic treatment - and even members of the IDSA have stated the spirochetes persist in their own research - the IDSA Lyme guidelines group currently question the spirochetes' ability to cause infection and has stated that they have no clinical significance. The IDSA has also stated that Lyme Disease is easy to treat and quick to cure.

For many Lyme patients, there is trouble with this stance because they have found research publications and patents by the same IDSA members which contradict their own position statements.

In the IDSA's and NIH's own research, Chronic Lyme Disease has been a consistently used term and their past usage of it has been connected with Borrelia infections which can persist in the host. As recently as 2005, IDSA members have filed a patent which mentions Lyme Disease as being difficult to eradicate. Also, researchers in other countries have found evidence that Borrelia infections can persist.

This leaves people questioning why it is they are finding contradictory statements about Lyme Disease coming from the same source - as well as from different ones.

Members of the IDSA guideline group have also stated that those with PLDS may be suffering from an autoimmune or immune dysregulation order. There has been no conclusive proof to date that CLD is caused by an autoimmune or immune dysregulation disorder, even though it may play a role in the disease process.  And unfortunately, unlike CLD, there is currently no treatment available for this disorder if it is the cause.

If I knew for sure this was the problem, and there was another treatment for it, I'd avoid taking one more milligram of antibiotics unless another infection came along - like bacterial pneumonia.

The Patient's Dilemma

So a patient in my position who is suffering from symptoms has these choices available to them:
  1. Believe the IDSA and do nothing. Maybe it will get better over time.
  2. Believe the IDSA and see a doctor or several doctors to find out if something else is wrong.
  3. Don't believe the IDSA, and try longer antibiotic treatment. Maybe it will help.
  4. Don't believe the IDSA, and try some alternative treatment. Maybe it will help.
  5. Don't believe the IDSA, and try longer antibiotic treatment and something alternative. Maybe it will help.
  6. Don't believe the IDSA and do nothing. Maybe it will get better over time.
It is not known how many CLD patients choose #1 or #6, and for how long that remains their position. Patients who have chosen #2 may start out with a non-CLD diagnosis and investigate whether or not they have CLD later on. The vast majority of CLD patients choose #3, #4, or #5 after they have been severely ill for some length of time and no other cause has been found.

Due to the severity of my symptoms that continued after the first three weeks of antibiotics, I made choice #3: continue antibiotic treatment. I tried additional treatment knowing what the risks were and went against the recommendations of the IDSA guidelines.

At the time, I was seeking to address what were not mild and vague symptoms but severe ones which prevented me from working and from even doing the most basic tasks like showering and preparing dinner.

I ended up visiting the ER more than a few times during my illness. If my condition were mild, I would not have been in the ER... I would have gone to work and made dinner.

In my case, extended antibiotic treatment eliminated a number of the symptoms I was experiencing - and for a time - diminished the intensity of my remaining symptoms. I did not think it was a poor choice to extend treatment, nor did my doctor. It was well thought out, and based on my responsiveness to treatment.

My issue now is that even as I have improved, I haven't regained my former health. Is this it,  have I hit the wall - or is there anything more I can do? I wish there was a definitive answer for me.

As it stands, I have the choice to either continue to follow treatment under an LLMD and/or alternative practitioner, self-treat holistically, or do nothing. I eliminate the other numbers in my spectrum of choices because I already see a primary care physician and other specialists concurrently to make sure I'm not missing anything else that could cause my symptoms as they come up. I have my bases covered.

What About The Original Question?

So we've gotten this far, and I guess I still haven't completely answered the question, "Is chronic Lyme real?"

What I've tried to do first in addressing that question is raise awareness that one's answer to that question depends on what they mean by the term, "Chronic Lyme Disease". The way the IDSA and its recent literature define CLD is the polar opposite of how the Lyme patient community defines CLD.

And I'm not entirely sure when the change in that use of the term took place and how consistently it has been applied - I still come across documents and research which use CLD in terms of persistent infection.

