tag:blogger.com,1999:blog-40733975887464304862024-03-13T22:46:17.553-10:00Lyme Disease, Science, And Society: Camp OtherLyme Disease, Science & Society: Camp OtherCamp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.comBlogger322125tag:blogger.com,1999:blog-4073397588746430486.post-82715595751728775572014-07-11T05:29:00.002-10:002014-07-12T06:18:58.463-10:00Antibiotic Resistance and Persisters In Lyme disease<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwoQooDB1suE6m-IQdzHgHohDBZdOJh9uaI1Sp5xSnEoWZxcTNL3OIWftxVfwAPvlkYO7ZWA0zSM4vEIuzXoafunX5wRX_MI2CtSFrZDfrmiKSVZmjaHSE3U9okMusK5o2D3h4siZt8fUt/s1600/greenbg_chetes.jpeg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><span style="font-family: inherit;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgwoQooDB1suE6m-IQdzHgHohDBZdOJh9uaI1Sp5xSnEoWZxcTNL3OIWftxVfwAPvlkYO7ZWA0zSM4vEIuzXoafunX5wRX_MI2CtSFrZDfrmiKSVZmjaHSE3U9okMusK5o2D3h4siZt8fUt/s1600/greenbg_chetes.jpeg" /></span></a></div>
The other day, someone asked me what the difference was between bacteria which is antibiotic resistant and bacteria which are persister cells, thinking they were the same thing.<br />
<br />
When one first hears about bacteria persisting, one often makes the assumption that must mean it's antibiotic resistant.<br />
<br />
But there is a difference between bacteria which are antibiotic resistant and bacterial persister cells - which are antibiotic <i>tolerant </i>.<br />
<br />
I'm going to provide a simple illustration (ragged as it is) to show what that difference is without getting too bogged down in terminology.<br />
<br />
First, since many people are familiar with the term "antibiotic resistant" and have heard it in the news a lot when journalists discuss MRSA and other major bacterial infections, I'll start there, and explain what it means for bacteria to be antibiotic resistant...<br />
<br />
<b>What Is Antibiotic Resistance, Anyway?</b><br />
<br />
When an antibiotic is used, susceptible bacteria are killed or inhibited by an antibiotic, resulting in a selective pressure for the survival of resistant strains of bacteria.<br />
<br />
Some bacteria are naturally resistant to certain antibiotics - they just happen to have the genetic makeup and qualities which make them instantly resistant to certain antibiotics. But in other cases, bacteria develop a resistance to antibiotics through genetic mutation or acquisition of genetic material from another source.<br />
<br />
Antibiotic resistance may take the form of a spontaneous or induced genetic mutation - that is, either a random mutation or one which arose due to changes in the bacteria's environment.<br />
<br />
It can also occur when bacteria acquire resistance genes from other bacterial species by horizontal gene transfer via conjugation, transduction, or transformation - in other words, bacterial sex, viral sharing of DNA via bacteriophage, or acquisition of DNA from another external source.<br />
<br />
Exposure to an antibiotic naturally selects for the survival of the organisms with the genes for resistance. A gene for antibiotic resistance may readily spread through a population of reproducing bacteria.<br />
<br />
This is a quick and dirty diagram illustrating what antibiotic resistance looks like: <br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<span style="font-family: inherit; margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgB0rAZ4ci3SDGLRw5eZe25HwLozJl-2WGV_EiLxc9JC0UtL01YDWLFIL8tj_ukPJqTvwiGd3baukafVZpotx_pzhGfwWN67B-LpCRAJ8D5ooBrSCYZx9ybLyNL3cE9-_rpzvrXpfaKWp9z/s1600/1whatIsDrugResistance.gif" height="297" width="320" /></span></div>
<br />
<br />
One thing to keep in mind in the illustration above is that non-resistant bacteria and drug or antibiotic resistant bacteria can exist at the same time in the same host. But eventually, all the non-resistant bacteria will die off and the antibiotic resistant bacteria will survive and reproduce, creating an <i>entirely resistant </i>population of bacteria.<br />
<br />
The infection will continue to spread - unless the host's immune system is strong and can manage to kill off the antibiotic-resistant bacteria - or a different antibiotic can be found that kills them.<br />
<br />
But some antibiotic resistant infections are so virulent and so successful, that neither antibiotics nor the host's immune system can overwhelm them.<br />
<br />
This is catastrophic when it happens on a large scale. Right now, we are headed that way, as we are having a worldwide antibiotic resistance crisis: Too many people are contracting infections which we are having difficulty effectively treating with existing antibiotics - or in some cases we cannot treat them at all.<br />
<br />
So, this explains what antibiotic resistant bacteria is: Bacteria which either naturally has a genetic makeup which makes it resistant to a specific antibiotic or bacteria which mutates (due to various factors) in such a way that it is more likely to survive the onslaught of antibiotics and produce a new generation of resistant bacteria.<br />
<br />
<b>How Are Persisters Or Persister Cells Different From Antibiotic Resistant Bacteria?</b><br />
<br />
Persister cells are a small subset of a given bacterial population which are <i>not</i> produced by genetic mutation, nor are they resistant to a specific antibiotic by default.<br />
<br />
Persister cells are a specific <i>phenotype</i> of the same bacteria. A phenotype results from the expression of an organism's genes as well as environmental factors and the interactions between the two.<br />
<br />
When we specifically think about a phenotype in terms of people, we think of their physical characteristics - such as blue or brown eyes, curly or straight hair, and so on. Phenotypes are physical characteristics which are expressed, based on an organism's genes.<br />
<br />
In terms of bacterial phenotypes, we can think more about size and shape, rod shaped or spiral cells, and so on. But we can also think in terms of tendencies towards dormancy, and that certain environmental factors can lead to bacteria expressing their innate tendency to go dormant.<br />
<br />
One difference between antibiotic resistant mutants and persister cells is that, unlike mutants, cells regrown from such persistent bacteria <i>actually remain sensitive</i> to the antibiotic. But the entire population <i>will not </i>be <i>as </i>sensitive, and there will be a subpopulation which will be antibiotic <i>tolerant</i>.<br />
<br />
Here is a simple illustration showing the difference between antibiotic resistant bacteria, and persister cells, which are antibiotic tolerant:<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEghKnfbN7AFBcT4WGokt2RW5iD4uRx9k3VHr51cqAMsprTns0oDXxoMDK1XwgxtjUJ3GdM4hNdV-pd1m9XikvyKLoj4vg-TsZQ7vsqFJU1SSbLGrBojGd43c3y8OWwiCRoCEzWdpq8VofWh/s1600/Suarezfig1final.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEghKnfbN7AFBcT4WGokt2RW5iD4uRx9k3VHr51cqAMsprTns0oDXxoMDK1XwgxtjUJ3GdM4hNdV-pd1m9XikvyKLoj4vg-TsZQ7vsqFJU1SSbLGrBojGd43c3y8OWwiCRoCEzWdpq8VofWh/s1600/Suarezfig1final.gif" height="292" width="400" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<span style="font-size: x-small;">Image from Kenyon College's awesome <a href="http://microbewiki.kenyon.edu/" target="_blank">MicrobeWiki</a>.</span></div>
<br />
The above illustration shows the key difference between antibiotic resistant bacteria and persister cells.<br />
<br />
In the first row, the bacteria in the first dish are <i>mostly </i>susceptible to antibiotics, except a small number of bacteria which are <i>resistant</i>. Almost all bacteria die when exposed to antibiotics - leaving behind the resistant bacteria, which multiply and fill the dish. Throwing more of the same antibiotic at these bacteria will <i>not</i> kill them.<br />
<br />
In the second row, we have bacteria which are also <i>mostly</i> susceptible to antibiotics, but a small number of bacteria are persisters. Almost all the bacteria die, and the persister cells become active and reproduce, creating a new population of bacteria of which some can still be <i>susceptible</i> to the same antibiotics and be killed off - but there will continue to be persister cells which could slowly multiply and <i>survive</i> more of the same antibiotic.<br />
<br />
Persister cells have a phenotypic "switch" which can turn on at random or in response to environmental events. There are <i>at least</i> three main phenotypes of persister cells:<br />
<br />
1) Those that reenter a normal growth phase and are quickly killed.<br />
<br />
2) Type I persisters exit the stationary phase very slowly, in a matter of hours (if not longer) rather than minutes after getting nutritional requirements met.<br />
<br />
3) Type II persisters occur via a spontaneous switch from a normal growth rate to a consistently slow growth rate - regardless of growth conditions and rarely switch back to the normal growth rate.<br />
<br />
Anyway, overall, the mechanisms of persisters are poorly understood, and it's only in the past several years that interest has been ignited (or actually, reignited, as it was known some cells persisted after antibiotic use in the 1940's!) in persister cells and these mechanisms are being more closely investigated.<br />
<br />
<b>Antibiotic Resistance And Borrelia Burgdorferi - Not So Fast?</b><br />
<br />
So what about the bacteria which causes Lyme disease, <i>Borrelia burgdorferi</i>? Is it antibiotic resistant? Has it shown signs of going the way of staph infections and tuberculosis, by becoming increasingly resistant to the antibiotics thrown at it?<br />
<br />
No - at least not so far. In general, there is no evidence of <i>acquired</i> antibiotic resistance by <i>Borrelia burgdorferi</i> in response to treatment.<br />
<br />
There is evidence, however, that some isolates have different preexisting susceptibilities to different antibiotics. Borreliae are known to be naturally resistant to aminoglycosides and quinolones, such as ciprofloxacin acid and ofloxacin. There have been <i>Borrelia burgdorferi</i> strains grown in laboratories and clinical isolates which show resistance to erythromycin. This particular resistance was <a href="http://aac.asm.org/content/46/11/3637.full">first written about in depth in a 2002 study</a>. Strain N40 is known to be resistant to erythromycin.<br />
<br />
Erythromycin resistance is not an issue for most people who contract Lyme disease because erythromycin is a second line antibiotic which is not used to treat Lyme disease very often. It is important to be aware of it in case a patient has an allergy to the other antibiotics which are typically given and is offered erythromycin.<br />
<br />
<a href="http://aac.asm.org/content/54/2/643.full">A study completed in 2010</a> demonstrated that <i>Borrelia burgorferi</i> is not eradicated by tigecycline, and in this study the issue of <i>Borrelia burgdorferi</i> potentially having persister cells and being antibiotic tolerant was raised. <br />
<br />
It is possible that in the future <i>Borrelia burgdorferi</i> will show signs of acquired antibiotic resistance, and studies will reveal this to be the case. There is recent evidence<a href="http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000009" target="_blank"> that<i> Borrelia burgdorferi</i> has an efflux pump</a> - also known as a membrane transporter protein - which could "pump" antibiotics out of cytoplasm as a mechanism of resistance. (More about efflux pumps here: <a href="http://en.wikipedia.org/wiki/Efflux_(microbiology)">http://en.wikipedia.org/wiki/Efflux_(microbiology)</a>)<br />
<br />
Intriguingly, the researchers who wrote about these efflux pumps in <i>Borrelia burgdorferi</i> stated, "Existing evidence indicates that the possible heterogeneity of <i>B. burgdorferi</i> may enable certain isolates to evade antimicrobial therapy and may account for the subsequent relapses suffered by some patients," and cited three papers which support this statement. <br />
<br />
At the time of publication up to the present, though, acquired resistance to specific antibiotics in specific isolates has yet to be confirmed.<br />
<br />
However, new research has identified that <i>Borrelia burgdorferi</i> does have evidence of a persister cell population <i>in vitro</i>. <br />
<br />
<b>Borrelia burgdorferi And Persister Cells</b><br />
<b><br />
</b> Some researchers - such as Dr. Stephen Barthold, who completed the study mentioned above on the effectiveness of tigecycline to treat Lyme disease - have suspected for some time that <i>Borrelia burgdorferi</i> might have a persister cell population.<br />
<br />
The issue of persistence in Lyme disease has become an oddly controversial topic, for which there is no reason - research will surely sort out what the nature of these wily spirochetes is one way or the other.<br />
<br />
And there is a renewed interest in determining what the nature is of <i>Borrelia burgdorferi</i> spirochetes which have been known to survive initial antibiotic treatment in animal models, and could survive treatment in humans as well.<br />
<br />
Recently, <a href="http://www.cdc.gov/lyme/pdfs/PersistenceWebinarSlides.pdf" target="_blank">the CDC webcast a seminar</a> via live streaming about government-funded studies touching on the persistence of Lyme disease spirochetes (this blog will discuss this seminar more in the near future). <br />
<br />
But even more recently, two publications were announced which discuss <i>Borrelia burgdorferi</i> persister cells as well as which antibiotic compounds to which those persister cells may be at least partially if not totally susceptible.<br />
<br />
The first publication was presented at the American Society for Microbiology conference this year (ASM2014) by Sharma et al, who are Dr. Kim Lewis' team which studies persister cells at Northeastern University. In their presentation, "Persister formation in <i>Borrelia burgdorferi</i>", the authors determined that 0.001% to 1% of <i>Borrelia burgdorferi</i> cells can survive lethal doses of various antibiotics <i>in vitro</i>.<br />
<br />
If 0.001% to 1% of the cells can survive lethal doses of various antibiotics <i>in vitro</i>, then once you've killed off all but the persister cells, the original population will be replaced <i>in vitro </i>in a range of times and conditions as follows:<br />
<br />
If only .001% of the spirochetes remain, and it takes 24 hours for each division, it will take 17 days for the bacteria to return to their original population size.<br />
<br />
If only .001% of the spirochetes remain and it takes 12 hours for each division, it will take 8.5 days for the bacteria to return to their original population size.<br />
<br />
If 1% of the spirochetes remain and it takes 24 hours for each division, it will take one week for the bacteria to return to their original population size.<br />
<br />
If 1% of the spirochetes remain and it takes 12 hours for each division, it will take 3.5 days or so for the bacteria to return to their original population size.<br />
<br />
All these are back-of-the-napkin calculations for what would happen to these bacterial persisters <i>in vitro</i>, provided they aren't environmentally challenged and have a stable medium; provided they don't lapse into dormancy. What exactly would happen <i>in vivo</i>, in the host, has yet to be clearly determined.<br />
<br />
The second paper, by Feng et al, "<a href="http://www.nature.com/emi/journal/v3/n7/full/emi201453a.html">Identification of novel activity against <i>Borrelia burgdorferi</i> persisters using an FDA approved drug library</a>", with Dr. Ying Zhang as PI, evaluated the use of specific FDA-approved antibiotics which affected persister cells. A series of fluorescing protein studies were completed which <a href="http://www.nature.com/emi/journal/v3/n7/fig_tab/emi201453f3.html#figure-title">gave visual confirmation</a> of which of the 1524 compounds reviewed were more effective at killing persister cells. So far, daptomycin appeared to be at the top of the list for effectiveness <i>in vitro</i>. Additional studies in the future may be performed on animal models.<br />
<br />
<u><b>The executive summary:</b></u><br />
<br />
Antibiotic resistant bacteria is resistant due to internal or induced genetic mutation of the bacteria, or by introduction of new genetic material to the bacteria.<br />
<br />
Persister cells have a phenotypic switch, and can become dormant <i>randomly or due to environmental stress</i>. All the genes the bacteria needs to do this are already there; they are not mutants. Persister cells can be susceptible to antibiotics, but a subset will be tolerant to antibiotics - and that degree of tolerance depends on which phenotype they are.<br />
<br />
<i>Borrelia burgdorferi</i> do not show signs so far of acquired antibiotic resistance. But the bacteria do have natural resistance to several antibiotics, and some specific resistance based on strain. <br />
<br />
<i>Borrelia burgdorferi</i> have a population of persister cells, on which further studies are needed to determine their role in the infection process and how best to address them.<br />
<br />
<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><span style="font-family: inherit;"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></span></a><br />
<small><span style="font-family: inherit;">This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</span></small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com4tag:blogger.com,1999:blog-4073397588746430486.post-28576698487069421592014-05-19T14:35:00.003-10:002014-07-13T10:06:31.653-10:00Op/Ed: Thoughts And Reflections On Worldwide Lyme Disease Awareness Protest<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKH2A5ZGtInEF2h5ZH-o2UCmxG9uCWtXSlnIIfsTdMMDI8lNAk3t3fmrBdh54uypQdvgSHaSHeK_OvF2FvQA6inPTtJwWIaAPK6abpA9nVCYPxnl1WZnE2r0IYJ8Ofqyk0oQvDIHtNO16G/s1600/CampOtherBadge2.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKH2A5ZGtInEF2h5ZH-o2UCmxG9uCWtXSlnIIfsTdMMDI8lNAk3t3fmrBdh54uypQdvgSHaSHeK_OvF2FvQA6inPTtJwWIaAPK6abpA9nVCYPxnl1WZnE2r0IYJ8Ofqyk0oQvDIHtNO16G/s1600/CampOtherBadge2.jpg" /></a></div>
This past weekend, May 16-18, many Lyme disease patients, their advocates, and organizations hit the streets, sent out tweets, and held events not only to spread awareness about Lyme disease around the world - but to be a vocal group protesting the current state of affairs regarding how the medical community manages tickborne diseases.<br />
<br />
I admit I'm late to the game on this one, having fallen behind on some of the activities going on in the Lyme disease advocacy world and focusing more on new research, a few Lyme disease related bills making their way through state and national governments, and as usual, my own medical concerns.<br />
<br />
This past weekend was particularly challenging while using of Twitter because I was in a position where many Lyme disease advocates were posting about various Lyme disease awareness events and, at the same time, microbiologists I follow began tweeting from a major microbiology conference which had just begun in Boston.<br />
<br />
Now, I'm not really good at multitasking even in the best of times - but it was a serious challenge to figure out how to divide my time, focus, and energy up in order to retweet items which caught my eye during the weekend.<br />
<br />
So I may not have split the difference that well, and for that I apologize to anyone hoping to see more of a specific type of content in my tweets and retweets. I was having a difficult time prioritizing what to post, in being mindful of my audience as well as my own interests.<br />
<br />
At the same time, I feel pretty confident that those who organized their regional protests for the worldwide Lyme disease awareness protests were doing well at the task ahead of them and doing a better job than I can about letting everyone know why they were protesting and how many different groups around the globe were involved. Advocacy can come in many different flavors and forms, and perhaps it's even fair to say I'm not the best person at organizing protests and rousing the crowds.(I don't know, by the way, on the basis of never having tried it.) <br />
<br />
And also I'm somewhat unnerved at the prospect. An active, outgoing role for advocacy is best left to people who are somewhat further along on their recovery from illness than I am, because they can go forth in the world with a stronger physical presence; they have the stamina to spend hours walking the pavement when I do not.<br />
<br />
But even as I sit here at home, catching up on some rest and periodically sitting down to write this blog, I wish I had given more of my attention to this protest earlier because of its mission statement and what it says.<br />
<br />
The home page which is the primary organizing force for these Lyme-aware activities around the world, <a href="http://worldwidelymediseaseprotest.blogspot.com/">worldwidelymediseaseprotest.blogspot.com</a>, posted the mission statement of the worldwide protest and what protesting patients and advocates around the world say they need…<br />
<br />
Worldwide Patients are raising awareness and protesting to highlight the need for:<br />
<br />
<blockquote class="tr_bq">
1. Recognition that Lyme disease/borreliosis, and other tick-borne infections, such as Babesia, Bartonella, Rickettsia, Ehrlichia, are serious, and sometimes fatal illnesses.<br />
<br />
2. Awareness of the fact that the transmission of tick-borne pathogens, such as borrelia, babesia, rickettsia, via blood transfusion is of global concern. </blockquote>
<blockquote class="tr_bq">
3. Agreement that Lyme disease/borreliosis should be listed as a notifiable infection. Notifiable status will aid in ensuring that the incidence and spread of this disease are monitored, a necessary precursor to determining the human suffering and socioeconomic impact of the disease. </blockquote>
<blockquote class="tr_bq">
4. Education of the healthcare sector regarding the accurate diagnosis of Lyme, which in some cases may be limited to clinical presentation due to limitations of serological testing.<br />
<br />
*Education should ensure all doctors are familiar with the CDC caution pertaining to criteria for blood tests for Lyme: “This surveillance case definition was developed for national reporting of Lyme disease; it is NOT appropriate for clinical diagnosis...Surveillance case definitions are created for the purpose of standardization, not patient care.”<br />
<br />
* Education that Lyme should be included as a differential diagnosis when considering other illnesses that are also reliant on subjective clinical presentation, or have no known cause. This includes, but is not limited to: Motor Neurone Disease (MND) also known as Lou Gehrig’s disease or Amyotrophic lateral sclerosis (ALS) ; Multiple Sclerosis ; Alzheimer’s; Parkinson’s disease; Sarcoidosis.<br />
<br />
5. Education of the healthcare sector regarding affordable and effective treatment of both acute and chronic Lyme and other tick-borne infections. This includes the need to update the outdated treatment guidelines of the Infectious Diseases Society of America (IDSA) and to take into account the treatment methods of other Societies such as: The International Lyme and Associated Diseases Society (ILADS) and the German Borreliosis Society (Deutsche Borreliose-Gesellschaft : DBG)<br />
<br />
6. Funding for research into tick-borne diseases. Including: Funding for medical research into accurate Lyme testing and treatment ; Funding for research into vectors and reservoir hosts to determine what diseases they may carry and transmit. </blockquote>
<br />
<u><b>Thoughts on the mission statement</b></u><br />
<br />
I agree with these statements in general: There is no argument that tickborne diseases are serious and can be fatal, that we need to be aware that they could be transmitted through blood transfusions and we don't necessarily screen for them or even have standardized high volume tests for them; that better tracking of Lyme disease suspected and confirmed cases would be helpful in getting a better estimate of cases and their socioeconomic impact, that the medical profession needs to be aware of the limitations of serological testing in diagnosing Lyme disease, that guidelines which are outdated need to be updated, and that more research needs to be conducted on Lyme disease including research that leads to improved testing and more effective treatment as well as achieving a better idea of which diseases are being carried and spread.<br />
<br />
<i>Phew. I need a deep breath after that paragraph.</i><br />
<br />
The mission statement as outlined is a good one - a starting point, a talking point on which more discussions can be built and more meaning added to it by those who are presenting it to a crowd by sharing it online and sharing it on the streets. <br />
<br />
I already know and understand the six items, intimately, because I have suffered with Lyme disease and Babesia, have been dealing with persisting symptoms for a long time - and after finding others in a similar situation want similar items addressed. <br />
<br />
And a large number of people came to an agreement on what this mission statement says because they, too, have shared my experience of not having been properly treated for Lyme disease as early as we could have been and have had to live with complications due to delayed treatment - as well as being co-infected and/or possibly due to other factors we have yet to fully understand.<br />
<br />
With this in mind, it's important for those who are not patients and advocates to understand that much of what is written is a cautionary statement, written through suffering and pain by people who have endured persisting symptoms after contracting Lyme disease who want to prevent even just one more person from having to experience the hell they have experienced. <br />
<br />
<i>And that would include me.</i> I don't want anyone to experience the hell I've been through and the problems I still have.<br />
<br />
The message to anyone healthy reading along from Lyme disease advocates to you is : <br />
<br />
<i>We want you to stay well. We want you to be healthy. </i>We want you to engage in jobs you enjoy, buy a house, finish that degree, have loving relationships, raise kids, play sports, go out and about and do lots of things. All the things that - by the way - a number of us can no longer do and fear we may never achieve.<br />
<br />
None of us would be here - either me writing this blog or these folks writing up a mission statement who are out protesting on the streets and from their computers - if we didn't each either suffer from the consequences of tickborne disease or are close to someone who has. We would be doing something else, and quite possibly doing something else our hearts yearned for, that we long dreamed about - only to have those possibilities crushed out of us due to being fatigued and enduring unpredictable cycles of dysfunction and pain.<br />
<br />
<b><u>Blood tests</u></b><br />
<br />
… That is why we want better blood tests - ones which are effective early on, and can catch the presence of a tickborne infection before the worst symptoms set in. <br />
<br />
We want to see those of you who are newly bitten swiftly tested with accurate tests and promptly treated so you can avoid more serious symptoms and worse, more serious persisting symptoms that disrupt your lives for months and years to come.<br />
<br />
The way things are now, it can take 4-6 weeks after a tick bite for antibodies to Lyme disease show up from a blood test. Sometimes it can take 8 weeks or even longer.<br />
<br />
If a patient has Lyme disease but never has a rash, the diagnosis may be missed. An early negative blood test can delay treatment. This is important because those who are treated with antibiotics early on are <i>far less likely</i> to experience severe symptoms and complications from Lyme disease.<br />
<br />
And now, there is a new relapsing fever spirochete carried by the same kind of tick which carries Lyme disease - <i>Borrelia miyamotoi</i>. And this spirochetal disease gives you symptoms very similar to Lyme disease - yet patients with it rarely see a rash and a blood test for Lyme disease will never be positive when you're infected with this organism. <br />
<br />
<i>Borrelia miyamotoi</i> is a serious infection which needs antibiotic treatment.The earlier it is diagnosed and treated, the better. In a Russian study of patients with infections with <i>Borrelia miyamotoi</i>, symptoms were more severe than those found in patients with Lyme disease and more patients needed hospitalization and intravenous antibiotics compared to patients with Lyme disease.<br />
<br />
<u><b>Doctor education</b></u><br />
<br />
It's not just that better objective testing for the presence of infection with Lyme disease is needed. It is - that's true. But it's also true that what's needed are better methods of assessing patients for the possibility a tickborne disease is causing their symptoms in the first place and that tickborne diseases beyond Lyme disease also have to be taken into account. <br />
<br />
The poor bastard who has flu-like symptoms, a migraine-like headache, high fever, and is severely fatigued who repeatedly tests negative for Lyme disease and is told it must be in his head needs to become a thing of the past; a relic. <br />
<br />
A Lyme disease test will never be positive for <i>Babesia</i> and <i>Borrelia miyamotoi</i> here in the United States, no matter how many times you run it - and yet the patient will still be sick. <i>Not crazy. Sick.</i><br />
<br />
The same applies to someone whose initial Lyme disease serology is negative yet they appear ill after having had a tick bite. Doctors need to look for coinfections. Retest for the presence of Lyme disease antibodies later, because the first test may have been too early even at 4 weeks for that specific patient. Read the literature about comparing different labs' tests for Lyme disease serology. And when it's clear the patient doesn't have a viral illness after symptoms continue to worsen and do not progress like the typical flu; when there's no recovery coming and the chest x-ray is clear... further investigation is needed.<br />
<br />
Doctors need to recognize this, grapple with it, and by default begin to look for a physical cause for patients' symptoms before resorting to psychiatric labels. After all, we can't all be "crazy". And if we are, then that is something our society seriously has to investigate - because either the numbers are being inflated or as a culture we are downright pathological.<br />
<br />
(This is, by the way, not to say that every patient with flu-like symptoms, a migraine-like headache, and high fever automatically has a tickborne disease. Not all all. It's just something that should be considered in the differential diagnosis more often than it has been in the past.)<br />
<br />
<u>Side note:</u><br />
<br />
I do not envy today's medical students, and the world they are entering as doctors. They will not only be facing the spectre of increasingly antibiotic resistant infections and the resurgence of measles and polio - they will be facing the onslaught of vector-borne diseases which are spreading to areas in which they had formerly receded or where they previously had never been. They will be facing diseases carried by mosquitoes and ticks that were previously viewed as exotic and foreign - only to find they knew no borders, and could travel here just as people and birds do.<br />
<br />
Any awareness of Lyme disease is just that - a narrow band of awareness focusing on one disease. Looking at other potential pathogens which can infect people is important, too, and becoming a medical detective is going to become a more prominent part of the job of being a doctor. <i>Who knows who will discover the next patient 0?</i><br />
<br />
<b><u>Make tickborne diseases reportable - and don't stop there</u></b><br />
<br />
Once someone has a tickborne disease, it needs to be reportable. Both suspected and confirmed, in order to get a better estimate of the number of cases out there - but also to help form a picture of how cases present themselves based on the clinical picture. <br />
<br />
Given that 10-20% of all patients who contract Lyme disease develop persisting symptoms after initial antibiotic treatment under existing IDSA Lyme disease panel guidelines,<b> I would also make chronic Lyme/post treatment Lyme disease a reportable condition. </b><br />
<br />
No one to my knowledge is reliably tracking this condition and the number of patients who get it. And while many patients claim they were diagnosed with chronic fatigue syndrome or fibromyalgia only to find out later on they had Lyme disease, I don't think anyone has made a point of looking back in time at all their patients' files to see if those diagnosed with chronic fatigue syndrome or fibromyalgia had a documented record of a tick bite or previous diagnosis with Lyme disease - which could very well mean what they're really seeing in front of them is a case of chronic Lyme/post treatment Lyme disease which needs to be recorded. <br />
<br />
Is it really 10-20% of an estimated 300,000 Lyme disease cases per year in the US - around 30,000-60,000 people a year who develop chronic Lyme or post treatment Lyme disease? Or is it more? <i>Or less?</i> Most patients I know would scoff at the idea of fewer cases. But the truth is, we don't know, because chronic Lyme disease or post treatment Lyme disease is not reportable. <br />
<br />
And as much as the CDC and other institutions prefer and support the use of the term "post treatment Lyme disease" or "post Lyme disease" over the usage of "chronic Lyme disease" in the US, it's not clear how often family doctors and specialists actually apply these diagnostic terms to their patients in clinical practice. Nor is it something I hear about much (though I have heard of one case of post Lyme disease syndrome as a diagnosis recently) within the Lyme disease patient community.<br />
<br />
People with a history of a tick bite and a flu-like illness which follows and doesn't go away after initial treatment report that they were usually first diagnosed with something else after initially having Lyme disease - but not usually "post-anything" and certainly not chronic Lyme disease.<br />
<br />
<b><u>Guidelines need updating - and it's not just about chronic Lyme disease</u></b><br />
<br />
In terms of guidelines… I'm possibly not going to have everyone jumping up and down in regards to what I write next, but I have to call it as I see it: Treatment guidelines for Lyme disease do need an overhaul, <i>period</i>. <br />
<br />
They either fall short of providing effective treatment for all patients who have been affected by Lyme disease or they lack studies which demonstrate high degrees of lasting positive outcomes for all patients. <br />
<br />
ILADS guidelines acknowledge that patients who fail initial treatment may need additional treatment and it's okay to try empiric treatment to see if it helps in an individual case. This approach may or may not help individual patients - but given some patients report marked improvement, this deserves further investigation.<br />
<br />
While their approach is something which requires more study and validation, at this point in time, patients have few options to explore in terms of treatment. Many are desperate for relief from pain, problems with short term memory and mental focus, fatigue, and other symptoms, and it would seem logical to try more antibiotics for treatment first as they are well studied, side effects are known, and it's thought a positive response to antibiotics confirms the presence of infection.<br />
<br />
This perspective by patients has been questioned and denounced by some researchers, who state that a positive response to antibiotics is not enough evidence that patients' infections persist and they could just be having a positive response to the anti-inflammatory effect of certain antibiotics.<br />
<br />
No one has conducted a study on this, however. And to this day, no one has conducted studies which apply the same antibiotic treatment methods ILADS does, either. There are no objective data on what works and what doesn't work beyond case studies and individual patient reports.<br />
<br />
And at the same time, the IDSA Lyme disease panel guidelines fall short by failing to offer any form of treatment at all, not offering any off-label treatments which may be helpful, nor are they suggesting future directions for research. Instead, their 2006 guidelines contain a long list of treatments that patients should not have including vitamin supplementation. (Nevermind that in some cases a Vitamin D deficiency may add to patients' pain and supplementation could help with symptoms. That's not mentioned here, but surely it could be included in an update?)<br />
<br />
If patients have any persisting symptoms past their initial guidelines-based treatment, most doctors currently offer patients antidepressants, anticonvulsants, and select pain medicine to treat the symptoms. Many patients report that these treatments do not consistently provide relief, though, and in some cases they do not help at all.<br />
<br />
But let's look at one key source of the problem: The 2006 guidelines for the treatment of Lyme disease by the IDSA are outdated, and they are partially outdated <i>by virtue of there not being any large, new, double-blind random controlled clinical trials and/or controlled studies having been completed in the past decade</i> <i>which would shed light on how more patients could be more effectively treated. </i><br />
<br />
The guidelines which the IDSA Lyme disease panel published in 2006 were largely a carbon copy of those published in 2000. Many of the cited studies in them were conducted in the late 1980s and early 1990s. The remainder of the guidelines are based on a few small clinical trials using a few months of antibiotics.<br />
<br />
Since that time, further research on Lyme disease has raised questions about its pathogenesis and persistence in animal models, but the findings from these studies have not been directly applied to the practice of human medicine. It seems a solid translational model for all aspects of Lyme disease does not appear to be ready.<br />
<br />
The chronic Lyme disease controversy is not the only one researchers need to investigate:<br />
<br />
At the first mention of a tick bite, we want to be certain that one 200 mg doxycycline pill is going to be adequate prophylaxis against Lyme disease. Research by Piesman and Hojgaard in 2012 suggests one 200 mg pill may <i>not</i> be adequate, and even before this 2012 study, one member of the 2009 IDSA review committee suggested that the strength of the quality of the evidence to support this recommendation was too high. (The committee as a whole also recommended grading of the evidence of this guideline needs to be carefully considered.)<br />
<br />
In early stage Lyme disease, there is documentation of there being up to a 10% treatment failure rate. <br />
<br />
In late stage Lyme disease, the guidelines state recovery after treatment may be incomplete. Late stage patients experience lingering symptoms, too.<br />
<br />
But surprisingly, there is no specific advice in the 2006 guidelines suggesting what to do about this and how to treat the patient, and the only later suggestion I could find independently is to give patients gabapentin for neuropathic pain.<br />
<br />
This, to me, sounds like more effective treatment is needed for early Lyme disease as well as late stage Lyme disease - regardless of what anyone thinks about chronic Lyme disease.<br />
<br />
As for chronic Lyme/post treatment Lyme disease:<br />
<br />
There are persisting symptoms in 10-20% of patients who contract Lyme disease, and some of these cases display symptoms which are equal in severity to cases of osteoarthritis and congestive heart failure.<br />
<br />
These severe cases are not the equivalent of someone with the "aches and pains of daily living" which are blithely mentioned in the 2006 Lyme disease guidelines. These are far more serious cases not to be written off - just as those who develop heartblock, autonomic system disorders, short term memory loss, moderate to severe fatigue, chronic pain, and other neurocognitive problems are not to be written off, either.<br />
<br />
In the end, people can (and will) argue all they want about whether or not extra antibiotic treatment is a good idea. What I'm doing, independently of that, is saying point blank that <b>regardless of that debate the current treatment approach under these guidelines isn't working for all patients. And it isn't working well for a sizable minority.</b><br />
<br />
Either way, no one has conducted any new treatment study for chronic Lyme disease or post treatment Lyme disease in years - either using antibiotics or on new immune modulating drugs or even supportive treatment such as better pain management approaches.<br />
<br />
And patients and their families and workplaces continue to pay that price, in the months and years of patients having debilitating illness, loss of income, and loss of productivity. <br />
<br />
<b><u>Research for tick-borne diseases</u></b><br />
<br />
After all I've written in this blog since it began years ago, my main complaint, my main rant has not been addressed and it is that many years have gone by and there has been very little solid research on patients with chronic Lyme disease or post treatment Lyme disease or post Lyme (one, the other, or both) and very little solid research on potential new treatments for those suffering.<br />
<br />
And all the concerns which are brought up, above, in the worldwide Lyme disease awareness protest mission statement are ones I share in terms of research: <br />
<br />
<b>We need more accurate Lyme disease testing</b>, <b>and to know who is actively infected and who has had infection in the past. </b>A solid direct detection test for this purpose would be great, and lack the issues a test for antibodies does. (In the meantime, perhaps a test like Spirofind will be helpful and offer additional support for diagnosis.) Right now, with the tests commonly used, it's not always easy to determine whether someone has an active infection or not.<br />
<br />
<b>We need better treatment and more options for those patients with persisting symptoms. </b>And before someone jumps in defensively and says they are against seeing patients being treated with long term antibiotics, I'd like to add here that no one - not one patient I've talked to - actually <i>likes</i> to be on long term antibiotics.<br />
<br />
They are trying it because they have nothing to lose and are incredibly miserable. They are trying it because in many cases they fear they will lose a lot more than they would if they <i>didn't</i> try it. <i>Their jobs. Their families. Their friends. Even their minds.</i><br />
<br />
They are also trying it because there are very few treatment options available, people report improvements on it, and because antibiotics are considered a "known" factor - they are evidence-based drugs which have been clinically tested, have been used long term for various indications including acne, and their safety profile and risks are known. Beyond this, of course, anything a patient tries is either indicated as a treatment to address pain, followed by alternative medicine.<br />
<br />
If there were more effective shorter term treatments which worked, if there were more effective pain treatments which worked - patients would be willing to try them. Just as patients are willing to try any of a number of treatments now to get some relief and get their lives back. <i>But they'll never get a chance to try anything new and evidence-based if no one does the research required.</i><br />
<i><br />
</i> People may argue that as long as they aren't sure what causes chronic Lyme/post treatment Lyme disease, then new treatments cannot be explored. <i>Nonsense. </i>There are plenty of other diseases and conditions which are not well understood for which treatment has been developed and tested. To some degree, it may be that new treatments <i>need</i> to be developed and tested in order to acquire more knowledge about what is causing patients' symptoms - and to understand whether or not all patients are suffering with the same condition or if there are different subgroups.<br />
<br />
<b>We need more research into what kind of pathogens ticks are carrying and if they are pathogenic for people. </b>This is a harder job to do, because new tickborne viruses, bacteria, and protozoa are always being discovered. I'm not sure how one is to stay on top of tickborne diseases in particular, relative to all the other new infections which are spreading across the globe. But it is a necessary part of understanding what is happening and be preemptive about zoonoses and the spread of vectorborne disease. <br />
<br />
<b>I'd also like to add here that we need more research into frontline prevention. </b>Development of a product like the Kite Patch (but a version used for ticks, not mosquitoes) and vaccines which work against multiple tickborne infections which can be used in oral bait in the wild seem to be solid ideas to develop to prevent tick bites and reduce infection in host animals.<br />
<br />
<b><u>Missing pieces:</u></b><br />
<b><u><br /></u></b>
<b>The need for better science communications on tickborne diseases in the media and public - and patient liaisons for those with persisting symptoms</b><br />
<b><u><br />
</u></b> An additional item I would add to this mission statement - or perhaps make it two items - is that patients and the public need better science communications on tickborne diseases in the media, and also a patient liaisons who are educated, articulate, and can work to represent patients in a research and public health context (refer to PCORI for an organization which already does this kind of work).<br />
<br />
The way Lyme disease is discussed in the media right now has to change. It's been dumbed down, the debate between two sets of doctors has been fired up in articles in order to sell papers, and the actual research being done on the disease is either seldom mentioned and sometimes when it is, important details get lost.<br />
<br />
I'd like to see more people in public discussing Lyme disease and other tickborne infections who actually do research on it, who are familiar with the debate over whether Lyme disease can persist or not, and who are not caught up in the middle of the debate share their knowledge and questions they think need to be asked to resolve controversies over persistence. I'd also like to see more medical professionals including immunologists and pain specialists write more about what kind of novel therapies they might suggest are worth trying now which would help patients feel better and improve their quality of life on top of or instead of treatments they are already trying - and to discuss the possibility of new research.<br />
<br />
Seeing more articles written about Lyme disease and other tickborne infections, more science blogs about Lyme disease and other tickborne infections, and more educational outreach in the form of websites and books by those educated about them who can outline the certainties and uncertainties about these diseases would go a long way towards reducing ignorance about them and provide an alternative to sites which are filled with misinformation and conspiracies.<br />
<br />
As for patient liaisons, patients with persisting symptoms related to tickborne infections need to have greater representation in the kind of research that is being funded and what will help those who are most severely affected by tickborne disease.<br />
<br />
As it stands, a lot of the frustration which is shared within the Lyme disease patient community is over the lack of more research on their condition and lack of communication about why there has been no patient-centered assistance from groups such as the IDSA Lyme disease guidelines panel (and if anything, some patients have been individually and collectively insulted by select members of this panel (documentation of this can be found elsewhere online)) and limited assistance and communication from those who make funding decisions for government funded Lyme disease research.<br />
<br />
Those with persisting symptoms question why there is yet another study on <i>erythema migrans</i> rashes and so little research on their condition, and want to know how study selection is determined and when and how their concerns can be addressed in a research context. But according to many patients, there has been little to no positive direct communication about these matters from certain organizations such as the IDSA panel with patients and their advocates.<br />
<br />
It is this attitude of disdain or act of avoidance of patients' concerns which many consider unprofessional and which prompts me to wish that a new panel could be elected which can better reflect patient concerns as well as represent the state of the science including uncertainties - and reduce the burgeoning weight of the history of the debate in Lyme disease.<br />
<br />
Clearly, more positive engagement is needed between patients who suffer with persisting symptoms, their advocates, and those who wield incredible power over making decisions as to how to treat their condition and what is worthwhile research.<br />
<br />
<b>And before I forget: We Need Open Access Research</b><br />
<b><u><br /></u></b>
One frustration I and others face in trying to understand the history behind how Lyme disease is tested for, diagnosed, and treated - as well as the current sociopolitical climate involving Lyme disease research and advocacy - is that most of the peer-reviewed publications about Lyme disease, chronic Lyme disease, and post treatment Lyme disease are behind paywalls.<br />