The IDSA needs to do more research on tickborne infections and clear up any inconsistencies in their research. It reflects poorly on them to contradict themselves, and to also base their guidelines on so few trials and limited understanding of not only Borrelia's pathogenesis but tickborne coinfections and immune factors as well.

Independent research groups and institutions with no investment or conflict of interests in tickborne disease research outcomes would be beneficial in providing unbiased confirmation of research that has been done - or better yet, do the research in areas the IDSA has been avoiding or under-serving.

I am not enamored of the one cause hypothesis when it comes to describing my own condition, because I don't think the issue is as simple as whether or not I have a chronic infection with Borrelia burgdorferi.

I may be infected with more than one strain of Borrelia and/or infected with a non-burgdorferi one.

There is objective evidence (serology) I have had at least one coinfection and it is one that has been proven to relapse. I may have other coinfections that have yet to test positive, and I may have additional coinfections for which there are no tests because they have not been identified.

It may be that coinfections are truly more my problem than Borrelia is.

I don't even think the issue is as simple as to whether or not I have an infection with Borrelia and Babesia, and possibly other coinfections, too. It's possible that I am a not only a polymicrobial soup du jour, but I am also suffering from an immune dysregulation disorder that was caused by the very pathogens which invaded me.

It's possible that my genetic profile left me more open to systemic disease than other people who have been bitten - but also possible that the specific genotypes of Borrelia are harder eradicate than others, that they have their own unique synergy with coinfections which make the infections harder to effectively treat, and that regardless of genetic background - would be difficult to treat in anyone.

And there are more possibilities which I am not listing here which may give rise to my condition.

So to say it's either persistent infection or an autoimmune/immune dysregulation disorder causing my problems seems a shortsighted simplification until more research is done and we really know what is going on.

After all of this discussion about whether or not chronic Lyme is real, the one thing to know is that the quote at the top of the page is definitely something to consider: the more you learn, the more there is yet to learn.

Any one post I make here - whether it's a study or commentary or article - is only going to touch on the edges of one facet of tickborne infections. The challenge is to take all of the information that is available and glean what is high quality, what is not, and what has yet to be determined to create a more informed picture of the problem.

Is Lyme Disease a disease that can be with you forever? Do certain conditions give rise to a lasting infection that can be eradicated eventually - and permanently? Is any symptom post-antibiotic treatment - even after much treatment - signs of a continuing infection or residual symptoms which will always be with you?

My suspicions are: conditionally yes, yes (but you could get re-infected), and maybe. More pieces of the picture are needed, and it will take separate posts just to begin addressing each of those questions on their own and confirm or even challenge my suspicions.

What does it take to confirm or challenge yours?

* I think that even in the Lyme patient community, many would think that CLD is a very basic definition of what they are suffering from and another term that I would use which may be more accurate based on their reported symptoms is this: Tickborne Disease Complex (TDC) or maybe even PTDC, where the 'P' stands for Persisting. Dr. Luft's term, "Lyme Borrelia Complex", isn't a bad idea, either.


  1. Excellent post. Good food for thought....I look forward to reading more.

  2. Yet another great post by camp other. My story is eerily similar to are my thoughts, but unfortunately my journalistic knowledge and skills are far less. How many others like us are there in the U.S. alone? How many will it take to make a difference? I find a frustrating sort of comfort knowing I am not alone, and possibly that is why I attempt to expose the gap between knowledge and ignorance of tick born diseases any way I can.

  3. Thank you, Anonymous. What in particular did you like, and what are you thinking about because you read it?

  4. Just Koz,

    Welcome to my journal, and thanks for your comment.

    How are our stories similar? I'm curious.

    I don't know how many are like us (if by "like us" you mean people who have extended symptoms of Lyme Disease and coinfections) because while there are people in the Lyme community who are trying to collect data on patients, it's not clear what criteria have to be met and how they are vetted in order to be counted.