<br />
Some of these papers have major implications for Lyme disease patients and yet many cannot access them and learn for themselves what the arguments are between academic doctors, medical organizations, advocacy organizations, and others actually are when it comes to Lyme disease.<br />
<br />
Often, misinformation about the content of different papers gets shared and spread amongst patients who do not have access to the original copy. From there, it's all over the internet, with facts mixed in with fiction. <i>Was something in that paper? Wasn't it? </i>Who knows, unless you have the $30 or more to shell out for it. (Most don't. And even if you do, 24 hours of access is not enough.)<br />
<br />
Some publications have old data which may have been overlooked and could be useful in revisiting in order to take new directions in research, and duplicate old studies and retest hypotheses. But patients and advocates can't even access many of these papers even though they may date back as far as the mid-1980's, not long after <i>Borrelia burgdorferi</i>, the spirochetal bacteria which causes Lyme disease, was discovered. To me, this is ridiculous and it needs to change.<br />
<br />
<u><b>Closing comments</b></u><br />
<br />
I agree with all that is within the mission statement and yet I think in actuality it needs to go further. The strength in a protest which has a petition or plea for certain changes to be made is improved by getting into the details more and asking for more specifics that would be useful in resolving the problems which have dogged Lyme disease patients and advocates for many years.<i> Decades now.</i><br />
<i><br />
</i> And I think it must be emphasized that there have been problems with the scene in Lyme disease for many years now, and nothing has changed in many ways. That's the biggest item to me really, that I'd like to protest.<br />
<br />
<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small><br />
<small><br />
</small> <small><br />
</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com2tag:blogger.com,1999:blog-4073397588746430486.post-42580049064385524852014-05-17T17:22:00.002-10:002014-05-17T17:24:31.485-10:00Lyme Disease Prevention: Tick Tack Toe Graphic<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjE7P6pTOHBn6M296dWEArI2cb0WAoXbz7ehSOeweqpdkX0myiVgGGPv7Vo2BguMxXeNK4qzbfYInINThQ1QHZCjMyKTM82bY8A0WrgIP5DFTwpdCroQIlVV4MWps5-G6070YDZQVXNIr68/s1600/supportlymeresearch2.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjE7P6pTOHBn6M296dWEArI2cb0WAoXbz7ehSOeweqpdkX0myiVgGGPv7Vo2BguMxXeNK4qzbfYInINThQ1QHZCjMyKTM82bY8A0WrgIP5DFTwpdCroQIlVV4MWps5-G6070YDZQVXNIr68/s1600/supportlymeresearch2.png" /></a></div>
This is just a brief post with a graphic about Lyme disease prevention created for Spring/Summer 2014 for use on Twitter, Facebook, or any of a number of social media sites. Camp Other's Tick Tack Toe game rules are simple: It is won by all players crossing off all squares to help avoid tickborne disease.<br />
<br />
Feel free to share... My only requirements are that you pass it on as it is with no further additions or subtractions - basically don't change it. Enjoy!<br />
<br />
<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZQJINcfv8XFUtfc6wKKnXHj995HFK915RfTgMvfshtcSeYaNtM-EzQzNm1a1NI-dQuy6k4jf1-mjclg3hRO2nPpfkTRp9DbUXSqhe9yey3H49CgDI4HWKe5_Qv393vYVF1hmPTF7QFMIc/s1600/CampOtherPreventionInfographic.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZQJINcfv8XFUtfc6wKKnXHj995HFK915RfTgMvfshtcSeYaNtM-EzQzNm1a1NI-dQuy6k4jf1-mjclg3hRO2nPpfkTRp9DbUXSqhe9yey3H49CgDI4HWKe5_Qv393vYVF1hmPTF7QFMIc/s1600/CampOtherPreventionInfographic.jpg" /></a></div>
<br />
<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ -->
<a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br /> Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com2tag:blogger.com,1999:blog-4073397588746430486.post-77819650554988118052014-04-30T14:57:00.002-10:002014-05-01T15:54:03.316-10:00Part 3: Sexual Transmission Of Lyme Disease - Is There Evidence?<div class="p1">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEir2ndwipgss9rSyxafsv2DocKFCdrTnq0YBe3VPbbssUVgs-6iHR76t-9_7NsiAbpR9iXxagUfvEmguEzhpAcLburd-sNa6d0Z_DepIR_o8WeFIIIYxl6o96TywQO4BcMJCGpna9A5vKNr/s1600/Raccoon_beside_blue_bin.jpg" imageanchor="1" style="clear: left; display: inline !important; float: left; margin-bottom: 1em; margin-right: 1em; text-align: center;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEir2ndwipgss9rSyxafsv2DocKFCdrTnq0YBe3VPbbssUVgs-6iHR76t-9_7NsiAbpR9iXxagUfvEmguEzhpAcLburd-sNa6d0Z_DepIR_o8WeFIIIYxl6o96TywQO4BcMJCGpna9A5vKNr/s1600/Raccoon_beside_blue_bin.jpg" height="200" width="179" /></a>This article is the continuation of "<a href="http://campother.blogspot.com/2014/04/part-2-sexual-transmission-of-lyme.html" target="_blank">Part 2: Sexual Transmission of Lyme Disease - Is There Evidence?</a>", our series on sexual transmission and contact studies involving <i>Borrelia burgdorferi</i>.<br />
<br />
To review the content of the first article briefly: We discussed the fact that no human sexual transmission studies of Borrelia burgdorferi have been conducted to date and reviewed the outcomes of animal studies on contact transmission and sexual (venereal) transmission. Based on all studies which could be found, there was evidence that <i>Borrelia burgdorferi</i> may be transmitted between at least some animals either via exposure to infected urine or by consumption of raw milk. The possibility that animals could transmit <i>Borrelia burgdorferi</i> to each other via sexual intercourse has only been examined in a few controlled studies, no cases have been confirmed so far, and it remains an issue of speculation in studies where uninfected animals came in contact with infected ones and developed a positive of antibody response (and in some cases, even signs of infection).<br />
<br />
What follows below is some notes on studies which are listed in Table 1 in "<a href="http://campother.blogspot.com/2014/04/part-2-sexual-transmission-of-lyme.html" target="_blank">Part 2: Sexual Transmission of Lyme Disease - Is There Evidence</a>?" as well as notes on additional papers on <i>Borrelia burgdorferi </i>transmission studies which were not included in that table as they were speculative and not based on controlled studies.</div>
<br />
<div class="p1">
<b>Additional Notes On Studies Included In Part Two's Table</b></div>
<div class="p2">
<br /></div>
<div class="p1">
The 1994 paper, "Distribution of <i>Borrelia burgdorferi</i> in host mice in Pennsylvania", is a study where samples are taken from ear tissue from mice from different counties around the state of Pennsylvania. When a sample was positive by darkfield microscopy and fluorescent-antibody testing, it was sent to the CDC for further evaluation.<br />
<br />
In the discussion section of this paper, the authors state that a group tagged mice in one county which repeatedly tested negative before began to turn up positive during the winter in areas where no vector ticks had been found - and because of this, the authors speculate this group of mice may not have been infected by ticks. However, there is no evidence in their paper which confirms an alternative method of infection. Because of this, I wouldn't cite this paper to support a method of contact or sexual transmission of Lyme disease between mice. It is a mystery how one specific group of mice in Indiana County were infected during the winter.</div>
<br />
<div class="p1">
I run into the same problem with the 1997 publication, "Tick-raccoon associations and the potential for Lyme disease spirochete transmission in the coastal plain of North Carolina". In it, <a href="http://www.jwildlifedis.org/doi/pdf/10.7589/0090-3558-33.1.28"><span class="s1">the authors discover that while raccoons in the South are highly infected with </span><span class="s2"><i>Borrelia burgdorferi</i></span><span class="s1">, none of the vector ticks which they find on them appear to have high spirochetal loads, and a low percentage of them are infected with </span><span class="s2"><i>Borrelia burgdorferi</i></span></a>. The ticks which latch onto the raccoons the most are <i>Amblyomma americanum</i> - Lone Star ticks - and <a href="http://labs.russell.wisc.edu/wisconsin-ticks/wisconsin-ticks/amblyomma-americanum-lone-star-tick/"><span class="s1">studies in the past showed they are incompetent vectors of B</span><span class="s2"><i>orrelia burgdorferi</i></span><span class="s1"> but are great at transmitting </span><span class="s2"><i>Ehrlichia</i></span><span class="s1"> and other pathogens</span></a>.<br />
<br />
The authors go on to speculate that maybe the raccoons are infected via urine, but also actually refer to the 1994 paper on host mice above, wondering if sexual or oral contact may be the cause for raccoons' high rate of <i>Borrelia burgdorferi</i> infection. There is no evidence here which confirms this method of transmission occurred in this study - it is just something the scientists are wondering about. More recent research supports the idea that <i>Amblyomma americanum</i> ticks are infected with other strains of <i>Borrelia</i>, and today raccoons in North Carolina may be infected with those - but at the time of this study, the raccoons' infections were considered unusual because the ticks collected did not appear to be full of spirochetes in general.</div>
<div class="p1">
<br />
<br /></div>
<div class="p2">
<b>Relevant Reviews, Summaries, and Editorials Outside The Scope of Part Two's Table</b></div>
<div class="p1">
<br /></div>
<div class="p2">
One of the most cited papers on <i>Borrelia</i>, "Biology of <i>Borrelia</i> Species"(1986) by Dr. Alan Barbour and Dr. Stanley Hayes, quotes research on the presence of <i>Borrelia</i> spirochetes in urine dating back to 1938: Chung and Wei's "Studies on the transmission of relapsing fever in North China I. Observations on the mechanism of transmission of relapsing fever in man." In a short passage, they mention that "Spirochetes in the urine could enter the host through the mucous membranes of the conjunctiva, mouth, or nose". It is this early research which perhaps set the stage for stringent laboratory rules about how to handle <i>Borrelia burgdorferi</i> spirochetes - that and the knowledge that other spirochetes, <i>Leptospira, </i>could infect people through contact with urine.</div>
<div class="p1">
<br /></div>
<div class="p2">
In another paper <i>not</i> included in the table in Part 2, "Epidemiologic Studies of Lyme disease in horses and their public health significance" there was passing mention of horse bite transmitting Lyme disease to a man in 1987 in Belgium. I am fortunate to have located the case study online describing the transmission of Lyme disease via a horse bite, "Horse Reservoir for <i>Borrelia burgdorferi</i>?" (<i>Lancet</i>, Apr. 25, 1987), and read the full text. It is an interesting case, in that it describes a man who was bitten on the neck by a horse with Lyme disease who went on to develop a erythema migrans (EM) rash and additional symptoms of Lyme disease shortly thereafter. No mention of the location of the rash was made in the case study, but had it stated it was directly at the bite site it would have strengthened the case for the infection being caused by the horse bite. As it stands, the history, timing of exposure, and clinical evidence do point to the possibility that a horse bite could have given this man Lyme disease - but this appears to be a rare case as I have not found other similar case studies.</div>
<div class="p1">
<br /></div>
<div class="p2">
A paper from 1991, "<i>Borrelia burgdorferi</i>: another cause of foodborne illness?" is an editorial letter which refers to studies mentioned in the table, and was written by researchers who questioned whether or not <i>Borrelia burgdorferi</i> was a risk to the food supply. They mention another study from 1990, "Thermal inactivation of <i>Borrelia burgdorferi</i>, the cause of Lyme disease," where it was discussed that refrigerated milk at 5° C contained viable <i>Borrelia burgdorferi </i>after 46 days<i> </i>and that high-temperature short-time (HTST) pasteurization may not kill all <i>Borrelia burgdorferi </i>in milk, thus raising questions as to whether the temperature should be raised and how much. The authors do not have an answer for their own questions - they only raise them for consideration.</div>
<div class="p1">
<br /></div>
<div class="p1">
</div>
<div class="p2">
The 1992 paper, "Lyme Borreliosis in dairy cattle" and 1994 paper, "Lyme Borreliosis in domestic animals" were not included in the table because both are overviews on Lyme disease studies on animals which refer to existing studies otherwise mentioned in the table and do not contain new experiments; references used in one paper are also used in the other. In the first paper, references to finding spirochetes in cattle milk, urine, and colostrum are cited which are mentioned in the second. In the second paper, it is mentioned that cats have been infected via experimental inoculation of <i>B. burgdorferi </i>by intravenous, oral, and conjunctival routes. Both papers cite other papers already listed in the table, and as such, I have not included these two papers in the table order to avoid duplication of data.</div>
<div class="p2">
<br /></div>
<div class="p1">
<b>While not directly addressed in the studies above, pasteurization seems likely to reduce odds of Borrelia burgdorferi survival.</b></div>
<div class="p2">
<br /></div>
<div class="p1">
Studies listed in Table 1 indicate that spirochetes can turn up in urine, milk, and colostrum samples, but positive samples in these studies came from animals which have not been treated with antibiotics (which affect Lyme disease) and/or fluids such as raw milk which has not been pasteurized - which suggests that the possibility of human infection from consuming animal products is going to be extremely low because most meat is cooked and milk is pasteurized.</div>
<div class="p2">
<br /></div>
<div class="p1">
"Thermal inactivation of <i>Borrelia burgdorferi</i>, the cause of Lyme disease" is the only paper I've reviewed which suggests that milk should be pasteurized at a higher temperature to ensure all spirochetes are dead.</div>
<div class="p2">
<br /></div>
<div class="p1">
What happens to milk during pasteurization all depends on how it's pasteurized: High-temperature short-time (HTST) pasteurization is when milk is subjected to a temperature of 71.5 °C (160 °F) to 74°C (165 °F), for about 15 to 30 seconds. Low-temperature long-time treatment is when milk is pasteurized at 63 °C (145 °F) for 30 minutes. And ultra-pasteurization is when one heats milk or cream to 138 °C (280 °F) for 2 seconds to extend the refrigerated shelf life of milk from 60 to 90 days.</div>
<div class="p2">
<br /></div>
<div class="p1">
This of course raises the question: At what temperature does <i>Borrelia burgdorferi </i>die?</div>
<div class="p2">
<br /></div>
<div class="p3">
<span class="s1"><a href="http://www.jci.org/articles/view/12484/version/1">Porcella and Schwan wrote</a></span><span class="s2"> in 2001 that:</span></div>
<div class="p1">
<blockquote class="tr_bq">
"In vitro cultivation of <i>B. burgdorferi</i> at various temperatures demonstrates that the spirochete replicates most quickly at 37 °C. An increase in temperature to 39 °C retards growth significantly, while a 24 hour exposure at 41 °C kills all spirochetes in the culture." </blockquote>
<br /></div>
<div class="p1">
According to <a href="http://www.urop.uci.edu/symposium/past_symposia/08/program_h-n.pdf"><span class="s3">a 2008 research study</span></a> by Juliet Kim, "Differential Temperature Susceptibility and Survival of <i>Borrelia burgdorferi</i> and <i>Borrelia hermsii</i>":</div>
<div class="p1">
<blockquote class="tr_bq">
"... on average, the Lyme disease bacterium had a higher survival at the higher temperatures than the relapsing fever agent, with a mean survival (95% confidence interval) of 1.62 (0.06– 43.6) X10-4 vs. 3.16 (1.02- 9.77) X10-4 at 50 °C and 38.3 (1.18- 1250) X10-6 vs. 1.96 (23.5- 16.3) X10-6 at 51 °C."</blockquote>
</div>
<div class="p1">
<br />
<span class="s3"><a href="http://europepmc.org/articles/PMC3561735">Laboratory techniques for semisolid plating of <i>Borrelia burgdorferi</i></a></span> require that samples do not exceed 52 °C, which is in the ballpark of the highest temperature on average that <i>Borrelia burgdorferi </i>die off<i> in vitro</i> in Kim's study.</div>
<div class="p2">
<br /></div>
<div class="p2">
</div>
<div class="p1">
It would seem either a lower temperature exposure of 41 °C over a longer duration is needed to kill all spirochetes or a higher temperature at shorter duration. Pasteurization is a minimum over 10 °C higher than these temperatures where spirochetes died off - so the question becomes<i> how long can spirochetes survive at temperatures this high</i>? Perhaps this is an issue requiring further research.<br />
<br />
<b>Summary of Findings From This Three Part Series</b><br />
<b><br /></b>
There is not one study to date which has been conducted which provides evidence sexual transmission of <i>Borrelia burgdorferi</i>, the spirochete which causes Lyme disease, occurs between humans. (I am reserving discussion on the Middelveen et al study for later - and so far the abstract does not indicate it is a transmission study.)<br />
<br />
Far as is known, there is no study to date which has been conducted which provides evidence sexual transmission of <i>Borrelia burgdorferi</i> occurs between animals, either - and very few controlled studies on venereal transmission in animals have been completed (Are there more than three?).<br />
<br />
There is some evidence that at least some animals under certain circumstances may contract infection with <i>Borrelia burgdorferi</i> through contact in some way. The two most plausible routes appear to be through exposure to urine and ingestion of raw milk.<br />
<br />
Studies on pasteurization of raw milk and the temperature at which <i>Borrelia burgdorferi</i> lead one to believe that most if not all of <i>Borrelia burgdorferi</i> will die when raw milk is pasteurized - but I would like an expert spirochetologist to weigh in on this, though, and cover what is posted about laboratory plating requirements.<br />
<br />
Researchers have at times speculated that sexual transmission of <i>Borrelia burgdorferi</i> may occur between animals, but there has been more speculation than there have been actual controlled studies to support this hypothesis.<br />
<br />
Some of this speculation came about after finding out uninfected contact animals exposed to infected animals developed a positive antibody response for <i>Borrelia burgdorferi</i> as well as signs of infection. If sexual contact between these animals occurred, it was not recorded as having been observed in the holding pen/cage.<br />
<br />
So, to answer the question about sexual transmission of Lyme disease between humans and also between animals: So far there is no evidence that it occurs. There are also few studies which test this possibility.<br />
<br />
<i>Thus ends another chapter in this ongoing notebook, Camp Other blog... I'm tired, I go crash now.</i><br />
<br />
[Placeholder for references of all papers listed in this three part series to be added soon.]<br />
<br /></div>
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com4tag:blogger.com,1999:blog-4073397588746430486.post-48510253040423456832014-04-27T18:41:00.001-10:002014-05-01T15:53:14.329-10:00Part 2: Sexual Transmission Of Lyme Disease - Is There Evidence?<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjwH-8XizTKQDJpSNpegMAbTV3aQ4HQWlSX906b8_9q1KLEyl3Xg7HUmy0_NRFY5D-L_exINH0OF9OxbW49IptWEHLlDuagOHawCsBEPgb8GRjjUJvb-PfCzucrah8QpvGOQtDvQ8GDQE45/s1600/250px-Breed-Syrian-Hamsters-Step-5.png" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjwH-8XizTKQDJpSNpegMAbTV3aQ4HQWlSX906b8_9q1KLEyl3Xg7HUmy0_NRFY5D-L_exINH0OF9OxbW49IptWEHLlDuagOHawCsBEPgb8GRjjUJvb-PfCzucrah8QpvGOQtDvQ8GDQE45/s1600/250px-Breed-Syrian-Hamsters-Step-5.png" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Syrian hamsters mating. From <a href="http://www.wikihow.com/Breed-Syrian-Hamsters">How to Breed <br />
Syrian Hamsters</a> on <a href="http://www.wikihow.com/">wikiHow</a>.</td></tr>
</tbody></table>
This article is the continuation of "<a href="http://campother.blogspot.com/2014/03/part-1-sexual-transmission-of-lyme.html" target="_blank">Part 1: Sexual Transmission Of Lyme Disease - Is There Evidence</a>?", our series on sexual transmission and contact studies involving <i>Borrelia burgdorferi</i>.<br />
<br />
To review the content of the first article briefly: We discussed three studies which are often used online to support the idea that Lyme disease could be a sexually transmitted disease between human patients. While two of those studies provided some evidence patients had spirochetal DNA in their bodily fluids, none of the studies provided evidence that Lyme disease is sexually transmitted by people. Setting aside the yet-to-be available Middelveen et al study, there are no studies to date which provide evidence that Lyme disease can be sexually transmitted in humans and there are very few studies which investigate this method of transmission in animals. We also had an introduction to Dr. Elizabeth Burgess' Lyme disease transmission studies, the criticism from Dr. Burgdorfer which they received, and took a glance at her study findings.<br />
<br />
In Part 2 of this series, we'll be looking more closely at the results of Dr. Burgess' studies and that of other researchers on contact transmission and the potential for sexual transmission of Lyme disease in animals.<br />
<br />
<b>The Tally So Far: Studies On Lyme Disease Sexual Transmission And Contact Transmission</b><br />
<br />
So far, I have not located <i>any</i> studies on Lyme disease and sexual transmission in humans, and found only a few studies about human sexual secretions containing <i>Borrelia burgdorferi</i> DNA.<br />
<br />
Is this lack of research on this method of transmission in people an oversight by researchers who are more focused on observing tickborne transmission? Or has the dominant view of researchers been that based on Lyme disease's pathogenesis, human sexual transmission of <i>Borrelia burgdorferi</i> is highly unlikely if not impossible - so why conduct more studies on it? Either way one answers, there is very little research on different transmission methods of Lyme disease in people.<br />
<br />
What we do have are early animal studies which were designed to investigate the nature of Lyme disease transmission through various methods - methods such as: how much more effective needle inoculation was compared to tick bites in transmitting infection; injecting mice with the urine of infected cattle to see if they would get infected; a few studies where it was hoped animals would copulate and that one could determine if sexual transmission could occur.<br />
<br />
To date, there are more animal studies which are about the potential for <i>contact</i> transmission of <i>Borrelia burgdorferi -</i>which means any kind of contact between animals either directly or indirectly via exposure to their blood, saliva, feces, urine, milk, or colostrum - than there are studies specifically about sexual or venereal transmission. It is the results of these early animal studies which were hoped would give one a better idea of whether or not other non-tickborne methods of transmission might also be possible in people, too.<br />
<br />
Given the wide range of data available from different animal model transmission studies over a period of nearly fifteen years, I've decided to place them into a table to view them all in one place.<br />
<br />
In general, the study data in the table below fall under the following five categories:<br />
<ol>
<li>Evidence of the presence or absence of <i>Borrelia burgdorferi</i> in different bodily fluids of animals. These are <i>not</i> transmission studies. These are studies which demonstrate spirochetes or spirochetal DNA can be found in various secretions, but they do not show that such spirochetes or infection can be passed on to another host animal.<br /><br />
</li>
<li>Evidence that the use of needle inoculation/subcutaneous injection of infected bodily fluids from animals can transmit <i>Borrelia burgdorferi</i> to uninfected animals and a tick was not required.<br /><br />
</li>
<li>Evidence pointing to oral inoculation as a potential route of transmission. These are studies where the researcher deliberately tried to infect an animal with <i>Borrelia burgdorferi</i> (or a substance assumed to contain it) either orally or oronasally, then looked at the results.<br /><br />
</li>
<li>Evidence supporting or rejecting sexual (venereal) transmission of <i>Borrelia burgdorferi</i> between studied animals.<br /><br />
</li>