    The definition of who has Lyme and coinfections and who does not is not being consistently applied even within the patient community - let alone from organizations such as the IDSA.

    While I think the IDSA's definitions are scientifically weak, I don't think one can say that if a person comes forward and just says, "I have Lyme Disease" that they are automatically counted. There is no criteria to be met in such a statement, and without confirming it somehow, anyone - my cousin Larry or Uncle George - could make the case.

    Someone has to come up with a clear case definition for this for all researchers and doctors. For scientific purposes, the definition has to be more specific and less vague, and I think the definition can be written in such a way as to include patients who are certain outliers and coinfections. (Maybe that comes with renaming the condition "Lyme Borrelia Complex" or "Tickborne Disease Complex" instead of "Chronic Lyme Disease"?)

    I really think closing the gap between knowledge and ignorance is huge. I have gaps, and I know I don't know enough. I'm trying to play catch-up and learn what I can.

  5. I wanted to address your other question, Just Koz - I'm sorry I didn't earlier.

    You said, "How many will it take to make a difference?"

    I think it will take all of us working together and pointing out where the IDSA has made errors and where their data is incomplete. It will take all of us doing our own homework and learning what we can to be as educated as we can about the studies that are out there already, that - if not support the role of persistence and other factors in Lyme and coinfections - at least expose some doubt about how much is known about them.

    It also would help to set an example, and find researchers to work with who are open-minded, scrupulously honest, and do not have any conflicts of interest over this Tickborne Disease Complex. If they do the work and tell me that not only is persistence an issue - immune issues are, too - I would be willing to listen to them.

    Right now, I have a hard time listening to those who are scrambling for vaccine development funding while those of us who are too late to benefit from one (IF they ever find one that works, that is) continue to suffer.

  6. Camp Other, if you don't believe that immune issues are a major problem in Chronic Lyme, that it is mainly an issue of persistence, how do you explain the Lyme-like symptoms that developed in certain idividuals that received the LYMErix vaccine? The vaccine contained no live bacteria, only their outer surface proteins.

  7. Anonymous,

    I don't think I said that it isn't a major problem. I'm thinking it is part of the problem.

    In the LYMErix vaccine, it's my understanding that a certain subset of the population - as much as 30% - has a genetic background that leads to an autoimmune reaction to OspA. So those people who had this background ended up developing Lyme-like symptoms in response to the vaccine even if they had never been bit by an infected tick.

    Even if we gave genetic testing to everyone with prolonged Lyme-like symptoms and showed that everyone with a given profile has this tendency for OspA-induced autoimmunity - how does that prove that persistence isn't also an issue? Or that an Osp autoimmune response is the only issue leading to ongoing symptoms?

    People could be symptomatic due to infection with Borrelia, or due to Borrelia and reaction to an Osp/lipopeptides like Pam(3)Cys-Ser, or other causes of inflammation (such as innate host deficiency, estrogen levels leading to increased proinflammatory cytokines, for example). And that's just Borrelia-induced problems - but you need the Borrelia first to get there.

    A vaccine with OspA in it is going to show one path where things can go wrong. It doesn't have the complexity of the organism in vivo.

    How do you know if it host infection or an autoimmune reaction in the host is currently taking place? Is this an "or" question, or an "and" question?

    I'm not saying that I don't believe immune system issues are a major problem. I just don't know how big a role it is and all the dependencies involved.

  8. In studies done on dogs it's close to 100% that show this exposure, while only 5-10% go on to develop symptoms. Of these dogs, most respond favorably to treatment. Unfortunately, for some it will be chronic and even fatal. I believe that retrievers are especially prone to the fatal kidney complications, which is an interesting genetic clue, I think.

  9. In comment #8, only a portion of my reply to Camp Other was posted. Here's my full reply:

    As another has commented on older posts, we know that antibiotics don't 100% eradicate an infection, likely any infection. They serve to bring the bacterial level down to a manageable level where the immune system is then able to take over.