<li>Evidence suggesting that an uninfected animal became infected somehow by being housed in the same space as an animal already infected with <i>Borrelia burgdorferi</i>. These studies suggest that contact transmission may have occurred because no direct action was taken by the researcher to infect the control/uninfected animal, and no ticks were deliberately introduced to the control/uninfected animal.</li>
</ol>
For the purpose of focusing discussion, the table below mostly displays information related to the possibility of oral, contact, and sexual (venereal) transmission and not much transmission data via needle inoculation (though some of the studies also focus on that method of transmission and may be mentioned in passing).<br />
<br />
<b>Table 1:</b> Evidence For The Presence of <i>Borrelia Burgdorferi</i> Infection Via Different Forms of Inoculation and Potential Contact Transmission<br />
<div>
<br />
<table border="2" bordercolor="#B5EAAA" cellpadding="10" cellspacing="0" style="background-color: white; border-collapse: collapse; font-size: 10pt;"><tbody>
<tr 4px="" 5px="" color:="" padding-bottom:="" padding-top:="" style="background-color: #b5eaaa;" white=""> <td style="text-align: center; vertical-align: top;"><span style="font-weight: bold;">Year</span></td> <td style="text-align: center; vertical-align: top;"><span style="font-weight: bold;">Publication</span></td> <td colspan="2" rowspan="1" style="font-weight: bold; text-align: center; vertical-align: top;">Oral<br />
<span style="font-size: 10pt;">Inoculation</span><br />
<br /></td> <td style="font-weight: bold; text-align: center; vertical-align: top;">Contact<br />
<br /></td> <td style="font-weight: bold; text-align: center; vertical-align: top;">Spirochetal<br />
<span style="font-size: 10pt;">DNA</span></td> <td style="font-weight: bold; text-align: center; vertical-align: top;">Whole Cell<br />
<span style="font-size: 10pt;">Spirochetes</span><br />
<br /></td> <td style="font-weight: bold; text-align: center; vertical-align: top;">Antibody<br />
<span style="font-size: 10pt;">Test</span></td> <td style="font-weight: bold; text-align: center; vertical-align: top;">Culture/<br />
PCR<br />
<span style="font-size: 10pt;">Status</span></td> </tr>
<tr> <td style="text-align: center; vertical-align: top;">1986</td> <td style="text-align: left; vertical-align: top;">Experimental <span style="font-size: 10pt;">inoculation of dogs with </span><i style="font-size: 10pt;">Borrelia burgdorferi</i></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">N<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">Y<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">N<br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">IFA+ n=1/1<br />
<span style="font-size: 10pt;">contact </span><br />
<span style="font-size: 10pt;">exposed dog</span></td> <td style="text-align: left; vertical-align: top;">no PCR<br />
<span style="font-size: 10pt;">completed</span></td> </tr>
<tr> <td style="text-align: center; vertical-align: top;">1986</td> <td style="text-align: left; vertical-align: top;">Experimental<br />
<span style="font-size: 10pt;">inoculation of </span><i style="font-size: 10pt;">Peromyscus spp.</i><span style="font-size: 10pt;"> with </span><i style="font-size: 10pt;">Borrelia burgdorferi</i><span style="font-size: 10pt;">:</span><br />
<span style="font-size: 10pt;">evidence of contact transmission</span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">N<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">Y<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">+ n=1/1 blood,<br />
<span style="font-size: 10pt;">contact mouse</span><br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">Exp 1: IFA+<br />
<span style="font-size: 10pt;">n=2/2 contact mice;</span><br />
<span style="font-size: 10pt;">4 log2, 6 log2</span><br />
<span style="font-size: 10pt;">Exp 2: +n=10/10 contact mice</span><br />
<span style="font-size: 10pt;">4 log2-6 log2</span><br />
<br />
<span style="font-size: 10pt;">Burgess speculates local IgA reaction possible instead of systemic IgG</span></td> <td style="text-align: left; vertical-align: top;">no PCR<br />
<span style="font-size: 10pt;">completed</span><br />
<br />
<br /></td> </tr>
<tr> <td style="text-align: center; vertical-align: top;">1986</td> <td style="text-align: left; vertical-align: top;">The prevalence<br />
<span style="font-size: 10pt;">and significance of </span><i style="font-size: 10pt;">Borrelia burgdorferi </i><span style="font-size: 10pt;">in the urine of feral </span><span style="font-size: 10pt;">reservoir hosts</span><br />
<br />
<br /></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">+ n=2 urine,<br />
<span style="font-size: 10pt;">via darkfield</span><br />
<span style="font-size: 10pt;">+n=21/22 kidneys, positive correlation w/ </span><span style="font-size: 10pt; font-style: italic;">Babesia</span><span style="font-size: 10pt;"> presence</span></td> <td style="text-align: left; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">no PCR<br />
<span style="font-size: 10pt;">completed</span><br />
<br />
<br /></td> </tr>
<tr> <td style="vertical-align: top;">1986</td> <td style="vertical-align: top;">Suspected borreliosis in cattle</td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">Y<br />
<span style="font-size: 10pt;">cat fed</span><br />
<span style="font-size: 10pt;">infected milk</span><br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">+ n=2/6 urine, via darkfield<br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">IFA+<br />
<span style="font-size: 10pt;"><br />
</span> <span style="font-size: 10pt;">+n=1/1 cat fed infected milk had </span><span style="font-size: 10pt;">1:164 titer</span><br />
<span style="font-size: 10pt;">+n=5/5 mice 1:8-1:32 titers with sc inoculation of milk</span><br />
<span style="font-size: 10pt;">+n=5/5 mice 1:32-1:64 titers with sc inoculation of urine</span></td> <td style="text-align: left; vertical-align: top;">- cultures<br />
<span style="font-size: 10pt;">negative in blood, urine, and milk</span><br />
<br />
<br />
no PCR completed<br />
<br />
<br /></td> </tr>
<tr> <td style="vertical-align: top;">1987</td> <td style="vertical-align: top;">Oral infection of <i>Peromyscus maniculatus </i>with <i>Borrelia burgdorferi </i>and subsequent <span style="font-size: 10pt;">transmission by </span><i style="font-size: 10pt;">Ixodes dammini</i></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">Y<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">N<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">+ n=1/10 blood, <br />
<span style="font-size: 10pt;">+ n=1/10 organs</span><br />
<span style="font-size: 10pt;">+n=1/10 blood (tick-fed)</span><br />
<span style="font-size: 10pt;">+n=1/10 organs (tick-fed)</span><br />
<br />
<br /></td> <td style="text-align: left; vertical-align: top;">IFA+ <br />
<span style="font-size: 10pt;">+n=10/10</span><br />
<span style="font-size: 10pt;">orally infected mice</span><br />
<span style="font-size: 10pt;">+n=10/10 mice from ticks that fed on orally infected mice; </span>6 orally infected mice developed symptoms</td> <td style="vertical-align: top;">no PCR completed<br />
<br />
<br />
<br />
<br />
<br /></td> </tr>
<tr> <td style="vertical-align: top;">1988</td> <td style="vertical-align: top;">The urinary bladder, a <span style="font-size: 10pt;">consistent source of </span><i style="font-size: 10pt;">Borrelia burgdorferi</i><span style="font-size: 10pt;"> in experimentally</span><br />
<span style="font-size: 10pt;">infected white-footed mice (Peromyscus leucopus)</span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">N<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">- 0/15 urine samples<br />
<span style="font-size: 10pt;">+ 2/15 blood samples</span><br />
<span style="font-size: 10pt;">+ tissue samples: bladder, kidney, spleen</span></td> <td style="vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">+ tissue culture, no PCR<br />
<br />
<br /></td> </tr>
<tr> <td style="vertical-align: top;">1988</td> <td style="vertical-align: top;">Clinical and serologic <span style="font-size: 10pt;">evaluations of induced </span><i style="font-size: 10pt;">Borrelia burgdorferi</i><span style="font-size: 10pt;"> infection in dogs.</span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">Y<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">IFA antibody +<br />
<span style="font-size: 10pt;">ELISA +</span><br />
<span style="font-size: 10pt;">n=1 control dog elevated + IgG</span></td> <td style="vertical-align: top;">no PCR completed<br />
<br />
<br /></td> </tr>
<tr> <td style="vertical-align: top;">1988</td> <td style="vertical-align: top;"><i>Borrelia burgdorferi</i><br />
<span style="font-size: 10pt;">infection in Wisconsin horses and cows</span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">Y <br />
<span style="font-size: 10pt;">n=3 mice inoculated with cow urine</span></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">+ n=2/10 cow urine<br />
<span style="font-size: 10pt;">+ n=2/3 colostrum</span><br />
<span style="font-size: 10pt;">- all milk samples</span></td> <td style="vertical-align: top;">IFA+ IgG<br />
<span style="font-size: 10pt;">n=2/3 colostrum titer, n=1/3 cows ~1:512</span><br />
<span style="font-size: 10pt;">n=2/3 mice 1:64; 1:28</span></td> <td style="vertical-align: top;">samples cultured,<br />
<span style="font-size: 10pt;">no PCR completed</span><br />
<br />
<br /></td> </tr>
<tr> <td>1989</td> <td><span style="font-size: 10pt;">Experimental inoculation of mallard ducks (</span><i style="font-size: 10pt;">Anas</i><br />
<div class="p1">
<i>platyrhynchos</i>) with <i>Borrelia burgdorferi</i></div>
<br /></td> <td colspan="2" rowspan="1" style="text-align: center;"><span style="font-size: 10pt;">Y</span><br />
<span style="font-size: 10pt;">n=4 ducks</span><br />
<br /></td> <td style="text-align: center;">n/a<br />
<br />
<br /></td> <td style="text-align: center;">n/a<br />
<br />
<br /></td> <td>+ n=1/4 cloaca secretion,<br />
<span style="font-size: 10pt;">+ n=1/4 kidney</span></td> <td>IFA+ n=3/4 kidneys of orally inoculated ducks; +n=1/4<br />
<span style="font-size: 10pt;">mesentery</span></td> <td>positive cultures, no PCR completed</td> </tr>
<tr> <td style="vertical-align: top;">1990</td> <td style="vertical-align: top;">Experimental infection of the <span style="font-size: 10pt;">white-footed mouse with </span><i style="font-size: 10pt;">Borrelia burgdorferi</i></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">Y<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="vertical-align: top;">+ n=1 blood<br />
<br /></td> <td style="vertical-align: top;">IFA+<br />
<span style="font-size: 10pt;">all asymptomatic mice</span></td> <td style="vertical-align: top;">tissue culture, no PCR completed</td> </tr>
<tr> <td style="vertical-align: top;">1991<br />
<br />
<br /></td> <td style="vertical-align: top;">Experimental infection of dogs <span style="font-size: 10pt;">with <i>Borrelia burgdorferi</i></span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">N<br />
<br /></td> <td style="text-align: center; vertical-align: top;">Y<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="vertical-align: top;">+ n=1 urine, blood of contact dog</td> <td style="vertical-align: top;">IFA+<br />
<span style="font-size: 10pt;">+n=1 uninoculated dog near 1 infected dog</span><br />
<span style="font-size: 10pt;">both asymptomatic</span></td> <td style="vertical-align: top;">no PCR completed<br />
<br /></td> </tr>
<tr> <td><br />
<br />
<div class="p1">
<br />
1991</div>
<br /></td> <td><span style="font-size: 10pt;">Relative infectivity of </span><i style="font-size: 10pt;">Borrelia burgdorferi </i><span style="font-size: 10pt;">in Lewis rats by various routes of inoculation</span></td> <td colspan="2" rowspan="1" style="text-align: center;"><span style="font-size: 10pt;">Y</span><br />
<span style="font-size: 10pt;">oronasally</span><br />
<br />
<br />
<br />
<br /></td> <td style="text-align: center;">N<br />
<br />
<br /></td> <td style="text-align: center;">n/a<br />
<br />
<br /></td> <td>- n=0/13 oronsally infected<br />
<span style="font-size: 10pt;">- n=0/6 males venereally</span><br />
<span style="font-size: 10pt;">- n=0/7 females venereally</span></td> <td>only needle inoculated rats +</td> <td>n/a</td> </tr>
<tr> <td style="vertical-align: top;">1992</td> <td style="vertical-align: top;">Experimentally induced infection <span style="font-size: 10pt;">of cats with </span><i style="font-size: 10pt;">Borrelia burgdorferi</i></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">Y <br />
<span style="font-size: 10pt;">n=2</span><br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="vertical-align: top;">+ n=2 blood smear; <br />
<span style="font-size: 10pt;">n=1 lung</span></td> <td style="vertical-align: top;">n=2 orally inoculated IFA+<br />
<span style="font-size: 10pt;">n=2 ocularly inoculated IFA+</span></td> <td style="vertical-align: top;">no PCR completed<br />
<br /></td> </tr>
<tr> <td style="vertical-align: top;">1993</td> <td style="vertical-align: top;">Detection of <i>Borrelia burgdorferi</i> in Urine of <i>Peromyscus leucopus</i> by Inhibition<br />
<span style="font-size: 10pt;">Enzyme-Linked Immunosorbent Assay</span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">N<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br />
<br /></td> <td style="text-align: center; vertical-align: top;">+n=57/87<br />
<span style="font-size: 10pt;">whole cells or subunits in urine</span><br />
<br /></td> <td style="vertical-align: top;">+ n=57/87 whole cells or<br />
<span style="font-size: 10pt;">subunits in urine</span><br />
<br />
<br /></td> <td style="vertical-align: top;">+IFA<br />
<span style="font-size: 10pt;">+ELISA</span><br />
<span style="font-size: 10pt;">+n=47/75 serum</span><br />
<span style="font-size: 10pt;">+n=57/87 antigens in urine</span></td> <td style="vertical-align: top;">+n=50/87 tissue culture;<br />
<span style="font-size: 10pt;">+n=36/50 infected bladders</span><br />
<span style="font-size: 10pt;">no PCR completed</span></td> </tr>
<tr> <td style="vertical-align: top;">1994</td> <td style="vertical-align: top;">Experimental infection of dogs <span style="font-size: 10pt;">with </span><i style="font-size: 10pt;">Borrelia burgdorferi</i></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">N<br />
<br /></td> <td style="text-align: center; vertical-align: top;">Y<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="vertical-align: top;">+ n=1/4 infected dog blood, urine<br />
<br /></td> <td style="vertical-align: top;">IFA+ <br />
<span style="font-size: 10pt;">+n=1/1 control dog, 1:128 (max titer)</span><br />
<span style="font-size: 10pt;">+n=2/2 guinea pigs inoculated with urine, 1:128</span></td> <td style="vertical-align: top;">no PCR completed<br />
<br /></td> </tr>
<tr> <td><br />
<br />
<div class="p1">
<br />
1994</div>
<br /></td> <td><span style="font-size: 10pt;">Distribution of </span><i style="font-size: 10pt;">Borrelia burgdorferi</i><span style="font-size: 10pt;"> in </span><span style="font-size: 10pt;">host mice in Pennsylvania</span><br />
<br /></td> <td colspan="2" rowspan="1" style="text-align: center;">n/a<br />
<br />
<br />
<br />
<br /></td> <td style="text-align: center;">Y<br />
<span style="font-size: 10pt;">see notes part 3</span></td> <td style="text-align: center;">n/a</td> <td>+ n=112 isolations/1619 mice (from ear tissue)<br />
<br /></td> <td>IFA+ in tick-bitten mice <br />
<span style="font-size: 10pt;">see notes <br />
part 3</span></td> <td>no PCR completed</td> </tr>
<tr> <td><span style="font-size: 10pt;">1996 </span><br />
<br /></td> <td><span style="font-size: 10pt;">Lyme Borreliosis in the laboratory mouse</span><br />
<br /></td> <td colspan="2" rowspan="1" style="text-align: center;"><br />
<br />
-<br />
<br />
<br /></td> <td style="text-align: center;">-</td> <td style="text-align: center;">-</td> <td style="text-align: center;">-</td> <td>- see below</td> <td>-</td> </tr>
<tr> <td style="vertical-align: top;">1996</td> <td style="text-align: left; vertical-align: top;">Dissemination <span style="font-size: 10pt;">of Borrelia burgdorferi after experimental infection in dogs</span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">N</td> <td style="text-align: center; vertical-align: top;">n/a</td> <td style="vertical-align: top;"><br /></td> <td style="vertical-align: top;">- n=0/6 urine culture</td> <td style="vertical-align: top;"><br /></td> <td style="vertical-align: top;">- culture bladder <br />
<span style="font-size: 10pt;">PCR completed</span><br />
- urine</td> </tr>
<tr> <td><span style="font-size: 10pt;">1997</span><br />
<br /></td> <td><span style="font-size: 10pt;">Tick-raccoon associations and the potential for </span><span style="font-size: 10pt;">Lyme disease spirochete transmission in the coastal plain of North</span><br />
<div class="p1">
<span style="font-size: 10pt;">Carolina</span></div>
</td> <td colspan="2" rowspan="1" style="text-align: center;">n/a</td> <td style="text-align: center;">Y <br />
<span style="font-size: 10pt;">see notes part 3</span><br />
<br />
<br /></td> <td style="text-align: center;">n/a</td> <td style="text-align: left;">n/a</td> <td>IFA+ <br />
<span style="font-size: 10pt;">see notes</span><br />
<span style="font-size: 10pt;">part 3</span></td> <td>no PCR was completed</td> </tr>
<tr> <td style="vertical-align: top;">1998</td> <td style="vertical-align: top;">Viable <i>Borrelia burgdorferi </i><span style="font-size: 10pt;">in the urine of two clinically normal horses</span></td> <td colspan="2" rowspan="1" style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="text-align: center; vertical-align: top;">n/a<br />
<br /></td> <td style="vertical-align: top;">+n=2/5 horses, urine</td> <td style="vertical-align: top;">+<br />
<br />
<br /></td> <td style="vertical-align: top;">+PCR FA on urine samples</td> </tr>
<tr> <td>1999</td> <td>Investigation of venereal, transplacental, and contact <span style="font-size: 10pt;">transmission of</span><br />
<span style="font-size: 10pt;">the Lyme disease spirochete, </span><i style="font-size: 10pt;">Borrelia burgdorferi</i><span style="font-size: 10pt;">, in Syrian</span><br />
<span style="font-size: 10pt;">hamsters</span></td> <td colspan="2" rowspan="1" style="text-align: center;">N<br />
<br />
<br /></td> <td style="text-align: center;">N<br />
<br />
<br /></td> <td style="text-align: center;">n/a<br />
<br />
<br /></td> <td>-n=0/6 female hamsters,<br />
-n=0/6 male hamsters infected<br />
<span style="font-size: 10pt;">venereally</span><br />
<span style="font-size: 10pt;">no mice contact infected</span></td> <td>- IFA in 6/6 venereal test hamsters<br />
<span style="font-size: 10pt;">and all contact mice</span></td> <td style="text-align: left;">- tissue samples, no PCR was<br />
<span style="font-size: 10pt;">completed</span></td></tr>
</tbody></table>
</div>
<br />
<br />
<b><u>Table Key:</u></b><br />
<br />
<b>+</b> positive <b>-</b> negative<br />
<br />
<b>n= #/# </b>number of samples or study animals infected or not infected out of the total studied<br />
<br />
<b>n/a</b> not applicable to study or no data available in given paper<br />
<br />
<b><br />
</b> <b>Notes On The Above Table</b><br />
<br />
While every effort was made for this table to be comprehensive, it may not be complete. (If you know of any additional publications and data which apply, please comment below so that I may add the paper to this table.)<br />
<br />
Note that certain papers which have been cited online pointing to different methods of contact transmission or evidence of <i>Borrelia burgdorferi</i> spirochetes or spirochetal DNA in bodily fluids were <i>not</i> included in the above table. This is because these specific papers were either review or editorial papers which cited more than one study already included in the above table, and I did not want to give the impression that additional studies were completed where the studies and findings were reproduced by another researcher. (I do, however, mention these papers in part 3 of this series on sexual transmission.)<br />
<br />
Note also that in certain columns data is lacking or relies on older methods:<br />
<br />
In some studies, antibody testing was not completed on animals because the research goal was to focus on finding evidence of <i>Borrelia </i>DNA and/or spirochetes in a given sample and not to measure antibodies in the host animal.<br />
<br />
In the 1980's and early 1990's, PCR studies were not performed on many samples. This is because at the time <a href="http://siarchives.si.edu/research/videohistory_catalog9577.html" target="_blank">PCR was a relatively recent invention, was at first a slow and labor intensive process, and not many researchers had access to it</a>. Also, there was some discussion over what the best method was to use on specific samples, and it hadn't been completely determined yet.<br />
<br />
Immunofluorescent antibody (IFA) assay testing was the primary method of testing samples for the presence of antibodies, rather than ELISA or Western blot. This method has been considered less sensitive than others, but given studies listed use one or more monoclonal antibodies specific to <i>Borrelia burgdorferi </i>(such as H5332, specific to North American OspA) the positive results obtained are noteworthy.<br />
<br />
<b>So What Do These Studies Indicate or Suggest?</b><br />
<b><br />
</b> <b>1. Contact transmission of <i>Borrelia burgdorferi</i> could occur between specific animals under specific conditions.</b><br />
<br />
While there is some evidence that some animals can be experimentally infected with Lyme disease through an oral or ocular route, it is unclear if animals end up infected through these routes in the natural world. It's important to note that dosages and the method used in a laboratory experiment may not have their parallel in real life conditions. Optimally, observing how infections occur in the wild would be best - but it is difficult to study animals in the wild to determine exactly when and how they get infected.<br />
<br />
What the data in this table reflects is that there is some evidence to suggest that contact transmission via urine <i>may</i> be a concern with some animals - particularly cattle and mice. One study on ducks points to the possibility of oral transmission, though no one has duplicated it thus far or extended additional transmission research to other kinds of birds.<br />
<br />
Based on the studies reviewed, if a form of contact transmission can occur in animals, it appears to happen inconsistently and in low numbers of animals - and so far appears to happen more frequently in specific species. Perhaps repeat studies with larger groups of animal subjects would be helpful - or perhaps they would demonstrate that contact transmission still only occurs in relatively few subjects under narrowly defined conditions. We just don't know.<br />
<br />
There is also some evidence that certain animals are highly unlikely to contract Lyme disease via contact transmission via urine, such as Lewis rats and Syrian hamsters.<br />
<br />
Additional autopsy studies in such cases that demonstrate where spirochetes are found in infected animals can be useful as they can indicate why spirochetes were not likely to be found in urine based on which tissues spirochetes colonized.<br />
<br />
<b>2. In some cases, it is not exactly clear <i>how</i> contact animals were infected in individual studies. All we know is they had positive antibody tests and some showed signs of infection.</b><br />
<b><br />
</b> Based on the studies within the above table, the following studies resulted in at least a positive IFA result in a contact animal, and in some cases evidence of spirochetal infection:<br />
<ol>
<li><span style="background-color: white; font-size: 13px;">Experimental </span><span style="background-color: white; font-size: 10pt;">inoculation of dogs with </span><i style="background-color: white; font-size: 10pt;">Borrelia burgdorferi.</i></li>
<li><span style="background-color: white; font-size: 13px;">Experimental </span><span style="font-size: 10pt;">inoculation of </span><i style="font-size: 10pt;">Peromyscus spp.</i><span style="font-size: 10pt;"> with </span><i style="font-size: 10pt;">Borrelia burgdorferi</i><span style="font-size: 10pt;">: </span><span style="font-size: 10pt;">evidence of contact transmission.</span></li>
<li><span style="background-color: white; font-size: 10pt;">Clinical and serologic </span><span style="background-color: white; font-size: 10pt;">evaluations of induced </span><i style="background-color: white; font-size: 10pt;">Borrelia burgdorferi</i><span style="background-color: white; font-size: 10pt;"> infection in dogs.</span></li>
<li><span style="background-color: white; font-size: 10pt;">Experimental infection of dogs </span><span style="background-color: white; font-size: 10pt;">with <i>Borrelia burgdorferi.</i></span></li>