    If you were able to test the population of a highly Lyme disease endemic area with a sensitive and accurate test you would find that a very large percentage of people would show exposure to Bb.

    Many of these would be asymptomatic; another segment would have had self-limiting symptoms; another group would have illness and respond well to antibiotic treatment whether their symptoms were mild or acute. Only the smallest segment of this population would have a lasting, chronic illness following even long-term antibiotic treatment. Pam Weintraub in her book Cure Unknown puts that number at 15% of Lyme disease patients, if memory serves me right.

    In studies done on dogs it's close to 100% that show exposure to Bb in areas of the Northeast, while only 5-10% go on to develop disease symptoms. Of these dogs, most respond very favorably to antibiotic treatment. Like people, for some dogs it will become chronic and even fatal. I believe that retriever breeds are especially prone to the fatal kidney complications of Lyme disease, which is an interesting genetic immune system clue, I think.

    To begin to understand what is happening, I think scientist need to know what is going on in not just the people who remain chronically ill, but also in those that don't get symptoms from their exposure to Bb infection, and those that get better from both antibiotic treatment and in self-limiting cases. What is causing these differing responses?

    In my humble, layperson opinion in most cases persistence is really the tail wagging the dog for those that have been treated with long-term antibiotics and are still chronically ill.

  10. I've read some of the canine studies, but thought that their physiological and immune response was so different compared to human hosts that I haven't known how much weight to place on them. They have a huge delayed response to infection and fewer symptoms as compared to humans - and respond to OspC very differently, for one thing.

    I've thought rodent models were more accurate for mapping what may happen in human hosts, and haven't been comfortable with the non-human primate studies (specifically Rhesus, apparently, develop neuroborreliosis like humans do).

    You think looking at the canine studies with fatal kidney complications (membranous glomerulonephritis) give one a genetic clue to why certain human hosts get chronic Borrelia and others do not? I thought membranous glomerulonephritis was pretty rare in humans, and they usually happen secondarily to viral hepatitis or malaria when it comes to infectious disease (and tumors otherwise).

    One thing I came across when reading about dog Borrelia that was interesting was this bit:

    "One of the most prominant of these insidious mechanisms involves formation of immune complexes composed of bound-together Borrelia antigen and dog-produced antibody. Deposition of these complexes in joints is primarily responsible for the lameness that has traditionally been thought of as a hallmark symptom of canine Lyme disease."

    I know the dogs with severe kidney problems after Borrelia infection have some autoimmune kidney dysfunction and it kills about 50% of them, but the problem is supposed to be rare to begin with.

  11. By the way, is it just me - or do you find that there are more full text publications on veterinary science that are available than full text publications on clinical microbiology on humans?

    I've always found it strange that government-funded research has to be paid for by the public at the tune of $28 on up to view peer-reviewed publications. Shouldn't our tax dollars give us full text access without the fee? I don't get it. (Well, I do get it, to a degree - not everyone can afford open access... but the principle of it... wow.)

  12. Ah, Anonymous, in regard to comment #8 - I see your entire comment came through now. I think I partially responded to it already, given the shorter comment beforehand.

    You also said later:

    "To begin to understand what is happening, I think scientist need to know what is going on in not just the people who remain chronically ill, but also in those that don't get symptoms from their exposure to Bb infection, and those that get better from both antibiotic treatment and in self-limiting cases. What is causing these differing responses?"

    I agree with you. And it would be good to show more evidence of the genetic connection and the role immune dysregulation by pathogen presence plays, too. If Borrelia has a latency stage, though, like Syphilis (many Lyme patients view this as a given; IDSA has contended it is not a given; some researchers think it is possible and can happen) then it is possible those who are asymptomatic simply have a dormant infection and have antibodies.

    "In my humble, layperson opinion in most cases persistence is really the tail wagging the dog for those that have been treated with long-term antibiotics and are still chronically ill."