<li><span style="background-color: white; font-size: 10pt;">Distribution of </span><i style="background-color: white; font-size: 10pt;">Borrelia burgdorferi</i><span style="background-color: white; font-size: 10pt;"> in </span><span style="background-color: white; font-size: 10pt;">host mice in Pennsylvania.</span></li>
<li><span style="font-size: 10pt;">Tick-raccoon associations and the potential for </span><span style="font-size: 10pt;">Lyme disease spirochete transmission in the coastal plain of North </span><span style="background-color: white; font-size: 10pt;">Carolina.</span></li>
</ol>
<div style="background-color: white; font-size: 13px;">
<span style="font-size: 10pt;"><span style="font-size: 10pt;"></span></span></div>
Of these studies, the last two listed above contained speculation by the researchers about whether or not mice and raccoons could contract Lyme disease through other methods outside of a tick bite - and neither of those two studies were completed under lab conditions and had control animals.<br />
<br />
As for the remaining four studies, there is no indication <i>exactly how</i> uninfected control animals ended up with positive antibody tests and signs of infection when in the presence of infected animals. Apparently it has happened - but <i>how</i> and <i>why</i> it happened in a number of these studies even when animals are in captivity is unclear.<br />
<br />
It is the unknown method of contact transmission in such studies which has led to speculation by others that sexual transmission may have occurred between animals. However, without a definite confirmation that sexual contact was the route of transmission, what happened remains a mystery.<br />
<br />
We do not have documentation in a number of cases of whether or not infected and contact animals were housed together indoors or outdoors, or if they were isolated from birds or other environmental factors which may have introduced infected ticks or <i>Borrelia burgdorferi</i>. Without more data, it is difficult to determine whether or not animals may have been infected via a different route.<br />
<br />
All the same, there is research above which indicates point #1 - that animals can be infected by other animals' secretions, although how often it happens and how is a good question. So far, urine and raw milk ingestion appears to be a plausible mode of transmission between some animals.<br />
<br />
<b>3. There haven't been many animal studies specifically focused on sexual or venereal transmission.</b><br />
<br />
Based on the studies within the above table, the following studies were specifically focused on sexual or venereal transmission and their results:<br />
<br />
<table border="0"><tbody>
<tr><td><b>Title</b></td><td><b> Sexual or Venereal Transmission?</b></td></tr>
<tr><td>Investigation of venereal, transplacental, and contact <br />
transmission of the Lyme disease spirochete,<br />
<i>Borrelia burgdorferi,</i> in Syrian hamsters</td><td> - negative</td></tr>
<tr><td>Relative infectivity of <i>Borrelia burgdorferi</i> <br />
in Lewis rats by various routes of inoculation </td><td> - negative</td></tr>
<tr><td>Lyme Borreliosis in the laboratory mouse</td><td> - negative</td></tr>
</tbody></table>
<br />
Of three papers where experiments were specifically designed to see if venereal transmission occurred between animals, the results of all three were negative.<br />
<br />
Three seems like a very small number of studies, and they were only completed on rats, Syrian hamsters, and mice. If you, the reader, knows of any additional studies on sexual or venereal transmission of Lyme disease in animals which were not included here - please comment below with the title(s) and link(s) to the paper(s).<br />
<br />
<b>Some Researchers Weigh In On Non-Tick Methods Of Transmission</b><br />
<br />
More has been said about the methods of transmission in mice than any other animal because mice are used more extensively in a lab environment for the study of Lyme disease than any other species.<br />
<br />
In 1996, Dr. Stephen Barthold wrote "Lyme Borreliosis in the laboratory mouse"in the <i><a href="http://www.lyme.org/journal/jstd_archive.html" target="_blank">Journal of Spirochetal and Tick-Borne Disease</a></i>. On pages 23-24, he states:<br />
<blockquote class="tr_bq">
"There has been no evidence of contact transmission or detection of viable spirochetes in urine of laboratory mice. Lung, bladder, and kidney are frequently infected, but spirochetes in these tissues are present in the connective tissue of the serosa, subserosa, submucosa (bladder), and periarterial connective tissue (lung, kidney), rather than lumina of tubules, ureters, bladder, or airways."</blockquote>
Based on his research up to that point in time, mice were not transmitting spirochetes through their urine to uninfected mice, and spirochetes which were found in autopsies were deeply embedded in connective tissue and not lining the vessels or surface of ureters, bladders, or bronchial tubes. In other words, if live spirochetes were present, they would be highly unlikely to be found in urine.<br />
<br />
His findings differ from those of Dr. Burgess, and those of Dr. Magnarelli.<br />
<br />
Magnarelli et al in the paper, "Detection of <i>Borrelia burgdorferi</i> in Urine of <i>Peromyscus leucopus</i> by Inhibition Enzyme-Linked Immunosorbent Assay" determined that 57 out of 87 mice had either subunits or whole cell <i>Borrelia burgdorferi</i> in their urine.<br />
<br />
Despite this high number, Magnarelli et al cited their own difficulties in detecting evidence of Lyme disease infection in mice consistently:<br />
<blockquote class="tr_bq">
"For more than half of the field-collected mice tested, there was concordance in the results of the serum antibody, culture, and urine analyses. Similar results were records for four of five laboratory-bred mice inoculated with <i>B. burgdorferi</i>. However, there were discrepancies. <i>B. burgdorferi</i> antigens sometimes were detected in urine from field-collected mice without supportive data from antibody assays or culture work. This was particularly noticeable in animals captured during October and November, a period after peak nymphal <i>I. scapularis</i> population levels had been reached."</blockquote>
The authors also pointed out that antibody-positive serum and titers can be low especially during early infection, successful culturing of <i>B. burgdorferi</i> depended partially on the number of spirochetes present in host tissues, and that occasionally, serum antibody analyses and culturing results were positive, while urine antigen test results were negative - antigens may not always be released into urine.<br />
<br />
In 2001, we have what may have been the last published words from Dr. Burgess on contact transmission in the book, "Infectious Diseases of Wild Mammals" published by Iowa State University Press, chapter 26. Authored by Dr. Richard Brown and Dr. Elizabeth Burgess, the chapter contains this quote:<br />
<blockquote class="tr_bq">
"Although direct transmission may occur in some situations, it has not been easily substantiated (Mather et al 1991) and has yet to be shown as epidemiologically important." </blockquote>
The authors supported the idea that direct transmission of spirochetes <i>may</i> occur between animals under certain circumstances - but it's not easy to provide evidence of what exactly happened and it occurs in only a very small number of cases.<br />
<br />
More recently, in 2010, in the book, <i>Borrelia: Molecular Biology, Host Interaction and Pathogenesis</i> by Horizon Press, on p. 381, the most recent note on transmission stated:<br />
<blockquote class="tr_bq">
"Mice are also susceptible to infection following intragastric inoculation of very high doses of <i>B. burgdorferi</i> N40, but there is no evidence for contact transmission (Barthold, 1991) or <i>in utero</i> (placental) transmission, although maternal infection may cause fetal death (Silver et al, 1995; Weis et al, 1997)."</blockquote>
Since our focus here is on contact, venereal, and oral transmission and not maternal/<i>in utero </i>(a topic worthy of a post in itself), it's notable that mice can be infected intragastrically based on Barthold's studies - though it takes high doses to do so, and it is a question how likely it is such doses would be found in nature. According to Burgess, <i>Peromyscus</i> are apparently susceptible to oral inoculation with <i>B. burgdorferi</i>, since oral infection with ~400 spirochetes resulted in sufficient spirochetemia to infect <i>Ixodes (</i>previously<i> dammini) scapularis </i>larvae.<br />
<br />
That there has been a variety of study outcomes regarding mice, transmission, and inoculation routes leads to questions about whether or not it is not just species that matters when it comes to how Lyme disease affects the host - but also the individual genetic background of the host animal.<br />
<br />
One should take note that anyone studying <i>Borrelia burgdorferi</i> in wild type mice should make sure they do not use mice which are <a href="http://www.sciencedaily.com/releases/2013/04/130404072925.htm">naturally resistant to infection with Lyme disease due to a particular genetic variant of the antigen receptor TLR2</a>, because such mice can greatly affect study outcome.<br />
<br />
Could it be that the discrepancies Magnarelli et al found in their research was due in part to the presence of mice in their study group which had this genetic variant?<br />
<br />
<b>Future Directions</b><br />
<br />
One question this raises for some reading along is how likely is it that <i>Borrelia burgdorferi</i> spirochetes can be found in human urine, and is there evidence of <i>non-sexual</i> transmission of Lyme disease between people? This is a question that will be discussed in an upcoming blog post, as there have been a number of studies on testing human urine samples for the presence of Lyme disease.<br />
<br />
But the main question which kicked off this post is this one: Will we have any evidence in the near future that <i>Borrelia burgdorferi </i>can be sexually transmitted between partners?<br />
<br />
So far, we do not, though a recent paper by Middelveen et al, "Isolation and Detection of <i>Borrelia burgdorferi</i> from human vaginal and seminal secretions" is the first publication to make the claim in its abstract that <i>live motile spirochetes</i> have been found in vaginal and seminal secretions, and that because two partners in the study share the same strain of <i>Borrelia burgdorferi</i> in their secretions, odds are greater than random chance that one partner passed <i>Borrelia burgdorferi </i>to the other.<br />
<br />
For these claims, I currently have no evidence. And unfortunately, my ability to give the paper a thorough review is limited without access to the full text of the paper. Once the Middelveen et al paper is out of embargo and I have read the entire paper, it deserves its own future blog entry given how important this topic has become for many patients.<br />
<br />
<b><u>To sum up:</u> </b>Sexual transmission of tickborne diseases - is there evidence? Answer: Not so far. But existing studies to date provide evidence that oral inoculation and urine transmission may occur in a few cases in animals.<br />
<br />
<b>Questions For Further Discussion:</b><br />
<ul>
<li>Why did different researchers have different results when it comes to the issue of contact transmission?<br />
<br />
</li>
<li>How much did animal species play a role in the outcome?<br />
<br />
</li>
<li>Why is it in a number of cases, uninfected animals exposed to infected animals had positive antibodies for <i>Borrelia burgdorferi</i> but were culture negative and no spirochetes could found in tissues post-mortem?<br />
<br />
</li>
<li>How did duration of untreated infection in the host relate to the odds of finding spirochetal DNA or a spirochete in a given sample?<br />
<br />
</li>
<li>How did the timing of testing of the host animal relate to the odds of finding spirochetal DNA or a spirochete in a given sample?<br />
<br />
</li>
<li>How do methods and materials and test conditions affect outcomes (e.g. urine acids can lyse cells) ?<br />
<br />
</li>
<li>How did the researchers demonstrate they had ruled out or eliminated other potential methods of transmission via experimental design?<br />
<br />
</li>
<li>What - if any - connection is there between nonsexual modes of Lyme disease transmission and a sexual one?</li>
</ul>
<div align="center">
<br />
<u>Coming up next: </u><br />
<br />
<a href="http://campother.blogspot.com/2014/04/part-3-sexual-transmission-of-lyme.html" target="_blank">Part 3: Sexual Transmission Of Lyme Disease - Is There Evidence?</a><br />
<br />
The next post will include notes on some of the above studies mentioned in the table and<br />
additional studies which have been cited when mentioning transmission methods of<br />
<i>Borrelia burgdorferi</i>. The temperature at which <i>Borrelia burgdorferi</i> dies<br />
off will also be discussed in relationship to pasteurization.<br />
<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
</div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com0tag:blogger.com,1999:blog-4073397588746430486.post-16805059806785948292014-03-10T13:12:00.001-10:002014-05-01T15:54:31.070-10:00Part 1: Sexual Transmission Of Lyme Disease - Is There Evidence?<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 10px; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKiCoH4VFe3SgJ95hlS1dBe75n-LEiLt5RG5WlFxPoDhE-sRaZhHv4x_AZEsxeRZj65yiTRNjCXwM07SqQnmOlVbkuIzHS2Lb8EhV5j3UQK6o6rNa3-VG7mjR5jev5tCK1vO0m2uA9xts0/s1600/IxodesricinusWTF.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Female and male Ixodes ricinus ticks mating" border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKiCoH4VFe3SgJ95hlS1dBe75n-LEiLt5RG5WlFxPoDhE-sRaZhHv4x_AZEsxeRZj65yiTRNjCXwM07SqQnmOlVbkuIzHS2Lb8EhV5j3UQK6o6rNa3-VG7mjR5jev5tCK1vO0m2uA9xts0/s1600/IxodesricinusWTF.jpg" title="Male and female Ixodes ricinus ticks mating" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Male and female <i>Ixodes ricinus </i>ticks mating. </td></tr>
</tbody></table>
A number of patients with Lyme disease have wondered if there is any other way to contract Lyme disease other than a tick bite. It's not an uncommon question to ask, given that not everyone remembers getting a tick bite, and nymphs are so small they can bite and infect someone without anyone ever knowing they were there.<br />
<br />
Of all the questions which lead one to pause for a moment regarding the possible methods of transmission of Lyme disease, it has to be this one: <i>Can Lyme disease be sexually transmitted between partners?</i><br />
<br />
This is an interesting question, and the overwhelming majority of researchers and medical professionals out there have stated that <i>no, Lyme disease cannot be sexually transmitted between people</i>.<br />
<br />
They will state other forms of transmission can occur outside of a tick bite: <i>Borrelia burgdorferi, </i>the bacteria which causes Lyme disease,<i> </i><a href="http://www.ingentaconnect.com/content/esa/jme/1996/00000033/00000003/art00010" target="_blank">could be transmitted between ticks while they are mating</a> (<a href="http://www.sciencedirect.com/science/article/pii/0014489482901254" target="_blank">sexual transmission of relapsing fever spirochetes also occurs between ticks</a>). It could be transmitted <a href="http://scholar.google.com/scholar?q=cofeeding+transmission+Borrelia+&btnG=&hl=en&as_sdt=0%2C5" target="_blank">between ticks during co-feeding</a> on the same mammal. It could be passed <a href="http://scholar.google.com/scholar?q=in+utero+transmission+Borrelia+&btnG=&hl=en&as_sdt=0%2C5" target="_blank">from a mother to her child's placenta in utero</a> during pregnancy, and in some cases, <a href="http://journals.lww.com/pidj/Citation/1988/04000/Borrelia_burgdorferi_in_a_newborn_despite_oral.10.aspx" target="_blank">to the fetus itself</a>. But they will state that thus far, there is no evidence that Lyme disease can be sexually transmitted between mammals including humans.<br />
<br />
<b>My Initial Thoughts On The Issue Of Sexual Transmission</b><br />
<br />
I didn't care much about answering the sexual transmission question when I first contracted Lyme disease. Partly because I was so sick, sex was the last thing on my mind, and I wasn't up to having any. Yeah, <i>sad but true</i>. For the most part, I concerned myself with treatment, rest, and getting better.<br />
<br />
Time and again, it's clear the question about whether or not Lyme disease can be sexually transmitted is important to others as it has been raised in support groups, on online patient fora, in chat rooms, and at conferences. So it's a question that keeps coming back, and now that <a href="http://www.reddit.com/r/science/comments/1w6u7x/lyme_disease_may_be_sexually_transmitted/cezah9a" target="_blank">a new abstract by Middelveen et al has been making the rounds concerning sexual transmission of Lyme disease</a>, the topic has become the focus of discussion by the media and among patients yet again.<br />
<br />
So I started investigating the issue of sexual transmission of Lyme disease, and while I came across a number of stories online where patients are convinced either they were infected by their spouse or had infected their spouse - actual studies regarding this phenomenon have been lacking. In reading of all the documentation on Lyme disease transmission I could get a hold of prior to writing this entry, I found one patient blog which offered a good layperson's summary of the literature regarding Lyme disease and sexual transmission: "<a href="http://gotlyme.wordpress.com/2009/08/13/sexual-transmission-of-lyme-disease/" target="_blank">Sexual Transmission of Lyme disease</a>" on <i>A Lyme Disease Journal</i> by J. Mankoff.<br />
<br />
Ms. Mankoff writes about the difficulty in finding scientific papers on Lyme disease sexual transmission studies using both animal and human models - and unfortunately, my own experience mirrored hers.<br />
<br />
In doing the research for this post, I initially learned the following things about publications to date:<br />
<ul>
<li>Setting aside Middelveen et al's recent abstract for now, there has not been one published study which provides any evidence that live<i> </i>spirochetes can be passed on from one human to another through sexual intercourse or sexual contact.</li>
<li>There is scant evidence that spirochetal DNA can be found in human seminal and vaginal secretions.</li>
<li>There is limited evidence that spirochetal DNA can be found in human breast milk.</li>
<li>There are animal studies which demonstrate uninfected animals placed in the same cages with infected animals can develop antibody responses to<i> Borrelia burgdorferi</i>.</li>
<li>There are animal studies which demonstrate that animals infected with spirochetes <i>do not</i> pass them on to uninfected animals in the same cage.</li>
<li>There are animal studies which indicate that the bladder and kidneys can be <i>very good</i> locations from which to culture spirochetes.</li>
<li>There are animal studies which indicate spirochetal DNA can be <i>high</i> in urine samples.</li>
<li>There are animal studies which indicate spirochetal DNA can be <i>absent</i> in urine samples.</li>
</ul>
When you look at this list, you'll notice that I went from discussing sexual transmission of Lyme disease to looking for spirochetes in sexual fluids and breast milk to looking for spirochetes in urine - probably not the direction anyone imagined I'd go. But that's because to date, more studies have been completed which indicate spirochetes are present in urine than studies which indicate spirochetes appear in sexual fluids - so I'm going to end up talking about those studies, too.<br />
<br />
<b>Evidence of Borrelia burgdorferi - Lyme disease DNA - in human semen and vaginal secretions</b><br />
<br />
So far, while there is research which indicates <i>Borrelia burgdorferi</i> DNA has been found in samples of vaginal and seminal secretions, there is no research to date which has conclusively shown that live motile <i>Borrelia burgdorferi</i> spirochetes have been passed from one partner to another.<br />
<br />
The distinction between having evidence of <i>Borrelia burgdorferi</i> DNA and having live motile <i>Borrelia burgdorferi </i>spirochetes is an important one: Having <i>Borrelia burgdorferi</i> DNA is like holding a strand of my hair in your hand - whereas having a live, motile <i>Borrelia burgdorferi</i> spirochete is like having me sitting in your living room drinking a beer. Hair DNA is a <i>part</i> of me, but it isn't <i>all</i> of me.<br />
<br />
This distinction is important to remember when reviewing one of the most frequently cited papers online on the presence of <i>Borrelia burgdorferi</i> DNA in human vaginal and seminal secretions, "Recovery of Lyme Spirochetes by PCR in Semen Samples of Previously Diagnosed Lyme Disease Patients" presented by Dr. Gregory Bach at the 14th International Scientific Conference on Lyme Disease in April, 2001.<br />
<br />
Unfortunately, when I reviewed all the major online repositories (Google Scholar, PubMed, Oxford Journals, etc.), this paper and its abstract was not listed anywhere and a general search outside of repositories did not point to any peer-reviewed sources. I eventually tracked down <a href="http://lymediseaseresource.com/wordpress/lyme-disease-on-the-rise-sexual-transmission/">a copy of the abstract on Jenna's Lyme Blog</a>, and am reproducing it here (with minor typo corrections) to make a few comments on it:<br />
<blockquote>
<b>Recovery of Lyme Spirochetes By PCR In Semen Samples of Previously Diagnosed Lyme Disease Patients (2001)</b><br />
<br />
Lyme disease, being a spirochete with pathology similar to syphilis, is often found difficult to treat due to the spirochete invading sanctuary sites and displaying pleomorphic characteristics such as a cyst (L-form). Because a significant portion of sexually active couples present to my office with Lyme disease, with only one partner having a history of tick exposure, the question of possible secondary (sexual) vector of transmission for the spirochete warrants inquiry.<br />
<br />
Additionally, sexually active couples seem to have a marked propensity for antibiotic failure raising the question of sexually active couples re-infecting themselves through intimate contact.<br />
<br />
METHODS:<br />
<br />
Lyme spirochetes/DNA have been recovered from stored animal semen. Recovery of spirochete DNA from nursing mother’s breast milk and umbilical cord blood by PCR (confirmed by culture/microscopy), have been found in samples provided to my office.<br />
<br />
RESULTS:<br />
<br />
Surprisingly, initial laboratory testing of semen samples provided by male Lyme patients (positive by western blot/PCR in blood) and the male sexual partner of a Lyme infected female patient were positive approximately 40% of the time.<br />
<br />
PCR recovery of Lyme DNA nucleotide sequences with microscopic confirmation of semen samples yielded positive results in 14/32 Lyme patients (13 male semen samples and 1 vaginal pap).<br />
<br />
ALL positive semen/vaginal samples in patients with known sexual partners resulted in positive Lyme titers/PCR in their sexual partners. 3/4 positive semen patients had no or unknown sexual partners to be tested. These preliminary findings warrant further study. Currently a statistical design study to evaluate the possibility of sexual transmission of the spirochete is being undertaken.<br />
<br />
Our laboratory studies confirm the existence of Lyme spirochetes in semen/vaginal secretions. Whether or not further clinical studies with a larger statistical group will support the hypothesis of sexual transmission remains to be seen. A retrospective clinical study is also underway.<br />
<br />
We are reviewing the medical records, collecting semen samples of patients who were previously diagnosed with current and previously treated Lyme disease are being asked to provide semen, pap, and blood samples for extensive laboratory testing.<br />
<br />
CONCLUSION:<br />
<br />
With the initially impressive data, we feel the subsequent statistical study on the sexual transmission of the Lyme spirochete will illuminate a much broader spectrum of public health concerns associated with the disease than the originally accepted tick borne vector.</blockquote>
At first glance, someone reading this study may get excited: <i>Hey, they found evidence of Lyme disease bacteria in semen and vaginal fluid.</i> But on further reading, it becomes clear that the paper focuses on PCR recovery of <b>Lyme DNA</b> nucleotide sequences and the results of western blots - <b>not</b> whole spirochetes.<br />
<br />
There are unanswered questions about this study based on the abstract: We don't know what kind of microscopic confirmation was conducted and why it was mostly conducted on semen. We don't know if patients had other possible routes of exposure to spirochetes. We don't know if the DNA sequences recovered matched between sexual partners. We don't know whether any of the patients who were sampled had recently taken antibiotics and if the spirochetal DNA that was detected was the result of their bodies trying to purge a massive die-off of spirochetes. What kind of treatment patients in the study had received so far is an unknown.<br />
<br />
I would agree with one message in the conclusion - that additional studies on spirochetal DNA or spirochetes in sexual fluids could be informative and help confirm or deny these findings.<br />
<br />
But finding Lyme disease <i>Borrelia burgdorferi</i> DNA alone in secretions is <i>not</i> evidence that spirochetes can be transmitted - it can be much like finding dead viral particles leaving the body of someone who recently had the flu.<br />
<br />
And in the case of figuring out who gave a flu to who, if Jane gets the flu - she may or may not have passed on the flu to John in her office. John could have picked it up from someone else or from <a href="http://en.wikipedia.org/wiki/Fomite" target="_blank">fomites</a> on a doorknob. Without more data, there's no compelling evidence to suggest that his active infection traces back to Jane in particular.<br />
<br />
The difference with a study on the sexual transmission of Lyme disease compared to transmission of the flu is that one has to demonstrate not only that the person contracted Lyme disease from a specific partner through sexual contact but one also has to provide evidence that the person <i>did not</i> somehow contract Lyme disease from a tick bite or by a different nonsexual mode of transmission.<br />
<br />
To my knowledge, further clinical studies with a larger statistical group have not been conducted by Dr. Bach to support his hypothesis about Lyme disease and sexual transmission, and his 2001 study abstract leaves the reader with unanswered questions.<br />
<br />
Here is another paper which examines <i>Borrelia burgdorferi</i> in human samples - but not semen or vaginal secretions:<br />
<blockquote class="tr_bq">
<b>Detection of <i>Borrelia burgdorferi </i>DNA by polymerase chain reaction in the urine and breast milk of patients with Lyme Borreliosis</b> <b>(1995)</b></blockquote>
<blockquote class="tr_bq">
Abstract</blockquote>
<blockquote class="tr_bq">
Current laboratory diagnosis of Lyme borreliosis relies on tests for the detection of antibodies to <i>Borrelia burgdorferi </i>with known limitations. By using a simple extraction procedure for urine samples, <i>B. burgdorferi</i> DNA was amplified by a nested PCR with primers that target the specific part of the flagellin gene. To control possible inhibition of the enzyme (polymerase), a special assay using the same primers was developed. We examined 403 urine samples from 185 patients with skin manifestations of Lyme borreliosis. Before treatment, <i>B. burgdorferi</i> DNA was detected in 88 of 97 patients with Lyme borreliosis. After treatment, all but seven patients became nonreactive. Six of these seven persons suffered from intermittent migratory arthralgias or myalgias, and one from acrodermatitis chronica atrophicans. Two of 49 control patients with various dermatologic disorders and none out of 22 presumably healthy persons were reactive in the PCR. In addition to urine, breast milk from two lactating women with erythema migrans was tested and also found reactive. <i>Borrelia burgdorferi </i>DNA can be detected with high sensitivity (91%) by a nested PCR in urine of patients with Lyme borreliosis. In addition, this test can be a reliable marker for the efficacy of treatment.</blockquote>
This study indicates that spirochetal DNA could be easily detected in urine using nested PCR, though today this is not a testing method for Lyme disease which is regularly used (and indeed there have been mixed reviews on how effective the use of urine is in testing for Lyme disease). While human breast milk was found to be reactive in PCR, it's important to note that no motile, whole spirochetes were recorded as being found.<br />
<br />
While interesting, this paper does not provide evidence that Lyme disease is sexually transmitted. It only has the potential to raise - but not answer - questions about the viability of spirochetes in urine and breast milk. Additional studies would have to be completed to determine that live, whole spirochetes are present in urine and breast milk, and that transmission of spirochetes can occur via human breast milk and urine.<br />
<br />
Others have cited a 1995 paper online as evidence pointing to <i>Borrelia burgdorferi </i>surviving in semen: "Viability of <i>Borrelia burgdorferi</i> in stored semen". That line of thinking is erroneous, however, and to clear up the matter here:<br />
<br />
This paper is <b>not</b> about <i>Borrelia burgdorferi</i> being found surviving in semen - it's about seeing if <i>Borrelia burgdorferi</i> which is <i>manually</i> added to semen from different animals (bull, ram, and dog) is a useful storage method. Storing <i>Borrelia burgdorferi</i> in semen samples is then compared to storing them in Barbour-Stoenner-Kelly (BSK) medium. Nothing in this study is relevant to providing evidence about <i>Borrelia burgdorferi</i> from an actual infection showing up in the host animal's semen. (And yes, I agree this is a weird experiment, and wonder what the authors were thinking when designing it - perhaps that semen's components may be nutritious for spirochetes and easier to use than BSK.)<br />
<br />
These studies are the top three studies often cited by some to support the position that Lyme disease can be sexually transmitted between humans - however, the first two only provide some evidence that <i>Borrelia burgdorferi</i> DNA can be found in semen, vaginal fluid, and breast milk - while the third is only about using animal semen to store spirochetes for research purposes.<br />
<br />
<b>The EC Burgess Studies</b><br />
<br />
One oft-cited researcher who investigated various routes of transmission of <i>Borrelia burgdorferi</i> in animal models was Dr. Elizabeth Burgess. Notes taken from a lecture by Tom Grier, microbiologist, <a href="http://madisonarealymesupportgroup.wordpress.com/2010/08/09/tom-grier-lyme-lecture-outline/">at Lac Court Oreilles Convention Center</a> said in reference to Dr. Burgess:<br />
<blockquote class="tr_bq">
"Dr Elizabeth Burgess, DMV at Madison: her work has been overlooked for decades.<br />
<br />
Her preliminary work showed that the <i>Borrelia</i> species of spirochete possessed some mechanism and ability to penetrate mucous membranes suggesting transmission in cattle could be through urine–to- mouth contact putting cattle at a risk, besides just ticks.<br />
<br />
Dr Burgess’ work was harshly and unjustly criticized without investigation or inspection. A decade later we see that <i>Borrelia</i> is a champion at penetrating mammalian blood vessels and endothelial cells that line the blood vessels. How hard is it to imagine mucosa capillaries in cattle are exposed targets for <i>Borrelia</i> to penetrate on contact? Since the introduction of the veterinary Lyme vaccines, we hear little about entire herds of cattle and horses being infected."</blockquote>
And it's true - Dr. Burgess' work was criticized. Some of this criticism was mentioned in <a href="http://www.nytimes.com/1989/07/04/science/medical-science-steps-up-its-assault-on-lyme-disease.html?pagewanted=all&src=pm">an article on Lyme disease from 1989 which was published in the New York Times</a>:<br />
<blockquote>
Dr. Elizabeth Burgess of the University of Wisconsin's School of Veterinary Medicine has suggested the possibility of direct spread through contaminated urine.<br />
<br />
But other experts expressed deep skepticism about her proposal, saying further studies are needed. They also say the disease probably would not follow a seasonal pattern if the spirochete were transmitted in this way. </blockquote>
<blockquote>
''If this were true, then virtually every veterinarian and every farmer would have Lyme disease,'' said Dr. Willy Burgdorfer, scientist emeritus at the Public Health Service laboratory in Montana. Dr. Burgdorfer led the team that in 1981 isolated the spirochete, which was named for him.</blockquote>
That same article later goes on to discuss the possibility of ticks spreading Lyme disease via migratory birds, with Dr. Burgdorfer then saying that ''just because they can be carried on birds does not mean that ticks will spread to every corner of the country.''<br />
<br />
Since this article's publication in 1989, <a href="http://scholar.google.com/scholar?q=migratory+birds+Borrelia+burgdorferi&btnG=&hl=en&as_sdt=0%2C5" target="_blank">numerous scientific studies have provided evidence that migratory birds spread infected ticks to various corners of the country as well as to neighboring Canada</a>. Dr. Burgdorfer has presumably revised his view on the role of migratory birds in spreading Lyme disease given these studies.<br />
<br />
But as of this writing, it is unknown if his criticism of Dr. Burgess remains the same. And to some degree, Dr. Burgdorfer's statement on record at the <i>New York Times</i> is interesting from a historical perspective because in 1989, he had co-authored <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC266481/">a paper with Dr. Tom Schwan</a> about the utility of culturing Lyme disease from mouse bladders and how spirochetes were not found in the urine of the mice they studied - but by 1998, he co-authored <a href="http://cid.oxfordjournals.org/content/26/1/122.full.pdf" target="_blank">a paper about tickborne relapsing fever</a>, citing a <a href="http://archpedi.jamanetwork.com/article.aspx?articleid=507816" target="_blank">Linnemann et al paper from 1978</a> mentioning that <i>Borrelia</i> spirochetes could be found in the urine of human patients with acute relapsing fever.<br />
<br />
One interesting note about Dr. Burgdorfer's paper co-authored with Dr. Schwan: He cited an earlier 1986 study by Bosler and Schultze, "The prevalence and significance of <i>Borrelia burgdorferi</i> in the urine of feral reservoir hosts" (mentioned in table in part two of this blog post) where 50% of the mice studied from Shelter Island had evidence of <i>Borrelia burgdorferi </i>in urine, but it was thought the reason that they were that highly spirochetemic was because 95% of the mice were also infected with <i>Babesia</i>.<br />
<br />
With this knowledge, I wonder if at some point years after his interview with the NYT, if Dr. Burgdorfer sat down with Dr. Burgess and discussed her work over a cup of coffee while <a href="http://www.lyme.org/journal/jstd_editors.html" target="_blank">they were both working on the <i>Journal of Spirochetal and Tick-borne Diseases</i></a> for the <a href="http://www.lyme.org/" target="_blank">now retired Lyme Disease Foundation</a>, and what conclusions they shared regarding the presence of spirochetes in urine samples. Did they discuss the role of <i>Babesia</i> in the presence of greater spirochetemia and spirocheturia in mice?<br />
<br />
But I digress...<br />
<br />
What did Burgess study? Burgess was known for her work on two infections - primarily <a href="http://en.wikipedia.org/wiki/Duck_plague" target="_blank">duck plague virus</a>, caused by anatid herpesvirus 1 - and <i>Borrelia burgdorferi </i>infections in a wide range of animals from cats and dogs to livestock; from black bears to coyotes. She was first author on 20 papers and co-author on 16 additional papers that I could find. This was her career, her lifeblood, and a record of her work can be viewed on <a href="http://scholar.google.com/scholar?q=Burgess%2C+EC+Borrelia&btnG=&hl=en&as_sdt=2005&sciodt=0%2C5&cites=6996562595376622527&scipsc=" target="_blank">Google Scholar</a>.<br />
<br />
Her most notable works related to <i>Borrelia burgdorferi</i> transmission in animals are:<br />
<div class="p1">
</div>
<ul>
<li>1986 Experimental inoculation of dogs with <i>Borrelia burgdorferi </i></li>
<li>1986 Experimental inoculation of <i>Peromyscus spp.</i> with <i>Borrelia burgdorferi:</i> evidence of contact transmission </li>
<li>1987 Oral infection of <i>Peromyscus maniculatus</i> with <i>Borrelia burgdorferi</i> and subsequent transmission by <i>Ixodes dammini</i></li>
<li>1988 <i>Borrelia burgdorferi</i> infection in Wisconsin horses and cows</li>
<li>1989 Experimental inoculation of mallard ducks (<i>Anas platyrhynchos</i>) with <i>Borrelia burgdorferi</i></li>
<li>1992 Experimentally induced infection of cats with <i>Borrelia burgdorferi</i></li>
</ul>
I tried to track down Dr. Burgess to ask her about her work, but this task was not successful; she appears to have retired and does not have an active online presence. However, I was able to acquire copies of the full text of her papers for my own review.<br />
<br />
Dr. Burgess' studies suggest that contact transmission from infected animals to uninfected animals can and does occur, though not consistently - and that even if there is no evidence of spirochetes being transferred from infected animals to uninfected animals, that uninfected animals housed with infected animals develop a positive antibody response to <i>Borrelia burgdorferi</i>. Her research also indicates that spirochetes can be found in animal urine and it is suggested that oral contact with that urine could lead to infection.<br />
<br />
Her findings - now as they were then - have been considered by some to be controversial. Other researchers have conducted similar experiments and their results conflicted with those of Burgess. Or they had negative results after running similar experiments using different animal models - which indicates that perhaps the ability for an animal to either transmit <i>Borrelia burgdorferi</i> via oral/urine contact or contract it that way is entirely species dependent.<br />
<br />
<b><u>Coming up next:</u> </b><br />
<b><u><br /></u></b>
We'll take a closer look at suspected cases of contact transmission between animals infected with <i>Borrelia burgdorferi </i>and uninfected animals, and how these cases may have led to the question of whether or not sexual transmission of Lyme disease between animals occurred in <a href="http://campother.blogspot.com/2014/04/part-2-sexual-transmission-of-lyme.html" target="_blank">Part 2 of "Sexual Transmission Of Lyme Disease - Is There Evidence?</a>"<br />
<br />
<br />
<br />
<div>
<div style="text-align: center;">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a> </div>
<div style="text-align: center;">
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> </small></div>
<div style="text-align: center;">
<small>is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons Attribution-</a></small></div>
<div style="text-align: center;">
<small><a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
</div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com1tag:blogger.com,1999:blog-4073397588746430486.post-11562357450307691142014-03-05T23:41:00.002-10:002014-03-07T06:27:41.525-10:00Admin Note: Pardon The Mess...But I'm Changing The Blog<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjN0-wWcBDcv7Jbwvm82Ys2XTPPre4TE46B5jdfzkT2aXbv-IuD1hasgQMS3lrsLyN_lFzxQpaGEg_edj333Bcj7vsSw4ooi4ILgjqd6is9_jCzz7Z3j7iEb9gYROC6qf2a1kkQ51_nHVxH/s1600/Va%CC%88garbete.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjN0-wWcBDcv7Jbwvm82Ys2XTPPre4TE46B5jdfzkT2aXbv-IuD1hasgQMS3lrsLyN_lFzxQpaGEg_edj333Bcj7vsSw4ooi4ILgjqd6is9_jCzz7Z3j7iEb9gYROC6qf2a1kkQ51_nHVxH/s1600/Va%CC%88garbete.png" height="176" width="200" /></a></div>
You might have noticed that this blog has had its format changed a lot in the past 24 hours. Apologies to anyone who found it disorienting, but it was something that had to be done.<br />
<br />
Initially my intent was to do one thing and one thing only: make room for an upcoming post which contains a wide table that wouldn't fit in my 3 column format. So I began pushing the links and widgets from two separate columns into one column so I could have a wider area for posts. Then I realized that it took much longer for the page to load, and there was a big white space below the posts next to the giant list of links I was forced to make when moving them all into one column.<br />
<br />
Suffice it to say, one thing lead to another and before I knew it, I was more than halfway through an overhaul of the site's layout.<br />
<br />
So here we are... I'm not sure I'm done with it (though hopefully close to it) and if you're a regular reader of this blog, it might be useful for me to point out what these changes have been, how they might affect you, and my thoughts on any near-future changes:<br />
<br />
<b>The logo has taken a vacation.</b><br />
<br />
It's nothing personal, it just needed a break (as I have as well) and was tired of holding up the top of the page. So I took it offline, where it has decided to go off to a spa in Bayern, lose some weight, and promised to introduce me to some new friends. (I'm not sure what to make of this, but at any rate, hopefully our new logo will come back, refreshed and resized.)<br />
<br />
<b>"Posts people are reading this week" list was removed.</b><br />
<b><br /></b>
The posts which were on that list were there mainly because people found them through a search engine or were already familiar with the blog and came back for a second look. Few people used them to read an older post, and more than half of my readers are regulars looking for new posts. Given this, I decided to retire this list.<br />
<br />
<b>The long list of blog post links which bordered the left side of the page have been moved.</b><br />
<b><br />
</b> They have not been deleted, they now live on their own page which is linked to on the toolbar at the top of this page: <a href="http://campother.blogspot.com/p/popular-links.html" target="_blank">Popular Posts</a>.<br />
<br />
Interesting as they were, they began slowing down the loading of this page and their presence prompted me to install a third column to the layout in the first place - which I now realize was a dumb decision if I ever intend to put tables of data on my blog or perhaps might want to post a diagram, scientific illustration, web comics, or a video with large dimensions. (<a href="http://campother.blogspot.com/2013/10/24-hours-of-attachment-is-estimate-not.html">The table on this page about tickborne disease transmission times</a> already looks better.)<br />
<br />
Sometimes less is more. So right. Gone.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh1i_vKv_pGXqnLTPweBznHF8uY2DWlZXYPdHsmSTEGRLRb2wmtDN-6asBviEbJ-NSbnK7fbgblFbSh3bBWpcMtCU6L0LaRN9uaayuIgiQiq8XYrcNGpft6BwQv1w4V4T6SZyVH0R3suXkX/s1600/PostIndex.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><br class="Apple-interchange-newline" /><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEh1i_vKv_pGXqnLTPweBznHF8uY2DWlZXYPdHsmSTEGRLRb2wmtDN-6asBviEbJ-NSbnK7fbgblFbSh3bBWpcMtCU6L0LaRN9uaayuIgiQiq8XYrcNGpft6BwQv1w4V4T6SZyVH0R3suXkX/s1600/PostIndex.jpg" /></a></div>
<< <b>The "view all posts" link is gone, along with its cool retro graphic. </b><br />
<b><br /></b>Sorry, it just had to go. I hadn't clicked on it in a while, but a few days ago I tried it and found out it didn't work. It didn't work on my laptop, it didn't work on phones... it didn't work on anything. I don't know if Blogger decided to no longer support this feature or if it just stopped working with my blog once it reached a certain number of posts. Either way, it isn't working so it's gone.<br />
<br />
If you used it a lot (or even at all), I recommend that instead you either search for a blog on a given topic by using the handy search tool on the sidebar or scroll down and browse the archives to find a specific blog post.<br />
<div>
<br /></div>
<br />
<b>The blog rolls for science blogs and Lyme disease patient blogs (relocated to the footer below) now display the 5 most recently updated blogs. </b><br />
<b><br />
</b> I have had a hard time deciding what to do with displaying blog rolls - particularly patient blogs. Two of the blogs on my patient roll as of this writing are no longer writing about Lyme disease. They have moved on, which is great news - but I'm not sure whether to retain their blogs since they are either unlikely to be updated or will be off topic. My compromise for the time being was to set the blog roll widget to only display the top 5 most recently updated blogs and the rest remain behind a link, where if you want to see them, just click it and the rest of the blogs - outdated as they are - will display.<br />
<br />
It may be that I end up removing some of the blogs from my rolls and replace them with others. I haven't decided yet, but I could use recommendations for good blogs by patients about science and chronic illness management in general to add to the rolls. I've been thinking broadening the category from "Lyme disease patient blogs" to something more general about chronic illness (but which is still focused more on Lyme disease and other tickborne infections). <strike>Nothing solid yet.</strike> Update: I added "chronic illness" to the blog roll title, and <a href="http://phdisabled.wordpress.com/" target="_blank">PhDisabled blog</a>.<br />
<br />
<b>Future changes?</b><br />
<b><br />
</b> I don't plan on making major future changes after this any time soon, unless one counts refreshing the logo (or header and logo area, to be precise) as a major change. My basic aim lately is to simplify everything, though, so you can at least make some predictions what direction near-future changes in the design and layout of this blog will be.<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com0tag:blogger.com,1999:blog-4073397588746430486.post-39695654475131665642013-11-17T23:00:00.001-10:002013-11-17T23:00:32.262-10:00On Stephen Hawking, Disability, and Capability: What Are Limitations?A few months ago, I read an article in <i>The Telegraph </i>about a doctor in the UK <a href="http://www.telegraph.co.uk/health/10217913/Stephen-Hawking-is-not-on-the-sick-so-disabled-should-not-be-says-GP.html">who made a statement about how people who receive disability benefits should not because if Stephen Hawking could work, then pretty much everyone could work</a>.<br />
<br />
<i>The Telegraph</i> quotes Dr. Peverley, who practices in Sunderland, England:<br />
<blockquote class="tr_bq">
“We are, as a profession, dedicated to making our patients as healthy as possible, and yet a proportion of punters are hell bent on trying to prove they’re really ill, and need us to confirm it." </blockquote>
<blockquote class="tr_bq">
“The fact is, nearly everyone is capable of some kind of work. I had considered, at one point, putting up a portrait of Professor Stephen Hawking in my consulting room with a caption that said, ‘This bloke is not on the sick’.”</blockquote>
<br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhAmaJ7xQro_40_hEyPjtuk5_3wgaTM8exIK1a3khSax_A18GnsIkL1VjYrTnMHyNihCiZ7pVo0QhkCZJ-vzJBBDU6nEsMiXhr_kDsIfjPs3_v5p2t670hp8PBBChxyVpf92zLIwLuJqYvE/s1600/320px-Stephen_Hawking_on_his_way_to_a_lecture_before_highschool_students_in_Jerusalem_10-12-2006.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: .5em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhAmaJ7xQro_40_hEyPjtuk5_3wgaTM8exIK1a3khSax_A18GnsIkL1VjYrTnMHyNihCiZ7pVo0QhkCZJ-vzJBBDU6nEsMiXhr_kDsIfjPs3_v5p2t670hp8PBBChxyVpf92zLIwLuJqYvE/s1600/320px-Stephen_Hawking_on_his_way_to_a_lecture_before_highschool_students_in_Jerusalem_10-12-2006.jpg" /></a> Dr. Peverley is one of a number of doctors and politicians who have been engaged in a strange war on the disabled in the UK. This war began during Prime Minister David Cameron's term in office, and has been reflected in the hiring of private firm, <a href="http://en.wikipedia.org/wiki/Atos_Healthcare">Atos</a>, to complete disability assessments on new patients and reassess those already disabled for the purpose of getting them off a disability pension and put them back to work.<br />
<br />
In theory, getting people with disabilities back to work who are capable of work sounds good. One problem is, though, that Atos doesn't appear to be doing a good job of determining just who is eligible to work again and who should remain on a disability pension.<br />
<br />
Since 2008, Atos has conducted more than 1.5 million disability assessments. However, during this time there have been more than 600,000 appeals at a cost of £60 million. A number of these appeals were based on reevaluations of disabled people who were in fact still quite disabled, but their new evaluation forms were filled with erroneous or incomplete information which did not characterize patients' degree of disability properly. <br />
<br />
One doctor, Dr. Greg Wood, who used to work as an evaluator for Atos <a href="http://www.theguardian.com/society/2013/jul/31/atos-fitness-work-test-greg-wood">became a whistleblower</a>. When interviewed by the newspaper he revealed that he had been not only encouraged - but ordered - to downplay the severity of patients' disabilities or misstate their limitations so as to get them off the disability pension rolls.<br />