    I hear what you're saying, and it's one possibility to consider. But I think it's not that simple, and once you add coinfections to the picture, the kinds of studies you mention above need to include them. Babesiosis can be resistant and relapse. Other tickborne infections can be difficult to beat and cloud the clinical picture. If up to 40% of the ticks in two counties in NY state were polymicrobial, odds are high people living in those counties who are bit by a tick will end up coinfected. So Lyme Borreliosis alone won't be shaping what happens in vivo.

    By the way, I don't entirely put stock in the term, "lay person". Some people use it as a way to separate those who know and those who do not as a form of elitist thinking. I don't like that form of thinking, for what it's worth - though I do appreciate people who know their stuff.

    You are asking intelligent questions and it doesn't matter that you're a lay person. We are all a lay person at any field that is outside our profession.

    The important thing is to ask and learn new things... I don't think any one person in the field of microbiology or outside of it knows all the answers here. We are all trying to figure it out. It's just some groups have different agendas as to what knowledge to pursue and what to do with it than others.

  13. I didn't intend to use the canine example as a direct, exact mirror for humans, but merely as an example, with enough similarities between species in the same environment, where such population studies and statistics have been analyzed for Lyme disease.

    I specifically mentioned the kidney complications seen mainly in retrievers as a good illustration of infectious disease pathogenesis with a genetic vulnerability component. It makes sense to me that these types of variables would also impact and explain the different courses and outcomes of the illness in humans with Lyme disease as well, specifically in relation to PLS or CLD. Who recovers and who doesn't.

    What I'd like to know is why the Bb titer tests for dogs are so much more accurate than those we currently have for humans. Why is that? Do you know?

    And yes, I agree with you about the scope and availability of veterinary related studies.

  14. Similar as in your words:

    "Several years ago I got bit by a tick and got a textbook case of Lyme Disease, and since then, I have not seen the same level of health I had before the bite and infection occurred. I suffer from fatigue, musculoskeletal pain, difficulties with memory and concentration, and a few other symptoms."

    My original diagnosis for Lyme Disease was met on these points:
    I was bitten by a tick in an endemic area.
    I had an expanding erythema migrans (EM) rash around my tick bite.
    The rash continued to expand and within ten days I began to show full-blown signs of a flu-like illness matching symptoms of Lyme Disease.
    I have had positive serology for Lyme including a CDC positive Western Blot.

    I could use the description nearly word for word of my own experience. However my memory was so far gone by the time of my clinical diagnosis I have had to work backwards as memory allows to recall events eight years passed. I am going to get my medical history soon to see if I can match my memory to approximate dates. My Western Blot had positive bands in both IgG and IgM but I am not sure if they meet CDC guidelines. I have chronic Candida and sinus infections also. I am almost two years into treatment with much physical improvement and not so much neurological improvement. To organize my thoughts is a challenge as are the obstacles of poor memory.
    I find it somewhat humorous that the burden of proof seems to fall on mentally challenged people like myself.

    PS. Please do not feel obligated to reply to my posts. You are going to burn out...and humanity needs articulate people like you to focus on the big picture and state our case in a way we cannot.

  15. Just Koz,

    Wow. I'm sorry to hear that you went through the same thing, pretty much word for word. You have my sympathy. This is not an easy road to travel.

    My memory was really bad when I first got ill. I had swollen glands all around my neck and a massive headache. I could barely move. I couldn't understand what I was reading after I read it. I tried. Multiple times.

    So it was pretty bad for me and I had to take a break from the contract I was working on (which involved a lot of research; reading, and writing).

    I've had a bit more neurological improvement in the past couple months but don't know if it is permanent or transient. Doing as well as I have encouraged me to continue the blog, but I have a voice at the back of my head that pings a message of concern occasionally about how long I can keep this up.

    I kept a private journal back when I first got infected and sick, but was not always good about keeping it up because I was so damn sick. But I tried. I can still look at it and print outs of symptom logs I gave to my doctor when I was too out of it to order my thoughts at my appointments.