<br />
Which brings me back to Dr. Peverley. Dr. Peverley sounds like the kind of doctor who would comply with whatever Atos asked him to do in order to get patients off disability and return them to work, no matter how sick or how poorly suited to work they would be.<br />
<br />
<i>The Telegraph</i> article later states, regarding Dr. Peverley:<br />
<blockquote>
He said that being declared “fit to work” did not mean patients had to do a laborious job.<br />
<br />
“Being found fit for some kind of employment by Atos does not mean you’re necessarily capable of being an FBI agent or a lumberjack”, Dr Peverley said.<br />
<br />
“However, you might be able to work at a desk on a telephone, or hold a lollipop on a zebra crossing."</blockquote>
On one hand, he makes a good point: Many people with disabilities and chronic illness can do something and many are not <i>completely </i>incapacitated. They may be disabled in some way, but they are capable of completing a task.<br />
<br />
On the other hand, he entirely misses the point that being able to work at a regular, part time or full time job is not just about being capable of doing a task once or even here and there - it's about being able to <i>consistently</i> perform certain tasks <i>repeatedly</i> on a <i>regular</i> basis, typically daily, often at long stretches of time without a break. And to do so in a workplace which may only allow you a minimum of flexibility in your work hours and may or may not permit you to work from home at all.<br />
<br />
Stephen Hawking, in a short BBC interview about his autobiographical film, <i><a href="http://www.vertigofilms.com/hawking/">Hawking</a> </i>(by Vertigo Films - not to be confused with the film, <i><a href="http://en.wikipedia.org/wiki/Hawking_(2004_film)">Hawking</a>,</i> starring Benedict Cumberbatch)<i>, </i>discusses his own disability and his view of it includes acknowledgments which Dr. Peverley does not make:<br />
<br />
<iframe allowfullscreen="" frameborder="0" height="315" src="//www.youtube.com/embed/H30PkZNMDv0" width="420"></iframe><br />
<br />
Stephen Hawking acknowledges that in his situation, he was very fortunate that his disability in some ways has been an asset which allows him to avoid teaching or attending more boring committee meetings so he can spend more time doing his own research on theoretical physics. He admits that because he cannot talk to people quickly, he tends drift off on a mental tangent about some aspect of physics while around other people. He also acknowledges that with his kind of disability, it has not been a drawback to working in his field because he can do theoretical physics in his head. His physical capabilities aren't necessary to do his work.<br />
<br />
Stephen Hawking recognizes his good fortune despite his misfortune - of this it's quite clear. And it's this message he wants everyone watching to hold on to. But he also states that some of his good fortune has been due to the support and love of his family and friends, his upbringing, the opportunity he had to get a solid education until his physical condition began to deteriorate, the care he received for many years from the National Health Service, and the fact that his condition has been a form of motor neuron disease which has given him a chance to go deep into his mind to explore new concepts while outliving doctors' expectations about his lifespan.<br />
<br />
It might have been more traumatic for Stephen Hawking to have lost his cognitive capabilities than it was to have lost his physical capabilities because his life up until the point his condition began to worsen was already about academia, about learning and innovative thinking.<br />
<br />
Only Stephen Hawking can really say what his choice would have been if it were given to him - I'm just guessing. But it's very clear that his complex internal mental world is where he lives, works, and plays - and if that were to be cut off from him, depression and losing the will to live might follow. This world is a big part of who he is.<br />
<br />
Stephen Hawking is visibly physically disabled. And yet <i>he has</i> certain abilities others with different disabilities do <i>not</i> have: He can see, hear, communicate with others on and off the internet, and think clearly and rationally. He can create whole models of the Universe inside his head. He can sleep 8 hours a night, wake up refreshed, and get around with the assistance of a wheelchair and a personal assistant. While he is physically impaired, others act as his physical extensions to care for him - whether it be eating, bathing, dressing, or using the toilet. With such support, he can focus on his work.<br />
<br />
But just because Stephen Hawking can do what he does does not mean all people with disabilities and chronic illnesses can do what he does. No one would expect someone with short term memory problems and difficulty learning and retaining new information to be able to explore problems of theoretical physics in their head any more than one would expect Stephen Hawking to start washing windows and painting the trim.<br />
<br />
I can think of any of a number of disabilities and chronic illnesses which could impair people to the degree that a regular part time or full time job would be impossible for them. Those with severe anxiety, severe depression, bipolar disorder, or PTSD can be so overwhelmed by managing their condition that at times it is enough work just to get through the next hour - let alone day or week. Those who have cancer and have many side effects from chemotherapy and fatigue may not be able to work. Those who have frequent flareups of autoimmune diseases or have conditions which require multiple surgeries over time and recoveries and/or multiple regular tests and scans every week or two may not be able work. Those who have more than one medical condition to manage may end up spending so much time and energy in their management that it would interfere with working.<br />
<br />
Some disabilities and illnesses get in the way of accomplishing things in a number of spheres in life more than others. Some disabilities and illnesses are more disruptive or have the potential to be more disruptive than others for holding down a regular job with regular hours and regular deadlines.<br />
<br />
It is this last bit around which I think Dr. Peverley - and those like him - has a blind spot: The issue of employment being contingent upon consistency and reliability.<br />
<br />
When it comes to someone being disabled or chronically ill, their <i>capability and consistent ability</i> to do work is different from their disability or illness. In the UK, the 2010 Equality Act defines disability as “a physical or mental impairment that has a ‘substantial’ and ‘long-term’ negative effect on your ability to do normal daily activities.” This definition covers a wide range of conditions, from mental illness and learning disabilities to chronic physical illness and long term physical impairments.<br />
<br />
Sure, someone with moderate myalgic encephalomyelitis, fibromyalgia, or chronic Lyme disease <i>might</i> be able to hold up up a sign as a crossing guard for a <i>few minutes</i> one day. But can they do it for the next <i>fifteen minutes</i>? Can they do it for <i>three hours a day</i>? Can they do it for <i>three hours a day, five days a week, for ten months of the year</i>? If they can't - and an employer witnesses that their crossing guard begins to fail to carry out this supposedly easy task (easy for whom?) by leaving their station early or calling in sick too many days in a row, then they will not be a crossing guard for long.<br />
<br />
Even if this crossing guard job were a job one could do, how on earth could it provide the disabled or chronically ill individual with enough financial support to keep a roof over their head? In all reality it can't, and so even if one could work 15-20 hours a week, within one's maximum capacity for work under the best of conditions, the wages earned from being a crossing guard are small. Anyone doing such work would need additional forms of support. And even if the disabled and chronically ill individual were to be capable of this type of job, one has to consider as an employer, if your employee will be capable of doing such job for at least an intermediate length of time if not the long run - and if one is a disabled or ill employee with such job, whether doing such a job with such frequency will have a negative impact on one's health.<br />
<br />
The same applies to Dr. Peverley's assumption about anyone with a disability or chronic illness being able to hold down a desk job. Maybe some people with disabilities or chronic illness can. Maybe some people can't. In this <i>Telegraph</i> article, Dr. Peverley makes it sound as if everyone can and this, again, brings up the same issues that the crossing guard job has: Someone could have trouble sitting for long periods of time due to pain and fatigue, someone could have trouble consistently performing other duties required of the job due to their individual disability or illness.<br />
<br />
In all of these situations, Dr. Peverley overlooks two realities:<br />
<br />
One is that the way most work is organized is that there is a daily routine and expectation where - no matter what the job is - employers want employees who will be able to show up to work on time, work at a consistent level, leave work at a certain time (often later than originally intended), work day in and out, and meet deadlines at regular intervals.<br />
<br />
Two is that in many ways, being disabled or chronically ill can interfere with this very structure of expectations and routine around which work is organized, and because of this, employers who fear the disabled or chronically ill will not meet expectations can either discriminate against hiring those who are visibly disabled or chronically ill, and/or more easily let go of employees with disabilities and chronic illnesses if simple accommodations aren't enough to help the employees accomplish their jobs under existing terms.<br />
<br />
The missing piece that would help empower more disabled and chronically ill people enter the workforce that is currently not part of our modern workplace culture is to <i>adapt jobs</i> and <i>adapt workplace infrastructures</i> to accommodate the person who is disabled and/or chronically ill - not the other way around.<br />
<br />
The situation for many disabled and chronically ill people is that they may not work at their best under circumstances which are normal and typical for the average able-bodied, healthy worker. In order to empower those who can work to some degree, the best accommodation comes from acknowledging the person with disability or chronic illness' circumstances and work with them to create a suitable position and environment.<br />
<br />
In this respect, Stephen Hawking has the kind of support that many people with disabilities and chronic illnesses do not: Throughout the film of his life, people value Hawking's opinion and ideas and bend over backward to accommodate him, with graduate students often also serving as personal assistants early in Hawking's career. As time goes on, hired nurses and assistants take their place. Personal care, assistive technology, and Hawking's research position are all created specifically to support him in doing his work as much as it is possible - rather than having Hawking be given only a few accommodations which might make the simple act of living possible.<br />
<br />
People with disabilities and chronic illnesses who could work and contribute something to society are better able to contribute if society as a whole begins to integrate a concept of working with disabilities and chronic illness into existing economies and workplaces. Workplaces and technology can evolve to create jobs which empower those with disabilities and chronic illnesses to work as much as it is possible.<br />
<br />
Rather than have the standard job with typical requirements and routines, jobs would have to be created which disabled and chronically ill people can do which do not rely on consistency or on meeting deadlines at regular - often short - intervals.<br />
<br />
Jobs and workplace infrastructures would have to be created which can flex around the circumstances of a person's reality, strengths, and weaknesses - rather than to try to shoehorn the disabled or chronically ill person into a job and workplace which permits a few small changes that help accommodate the person to try to work at the job in the same way able-bodied and healthy people do.<br />
<br />
The support should be there to accommodate people in reaching goals whether or not they conform to standard workplace expectations. And not to do so in order to make the Dr. Peverleys of the world shut up and feel righteous about their idea that those with disabilities and chronic illnesses should be able to get off disability pensions and work - but to empower <i>anyone</i> to pursue goals, to follow dreams, to have some hand in supporting themselves and having a sense of a future despite the cards they've been dealt.<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com5tag:blogger.com,1999:blog-4073397588746430486.post-69389608537193876052013-11-11T08:26:00.002-10:002013-11-12T07:02:20.250-10:00Thoughts on "Canary In A Coal Mine" and "Under Our Skin"It's been five years since the controversial award-winning film about chronic Lyme disease, <i>Under Our Skin</i>, was first released.<br />
<br />
<iframe allowfullscreen="" frameborder="0" height="315" src="http://www.youtube.com/embed/z5u73ME4sVU" width="560"></iframe><br />
<br />
<br />
When it was first released, <i>Under Our Skin</i> provided catharsis for me as a patient who developed chronic pain and chronic fatigue since that fateful day I received an infected tick bite and fell ill. It was the first film - the only film, in fact - that I could point to, share, and say to others, "Look. <i>Watch.</i> I'm not the only one who is dealing with this problem".<br />
<br />
And share I did. I bought the DVD and gave it to a therapist who at the time was working with me on tips for coping with secondary depression. I showed it to a few close friends who wanted to know more about the chronic Lyme disease controversy. And I sent a copy to my parents.<br />
<br />
<i>Under Our Skin </i>helped open the door for discussion about my illness, it made me feel less alone in my suffering, it validated my condition for others, and it brought up the very controversies involving chronic Lyme disease I'd been discussing with other patients in a way which easily summarized them for those new to it.<br />
<br />
Lately, I think more about <i>Under Our Skin</i> in a broader sense and less about it being a piece of my own personal chronic illness manifesto. Here was a film which scored an Academy Award nomination and several international film festival awards - no small feat for a documentary film of this nature. Here was a film which took Lyme disease into the spotlight and encouraged people to take more steps to prevent tick bites so as to avoid having the kind of experience I've been having. Here was a film that spoke to a larger proportion of the population than I originally thought possible.<br />
<i><br />
</i><i>"Lyme disease?" </i>I remember muttering to myself,<i> "Who the hell wants to watch a film about that except patients?" </i>But watch it they did<i>.</i><br />
<i><br />
</i> Whatever your personal opinion about <i>Under Our Skin</i> is - like it or loathe it - it spread awareness about the issue of chronic Lyme disease and touched on why the topic of persisting symptoms in patients has become a loaded subject.<br />
<br />
Conditions like chronic Lyme disease, fibromyalgia, and myalgic encephalomyelitis - also known as chronic fatigue syndrome - fall outside the usual diagnostic box and frustrate doctors and patients alike.<br />
<br />
Patients inexplicably report being diagnosed with depression or anxiety when they're running a fever and have joint pain, or report being diagnosed with anxiety when they're dizzy and have signs of orthostatic intolerance. Instead of more involved investigation and attempts to improve patients' symptoms, some are only sent home with a prescription for psychiatric medication and told to call if there are any side effects.<br />
<br />
Doctors, likewise, mention patients who clearly have something going wrong but they have no idea how to help them because the literature just isn't there; the guidelines they are supposed to use have no contingency plans for those who fall outside the box. Some want to help, but they don't know where to begin. A rare few are willing to experiment and try an out-of-the-box treatment for the out-of-the-box patient, and some do so at a risk to themselves.<br />
<br />
If there were more research, if people invested more in projects to help people with such conditions, then maybe we would already have more answers which would help people. As it stands, funding for such research is slim, people are not aware of how profound an impact these conditions can have, and as long as many patients are so sick that they venture outside tentatively (if at all), the only way they can stop slipping through the cracks is to make their voice heard without leaving their beds.<br />
<br />
It is these kinds of points which were made during the Kickstarter campaign for the film, <i>Canary In A Coal Mine</i>, that grabbed my attention, including this one statistic: "Male pattern baldness gets more money for research than myalgic encephalomyelitis/chronic fatigue syndrome".<br />
<br />
It has to be one of the most ridiculous statements made in remarks sandwiched between footage for the film. Or rather, it would be ridiculous if it weren't for the fact that it's actually true. The reality is sad: <a href="http://report.nih.gov/categorical_spending.aspx">ME/CFS only receives about $5 million in NIH research funding annually</a> compared to the hairless wonder's many million dollar pot (hell, just this <i>one</i> private company announced <a href="http://www.thebaldtruth.com/news/eleven-million-dollars-hair-loss-treatment-research/">an $11 million funding round for research</a>) and an industry which generates hundreds of millions in profit. Bill Gates also stated earlier this year <a href="http://www.wired.co.uk/news/archive/2013-03/14/.UUGe-5TS1fE.reddit">that male pattern baldness received more research funding than malaria</a> - another sad surprise. So when <a href="http://phys.org/wire-news/124119794/nih-awards-nearly-2-million-to-3-nyc-institutions-for-chronic-fa.html">$2 million of NIH funding is given to 3 different institutions to study ME/CFS</a>, it's considered a big deal - however, that amount of money pales in comparison to the funding for research on other conditions.<br />
<br />
Sadly, somewhere along the line, it was decided that vanity was more important than a person's ability to get through their day like a normal human being, such as being able to hold down a job and go out to a movie after work - maybe even have a family. Things like that. <i>Normal, you know?</i><br />
<br />
(I don't know about you, but screw my insecurities about going bald - If I had to choose between being bald and having ME/CFS or chronic Lyme disease, well, show me the god that can grant me this wish and let's get that shaver rolling. I can join the Hair Club for Men later and get a transplant or an outrageous selection of hair pieces.)<br />
<br />
Chronic Lyme disease falls into its own funding hell, because while Lyme disease receives a fair amount of funding compared to ME/CFS, it's still relatively less compared to other conditions and projects which are specifically about chronic Lyme disease are rare.<br />
<br />
Twelve years ago, the NIH Lyme disease program officer said data collected from the Klempner antibiotic trial for chronic Lyme disease <a href="http://www.nlm.nih.gov/databases/alerts/lyme.html">would be used to help develop new innovative treatments for patients</a>. Well, it's twelve years later, and the number of innovative treatments for chronic Lyme disease which have been developed from this NIH-NIAID project data <i>are exactly zero</i>.<br />
<br />
But getting back to <i>Canary In A Coal Mine</i>...<br />
<br />
When I first saw the appeal for <i>Canary In A Coal Mine</i>, it came via a tweet from a member of the ME/CFS community. I didn't know what to expect, and when I played the trailer, I was immediately taken in by it.<br />
<br />
<i>Canary In a Coal Mine</i> began as a Kickstarter project initiated by Jennifer Brea, a Harvard doctoral student on medical leave whose life has been changed dramatically by myalgic encephalomyelitis (more commonly referred to as chronic fatigue syndrome, a name which does not do the condition justice) and Kiran Chitanvis, an independent filmmaker who attended NYU Tisch School of the Arts. Jennifer Brea directs the film, Kiran and Jennifer are both producers, and Kiran is director of photography.<br />
<br />
Within days of posting <a href="http://www.kickstarter.com/projects/959776320/canary-in-a-coal-mine">the project on Kickstarter</a>, the initial funding drive exceeded its first goal of $50,000 and today, weeks after posting, it has received over $150,000 funding towards the entire $200,000 needed to complete the film.<br />
<br />
How has this independent film produced in dimly lit bedrooms using iPads and video cameras gained such a meteoric rise in support in so short a time? The answer lies in the trailer presented on Kickstarter, which struck such a note with viewers that they immediately felt inspired to donate:<br />
<br />
<iframe allowfullscreen="" frameborder="0" height="315" src="http://www.youtube.com/embed/YNZai25bOjQ" width="420"></iframe><br />
<div>
<br />
<br />
I've viewed the trailer several times, and with each passage the same scenes stand out for me, over and over. As a whole, it is a masterful piece which builds suspense around the mysterious beginnings of ME/CFS with a history of unusual outbreaks of illness where no one could pinpoint the cause to demonstrating how ME/CFS has had a profound impact on its sufferers and the current controversy over the scientific positions on what causes ME/CFS.<br />
<br />
In this regard, the trailers for <i>Canary in A Coal Mine</i> and <i>Under Our Skin</i> are similar: Both hint at a history of controversy and mystery surrounding the condition. Both highlight the patient experience, by capturing the suffering and changed lives of individuals and families whose lives are abruptly jarred by disease. Both point fingers at doctors who claim patients' symptoms are psychological in nature rather than looking at evidence that the condition is physical. Both open the door into sharing moments in people's lives which are difficult and usually suffered alone in silence or only with those closest to them.<br />
<br />
But where <i>Canary In A Coal Mine</i> immediately diverged from <i>Under Our Skin</i> as a concept is what truly got to me, and almost made me break inside: The trailer is in large part made by the very person who is invested in it the most: Jennifer Brea, a patient suffering with ME/CFS.<br />
<br />
As Kiran Chitanvis, the independent filmmaker directing the project states, the film is intended to be a narrative which pulls the viewer into the experience of what it's like to have ME/CFS in a way that hasn't been done before. And this is one reason why the trailer has been a success: It subtly places the viewer in the position of imagining what it is like to have ME/CFS and have to live life around and through it.<br />
<br />
It can do so effectively because Jennifer Brea is telling her own story, filming her story, interviewing others about her story, and by extension, the making of the trailer and the film actually <i>become</i> part of her own story.<br />
<br />
Footage in the trailer and supplemental videos on the Kickstarter page show the viewer how difficult it is for Jennifer to work on the film and the costs on her body of pushing through a 12 hour day of shooting - a day which will not be repeated because the cost is too high. To emphasize this decision, the statement is made that pacing is important to preserve Jennifer's health, and that if 6 weeks' worth of shooting the film has to be done over the course of a year or more, then so be it. There is no race to finish the film. The important thing is to finish it, period.<br />
<br />
We witness the difficulty involved in watching Jennifer slowly walking, staggering towards a vehicle and outlining the planning required for a journey that most people don't give much thought when they get in a car for a one hour trip to New York City. We see Jennifer slowly struggling to stand up with a laptop in her arms, only to watch her fall forward. We observe Jennifer lying down on a couch in a dimly lit room, too exhausted to stand while friends socialize in a kitchen down the hall. As time trickles by, we catch glimpses of how plans and key milestones Jennifer had planned for her life have been railroaded into some murky unknown future where it's uncertain what will happen.<br />