    You're probably right about needing a break. It's been a busy day for commenting and I am getting a lot of traffic... One annoying thing about being ill though is that with concentration problems and fatigue, just writing these posts takes a lot of time and energy... I am doing better lately than I used to in terms of brain fog - but the fatigue and pain can slow me down a lot in terms of quality and frequency of posting.

    And I see a lot of value in the comments over time - more than my posting in a number of cases, because my post triggers a discussion that takes us in new directions sharing more info that what I put out originally. So it's hard not to respond sometimes.

  16. Excellent blog, CO.

    Thanks for this.

  17. Hi Camp Other
    I just found your blog Great idea, I rather like the middle ground but then I have faired well on long term antibiotics but not quite so aggressive as some of the US LLMD's would have given. I live in the UK where we don't have many LLMD's.

    I never had a positive test result but then the 20 months of steroids given for wrong diagnosis of PMR most likely would have muddied things for me.

    Now virtually 100% after the best part of 4 years antibiotics life is such a joy. My story is on my side bar of my Looking at Lyme Disease blog.

  18. Joanne, I am in support of use of long term antibiotics if that is what it takes to fight Borrelia infections - though I do wish other drugs and treatments were available because the risk of secondary infection and side effects is there. Something lower risk would be welcome, even if some of the same effects continued.

    Being in the middle is about questioning all of it - whether it comes from the IDSA or ILADS or my neighbor next store. And it's also about trying to find a way to bridge differences by uniting under the truth once found. I think a lot of the research that is out there helps find that truth, and basic scientific research is what we need more of to expose it and question our current understanding.

    I'm sorry that you were on 20 months of steroids and got the wrong diagnosis. That would set anyone back, and the side effects of steroids are not fun, as I can attest (mood swings, insomnia, edema, weight gain...). I wasn't on them nearly as long as you were, though.

    I am so glad to hear you are nearly 100% - that's great news! May you continue to heal and thrive.

    One question: Is it hard to continue writing the blog when you are doing so well now? A comment often said on Lyme support fora and groups is that those who have recovered don't come back - they just want to put it behind them - so we never hear of their success. I hope you will continue to write in your blog, but do you ever feel like doing something else? Or rather: I'm imagining a lot of your energy is back and you can do more - how much goes into Lyme disease education and advocacy, and how much is finally going into the backlog of things you hadn't been doing while ill?

  19. I meant to say "neighbor next DOOR", but of course, Lyme brain, and here one cannot edit comments but only delete them. So it remains.

  20. Camp Other,
    This may not be the correct thread to ask this----- but will you comment on all the advice on 'clear up the immune system' given in all forums and even in some articles you've referenced here.

    Just HOW does one go about 'fixing' the immune system. And which one, acquired or innate? Or both.

  21. Hey cave76,

    I don't think there's a right or wrong thread for this comment - here is fine.

    That's a very good question.I think it requires its own post and not just a comment - along with at least a top-level explanation of the immune system.

    Which articles are you referring to - can you point them out?

    I'll see what I can do to write a post about this, once I'm feeling better.

    Thanks for the question.

  22. I mis-spoke. I shouldn't have implied that you had articles on this blog addressing that. (If you do, I've missed it.)

    I mean what the general population receives in most forums and on the Internet. A google search brings up thousands of hits but as far as I can see they're all sites that are selling 'something to help your immune system'!

    The 'science' of the immune system, I'm sure is VERY convoluted and hard to tease out. And it probably varies from person to person.

  23. cave76,

    Thanks for further clarification. And yes, the immune system is pretty complicated overall and a field that is making new strides in research all the time. Immunology, biochemistry, cell biology, molecular biology, and genetics are fields which work towards our understanding of the immune system.

    A short answer to address your question is that so far, what I've learned is that much of what helps 'build' the immune system is more about what *not* to do rather than what *to* do - that is, avoid damaging one's body so the immune system isn't impaired versus actively do things to improve it. Good basic self care is a start. But as I said, I think in order to give a pretty good picture of it requires at least one post.


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