<br />
This is a trailer which inspired other patients, caregivers, and advocates to fund the project because it is a film that is not only speaking on behalf of all the patients who cannot march on Washington to request funding for more research, who cannot stand for more than a few minutes or even a second, who cannot speak for themselves - it inspired others because it is by a patient, about a patient, and for patients in the voice of a patient - and using this perspective to spread awareness to those who do not have ME/CFS. This angle is one way in which it is very different from a documentary like <i>Under Our Skin</i>.<br />
<br />
One of the scenes in the trailer which put a catch in my throat is shown in this still:<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhzPfFOBjUiM6n5imAB1TDRnYwQOEsdQ9wgOlwC1VmE63kZJfLdLUHDa9auJ3NBaxTrNDqW9kknDC1I8vFkbgz4w0UJMym68cqVZdNge8OdKB0usHqCuU9fR8p3IWyAfZsEwxm9yLnvIHmS/s1600/Jen_wall_of_mystery.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="290" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhzPfFOBjUiM6n5imAB1TDRnYwQOEsdQ9wgOlwC1VmE63kZJfLdLUHDa9auJ3NBaxTrNDqW9kknDC1I8vFkbgz4w0UJMym68cqVZdNge8OdKB0usHqCuU9fR8p3IWyAfZsEwxm9yLnvIHmS/s640/Jen_wall_of_mystery.jpg" width="550" /></a></td></tr>
<tr><td class="tr-caption" style="font-size: 13px;">Jennifer Brea mapping out the pathways and immunological profiles which underlie part of the myalgic encephalomyelitis (ME) puzzle, or what American researchers renamed "chronic fatigue syndrome" (CFS).<br />
© 2013 Canary Films with permission</td></tr>
</tbody></table>
<br />
I can't get this scene out of my mind, because this one moment captures so much of my own experience as chronic Lyme disease patient with an diagnosis of ME/CFS as well.<br />
<br />
While much of my limited energy goes into a few mundane tasks during the day, it also is spent on research related to Lyme disease and immunology, microbiology, molecular biology, and genetics. It is spent pouring over many documents, where I am trying to piece together parts of the chronic Lyme disease puzzle and figure out what happened to me - and to see what novel ideas I can come up with that might make my quality of life better.<br />
<br />
This one snapshot of Jennifer Brea's life could just as easily be a snapshot of my own. I couldn't help but be moved by watching someone else having an experience similar to my own; someone who wanted to do the hard work of getting answers and learning as much as they could even with the challenge of brain fog, overwhelming fatigue, and other disruptive symptoms getting in the way.<br />
<br />
And at the same time, this scene is also one which triggers tremendous anger. Why should she - and why should I - have to be placed in a position where we are compelled to figure out what is going on with our conditions? Why isn't there more research for people in our situation? Why aren't there more doctors who can help us? And most of all: <i>Why the hell do people value a full head of hair over helping people be able to sit up and feed themselves - let alone go to work every day and have a life?</i> Because that's what the dollar signs say. That's where the money is going.<br />
<br />
Another scene which struck me is near the end of the trailer, when Jennifer sits in a wheelchair in the yard and watches others doing yard work:<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiCwW9gBSggQtWdfRRVYXqSbDwNfTXJ44ysTyoVUt28tSro64LAqXCfsU_5zimFEQejLwuK1WSmam8SDJFcH13Jyz5Bfbe_QD_thyphenhyphenO_1Rl2jaxR9KIELSJd3bqeWQdVwxx-3WU33_ErKIIO/s1600/Jen-coop-outside.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="280" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiCwW9gBSggQtWdfRRVYXqSbDwNfTXJ44ysTyoVUt28tSro64LAqXCfsU_5zimFEQejLwuK1WSmam8SDJFcH13Jyz5Bfbe_QD_thyphenhyphenO_1Rl2jaxR9KIELSJd3bqeWQdVwxx-3WU33_ErKIIO/s640/Jen-coop-outside.jpg" width="540" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Scene from <i>Canary In A Coal Mine</i> © 2013 Canary Films with permission</td></tr>
</tbody></table>
<br />
Howard Bloom, writer and former publicist in the music industry who came down with ME/CFS years ago does a voice-over during the scene, saying:<br />
<blockquote>
"There is a future you take for granted every day and never articulate to yourself - and yet it's always there. And when you come down with an illness that has no end, it strips away that idea of a future."</blockquote>
Howard later discusses the ability to see the infinite in the smallest detail as one of the benefits of having to slow down due to a chronic illness, and while this experience can soften the edges of the blow of having a bad day, it in no ways diminishes awareness that one's life plans have been altered - in some cases, irrevocably.<br />
<br />
These scenes are not about the science behind ME/CFS, yet they strike a personal chord for someone in my shoes and I suspect they stand out for others who have been on the same path. Some of us have been up to our eyeballs in research and controversy - just for a moment let us reflect on our humanity in facing a difficult situation.<br />
<br />
While all I can write about at this stage of the production is about <i>Canary In A Coal Mine </i>the trailer, I am hopeful that <i>Canary In A Coal Mine</i> the film will retain the same focus I saw in the trailer which put the patient experience front and center. I am hopeful there will be more discussion about the realities of ME/CFS and the scientific evidence supporting it as a physical, immunological condition and not something akin to the 19th century version of hysteria. And most of all, I am hopeful it is an experience Jennifer Brea will get through, intact, with adequate rest and a sense of major accomplishment on the other side of it.<br />
<br />
<span style="font-size: x-small;"><br /></span>
<span style="font-size: x-small;"><br /></span>
<span style="font-size: x-small;">[Edit Nov. 12: Updated to include info on director and producer roles by Jennifer Brea and Kiran Chitanvis</span><span style="font-size: x-small;">.]</span><br />
<br />
<br />
<div align="center">
<a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>The written content of this work by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small><br />
<span style="font-size: x-small;">All images subject to copyright and are used with permission of Canary Films.</span></div>
</div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com10tag:blogger.com,1999:blog-4073397588746430486.post-66932477923120077392013-11-04T06:50:00.002-10:002013-11-14T16:45:34.994-10:00Meta: Post of Upcoming Post Topics<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhsHm1HZ_wkWdlZFJHClwhzqTzTp6lJEmcrRb4vidg26yVW6lvfkl-6taFN56dfBNwmgFi_WT91Wx8znxxxh4ABZd1cCu4HFoq9IQelJq1_NXHyxBq1Gl-qfDeHjh_dgPIqmtZuLwnMn14Z/s1600/escherhands.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhsHm1HZ_wkWdlZFJHClwhzqTzTp6lJEmcrRb4vidg26yVW6lvfkl-6taFN56dfBNwmgFi_WT91Wx8znxxxh4ABZd1cCu4HFoq9IQelJq1_NXHyxBq1Gl-qfDeHjh_dgPIqmtZuLwnMn14Z/s1600/escherhands.jpg" /></a></div>
<br />
It's been a few weeks since my last post, and I would like to get back to blogging on a regular basis. How regular remains to be seen but certainly more than once every 6 months, which has been the largest gap between entries since I began this blog.<br />
<br />
I haven't blogged much this year for a variety of reasons. One reason is that there has been a lot going on in real life, so in my virtual life I took to tweeting more and writing at length less. Another is that I've been exhausted, and writing at length hasn't been coming as easily as it has other times.<br />
<br />
So I have taken a break, even if that meant having to put off writing a number of posts which I originally intended to do. I think it was necessary to take a step back and use my energy elsewhere for a while - including discussing tickborne diseases in other venues outside of this space.<br />
<br />
I'm hoping to make a reentry and post more often as it works for me. It's going to be an experiment to see how frequently I can manage it because I can't predict what the future is going to bring between happenings in my life and the status of my health, but I want to give it another try even though at times I feel like<a href="http://downwithtime.wordpress.com/2013/10/29/no-one-reads-your-blog-reflections-on-the-middling-bottom/"> no one reads this blog</a> (though clearly they do, as Blogger's stats indicate several thousand pageviews each month even if I don't post anything in a long time) and few people comment lately.<br />
<br />
My intent is to begin working through these topics, order to be determined:<br />
<br />
<br />
<ul>
<li>Thoughts on the trailer for the film, <i><a href="http://www.kickstarter.com/projects/959776320/canary-in-a-coal-mine">Canary In a Coal Mine</a></i>, and how the film may differ from <i><a href="http://underourskin.com/">Under Our Skin</a><br />
</i></li>
<br />
<li>Thoughts on the difference been disability and capability and where they intersect<br />
</li>
<br />
<li>The "it's all in your head" diagnosis: why it does everyone a disservice and can even be deadly<br />
</li>
<br />
<li>So about that 10-20% of Lyme disease patients with persisting symptoms after initial treatment...<br />
</li>
<br />
<li>Individual issue posts in response to the <a href="http://www.healthunit.org/hazards/documents/Advocacy_of_Lyme_Disease.pdf">anti-science letter Panel 1 items</a>:</li>
<ul>
<li>Sexual transmission of tickborne diseases: Is there evidence?</li>
<li>Whether or not Lyme disease <i>Borrelia</i> are restricted geographically</li>
<li>Subjective versus objective symptoms in Lyme disease</li>
<li>Lyme disease as a trigger for other conditions</li>
<li>How common tickborne coinfections are</li>
<li>The pathobiology of <i>Borrelia burgdorferi</i> (this may be 3 separate posts)</li>
<li>Serological testing and its value in diagnosis when there is no EM rash</li>
<li>The use of IgM testing </li>
<li>Serological sensitivity in Lyme disease based on gender</li>
<li>(Will <i>not</i> be addressing treatment topics on this panel at this time.)<br />
</li>
</ul>
<br />
<li>The who, what, where, how, and why of blogging here: Should the focus change?</li>
</ul>
<br />
So, I have a number of posts here I would like to write, and hopefully the energy and focus can be found to move forward.<br />
<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com6tag:blogger.com,1999:blog-4073397588746430486.post-2785043922684285662013-10-11T08:45:00.001-10:002013-10-14T04:59:40.677-10:0024 Hours Of Attachment Is An Estimate - Not a Safety BlanketBy now you may have heard the news that <a href="http://www.cdc.gov/media/releases/2013/p0819-lyme-disease.html">the CDC announced that there are over 300,000 estimated cases of Lyme disease in the United States each year</a>.<br />
<br />
For many people, this estimate came as a shock, but it really shouldn't be - the CDC itself has stated in the past that reported cases are a fraction of actual case numbers - especially in highly endemic areas - and researchers have also stated a case count of 30,000 was an underestimate.<br />
<br />
Many Lyme disease patients and advocacy groups felt vindicated by the announcement, as it confirmed their position that the number of people contracting Lyme disease was always much larger than official numbers which were originally reported. The below chart, for example, was created by Open Eye Pictures, which produced the controversial film on Lyme disease, <i>Under Our Skin</i>:<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrfkLBNqxixxn3flynRk3s4kZ-9-i2Lcjm-d9HolN_bw3nBPwfqgyI6Qan2zFq4QgOP9lnSdFVOtPj5bZ2mdBpO7eTC5kt6oaW3ttm6bY-k0D3Y01YHwHdUrlxvZFvHKzGLSHUgQqrzHSV/s1600/Lyme_Cases_1982-2009.jpeg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img alt="Lyme Disease in the US as of 2009 - 0ver 461,000 estimated cases" border="0" height="270" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhrfkLBNqxixxn3flynRk3s4kZ-9-i2Lcjm-d9HolN_bw3nBPwfqgyI6Qan2zFq4QgOP9lnSdFVOtPj5bZ2mdBpO7eTC5kt6oaW3ttm6bY-k0D3Y01YHwHdUrlxvZFvHKzGLSHUgQqrzHSV/s400/Lyme_Cases_1982-2009.jpeg" title="" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Click to zoom in for a closer look.</td></tr>
</tbody></table>
<br />
Open Eye Pictures created this chart back in 2011, based on data directly from the CDC but without direct access to the insurance study, patient survey, and other information the CDC used recently to adjust their new estimate to 300,000 annual cases of Lyme disease. As one can see, their estimate managed to come pretty close to the CDC's - if not potentially higher.<br />
<br />
With this announcement, news outlets, park rangers, and medical experts began warning the public once again to take proper precautions to prevent tick bites and to do body checks for ticks after being outdoors.<br />
<br />
Some are also informing people that if they don't spot a tick right away, not to worry - if a tick is removed properly within 24 hours, it is highly unlikely to transmit any tickborne disease.<br />
<br />
While there is truth in that statement, unfortunately it isn't exactly accurate and doesn't cover all kinds of ticks and any tickborne infections they might be carrying.<br />
<br />
This chart shows only a small fraction of tickborne infections currently known to be pathogenic to people along with their transmission times (and in some cases, typical attachment times):<br />
<br />
<b>Sample of Well-known and Newly Emerging Tickborne Diseases in North America and Europe and Their Estimated Transmission Times</b><br />
<br />
<table border="1" cellpadding="1" cellspacing="4"><tbody>
<tr><td><div style="text-align: center;">
<b>Tickborne Infection</b></div>
</td><td><div style="text-align: center;">
<b>Pathogen</b></div>
</td><td><div style="text-align: center;">
<b>Tick Species</b></div>
</td><td><div style="text-align: center;">
<b>Location</b></div>
</td><td><div style="text-align: center;">
<b>Estimated Transmission Time </b></div>
<div style="text-align: center;">
<b>Upon Attachment</b></div>
</td></tr>
<tr><td rowspan="4">Lyme disease Borreliosis</td><td><i>Borrelia burgdorferi sensu strictu</i></td><td><i>Ixodes scapularis, </i><br />
<i>Ixodes pacificus</i></td><td>North America</td><td>36-48 hrs;<br />
24 hours or more;<br />
potentially less </td></tr>
<tr><td><i>Borrelia burgdorferi </i></td><td><i>Ixodes ricinus</i></td><td>Europe</td><td>Less than 24 hours</td></tr>
<tr><td><i>Borrelia afzelii</i></td><td><i>Ixodes ricinus</i></td><td>Europe</td><td>Less than 24 hours</td></tr>
<tr><td><i>Borrelia garinii</i></td><td><i>Ixodes ricinus</i></td><td>Europe</td><td>Less than 24 hours</td></tr>
<tr><td rowspan="4">Tickborne<br />
Relapsing Fever</td><td rowspan="2"><i>Borrelia miyamotoi</i></td><td><i>Ixodes scapularis, Ixodes pacificus</i></td><td>North America</td><td>unknown</td></tr>
<tr><td><i>Ixodes ricinus</i></td><td>Europe</td><td>unknown</td></tr>
<tr><td><i>Borrelia turicatae</i></td><td><i>Ornithodoros turciata</i></td><td>North America</td><td>30 seconds with a total tick attachment time 15-90 minutes</td></tr>
<tr><td><i>Borrelia hermsii</i></td><td><i>Ornithodoros hermsii</i></td><td>North America</td><td>30 seconds with a total tick attachment time 15-90 minutes </td></tr>
<tr><td>Human Monocytic Ehrlichiosis</td><td><i>Ehrlichia chaffeensis</i></td><td><i>Amblyomma americanum, </i><i>Ixodes pacificus,</i><br />
<i>possibly Dermacentor variabilis </i></td><td>North America</td><td>12 to 24 hours </td></tr>
<tr><td>Human Ewingii Ehrlichiosis</td><td><i>Ehrlichia ewingii</i></td><td><i>Amblyomma americanum</i></td><td>North America</td><td>suspected 12 to 24 hours</td></tr>
<tr><td>Anaplasmosis<br />
(formerly HGE)</td><td><i>Anaplasma phagocytophilum </i>(formerly <i>Ehrlichia phagocytophilum</i>)</td><td><i>Ixodes scapularis, Ixodes pacificus, Dermacentor variabilis</i></td><td>North America</td><td>12 to 24 hours</td></tr>
<tr><td rowspan="3">Babesiosis</td><td><i>Babesia duncani</i></td><td><i>Ixodes pacificus</i></td><td>North America</td><td>24 to 36 hours</td></tr>
<tr><td><i>Babesia divergens</i></td><td><i>Ixodes ricinus</i></td><td>Europe</td><td>24 to 36 hours</td></tr>
<tr><td><i>Babesia microti</i></td><td><i>Ixodes scapularis</i></td><td>North America</td><td>24 to 36 hours</td></tr>
<tr><td>Rocky Mountain Spotted Fever</td><td><i>Rickettsia rickettsii</i></td><td><i>Dermacentor </i><i>andersoni, Dermacentor variabilis</i></td><td>North America</td><td>4 to 6 hours</td></tr>
<tr><td rowspan="2">Q Fever</td><td rowspan="2"><i>Coxiella burnetii</i></td><td><i>Dermacentor </i><br />
<i>andersoni (rare*)</i></td><td>North America</td><td>unknown - suspected fast as highly infectious</td></tr>
<tr><td><i>Ixodes ricinus, others</i> (rare*)</td><td>Europe</td><td>unknown - suspected fast as highly infectious</td></tr>
<tr><td>Powassan Virus or Powassan Encephalitis</td><td>Lineage 1 or 2 <i>Flavivirus</i></td><td><i>Ixodes cookei, Ixodes scapularis</i></td><td>North America</td><td>~15 minutes</td></tr>
<tr><td>Heartland Virus</td><td>Group V <i>Phlebovirus</i></td><td><i>Amblyomma americanum</i></td><td>North America</td><td>unknown</td></tr>
<tr><td>Tickborne Encephalitis (TBE)</td><td><i>Flaviviridae Flavivirus</i></td><td><i>Ixodes ricinus</i></td><td>Europe</td><td>Within minutes</td></tr>
</tbody></table>
<span style="font-size: x-small;"><br />
</span> <span style="font-size: x-small;">* Q fever is usually transmitted to people by exposure to contaminated raw dairy products, inhalation of aerosol fluids from pregnant animals, blood transfusions, and in utero. Tickborne infection with Q fever can happen - either through a tick bite or exposure to tick fecal matter - but along with cases of sexual transmission, this is rare compared to other methods.</span><br />
<span style="font-size: x-small;"><br />
</span> <b>There Are Unknowns In Tickborne Disease Transmission Times</b><br />
<br />
Note that in the above chart, some items are marked unknown. This is because - as far as could be determined, no lab animal model transmission studies for that specific organism have been completed.<br />
<br />
Incubation research may have been conducted - and this can inform us how long it takes before animals show signs and symptoms of being infected - but it does not inform us how long a tick must be attached before an infection can occur.<br />
<br />
For example, the chart above contains information on <i>Borrelia miyamotoi</i> as one causative agent of relapsing fever, but transmission time from a hard-bodied <i>Ixodid</i> tick is currently unknown.<br />
<br />
Until recently, it was thought relapsing fever spirochetes only colonize soft-bodied ticks and persist in their salivary glands, where they can transmit infection to blood quickly. But does the same situation apply to all hard-bodied ticks <i>Borrelia miyamotoi </i>colonizes? Is it the organism, or the tick's physiology, or both which determines how quickly <i>Borrelia miyamotoi</i> can be transmitted on average?<br />
<br />
Heartland Virus is another example where transmission time is unknown. Heartland Virus is so new, very little is known about it.<br />
<br />
<b>Transmission Time Varies Based On Pathogen And Tick Species</b><br />
<br />
Some pathogens are transmitted from a tick to its host in a few minutes - not hours - and so the 24 hour guideline does not apply to them. Relapsing fever organisms and tickborne viruses often fall into this category.<br />
<br />
Some pathogens are transmitted more rapidly from one tick than they are from another. In Europe, there is evidence Lyme disease spirochetes are transmitted to their host more rapidly due to <i>Ixodes ricinus</i>' physiology. So if you live in Europe or visit there and get bitten by <i>Ixodes ricinus</i>, if the tick was attached for under 24 hours you are more likely to contract Lyme disease than if you were bitten by an <i>Ixodes</i> tick in North America.<br />
<br />
Note, too, that transmission times can be periodically revised based on new data - and if anything, the trend has been demonstrating infection transmission could take place in less time than originally determined.<br />
<br />
<b>Overview Of Risk Factors In Tickborne Disease Transmission</b><br />
<span style="font-size: x-small;"><br />
</span> What your risk is for contracting particular tickborne infections can vary, depending on:<br />
<br />
<ul>
<li>The geographic location you were in when you were bitten; </li>
<li>The type of tick which has bitten you;</li>
<li>How recently the tick may have fed on another host;</li>
<li>How many infectious organisms it has in its salivary glands;</li>
<li>Whether or not the tick is carrying other pathogens;</li>
<li>How long the tick has been attached; </li>
<li>How the tick has been removed.</li>
</ul>
<br />
Those are risk factors involving the tick. But there are also host factors as well. Different hosts - including humans - have different immune systems and responses to specific tickborne strains of pathogens, and this, too, can determine the outcome of how or<i> even if</i> an infection will occur.<br />
<br />
<b>The Bottom Line</b><br />
<br />
<i>So what does the 24 hour guideline mean?</i> It means many tickborne infections are less likely to infect you if a tick has been removed within 24 hours, but it isn't an ironclad guarantee that you won't contract an infection.<br />
<br />
The best thing to do, of course, is to prevent ticks from getting on you in the first place. <i>Prevention is key.</i> No ticks means no tick bites, and not having to worry about what kind of tick has bitten you and what disease it might be carrying.<br />
<br />
Wear permethrin coated clothes and use DEET spray on exposed skin. Wear pants tucked into socks and long-sleeved shirts and stick to the middle of the trail when hiking.<br />
<br />
The second best thing to do is to do a regular tick check outdoors with a friend and not wait until you come home. Brush off any loose ticks, and <i>carefully</i> remove ticks with tweezers or narrow forceps as soon as you find them. Clean the tick bite area and place antibiotic lotion on it, then save the tick(s) you find in a well-sealed container for identification and testing at a tick testing lab.<br />
<br />
There is no 100% guarantee that even with early tick removal, you will avoid contracting a tickborne infection. But your odds of getting infected are greatly reduced the sooner you properly remove a tick. <br />
<br />
<br />
<b><u>References</u></b> <br />
<br />
Lyme disease. Centers for Disease Control. http://www.cdc.gov/lyme/transmission/index.html Downloaded September 28, 2013.<br />
Lyme disease. Centers for Disease Control. http://www.cdc.gov/features/lymedisease/ Downloaded September 28, 2013.<br />
Piesman J, Mather TN, Sinsky RJ, et al. Duration of tick attachment and Borrelia burgdorferi transmission. J Clin Microbiol. 1987;25:557–8. <br />
Joseph Piesman, Andrias Hojgaard, Protective value of prophylactic antibiotic treatment of tick bite for Lyme disease prevention: An animal model, Ticks and Tick-borne Diseases, Volume 3, Issue 3, June 2012, Pages 193-196.<br />
Kahl O, Janetzki-Mittmann C, Gray JS, Jonas R, Stein J, et al. Risk of infection with Borrelia burgdorferi sensu lato for a host in relation to the duration of nymphal Ixodes ricinus feeding and the method of tick removal. Zentralbl Bakteriol 1998; 287: 41–52.<br />
Leuba-Garcia S, Kramer MD, Wallich R, Gern L. Characterization of Borrelia burgdorferi isolated from different organs of Ixodes ricinus ticks collected in nature. Zbl Bakt 1994; 280: 468–475.<br />
Crippa M, Rais O, Gern L Investigations on the mode and dynamics of transmission and infectivity of Borrelia burgdorferi sensu stricto and Borrelia afzelii in Ixodes ricinus ticks. Vector Borne Zoonotic Dis 2002; 2: 3–9.<br />
Hofhuis A, Herremans T, Notermans DW, Sprong H, Fonville M, et al. A Prospective Study among Patients Presenting at the General Practitioner with a Tick Bite or Erythema Migrans in the Netherlands. PLoS ONE 2013; 8(5): e64361.<br />
Franc Strle, Jeffrey A. Nelson, Eva Ruzic-Sabljic, Joze Cimperman, Vera Maraspin, Stanka Lotric-Furlan, Yu Cheng, Maria M. Picken, Gordon M. Trenholme, and Roger N. Picken. European Lyme Borreliosis: 231 Culture-Confirmed Cases Involving Patients with Erythema Migrans. Clin Infect Dis. 1996; 23 (1): 61-65.<br />
Davis GE. The endemic relapsing fevers. In: Hull TG, editor. Diseases transmitted from animals to man. Springfield (IL): Charles C Thomas; 1955. pp. 552–565. <br />
Dworkin MS, Schwan TG, Anderson DE, Jr, Borchardt SM. Tick-borne relapsing fever. Infect. Dis. Clin. North Am. 2008; 22:449–468, viii. <br />
Wisconsin Ticks and Tick-borne Diseases, Department of Entomology, University of Wisconsin-Madison <a href="http://labs.russell.wisc.edu/wisconsin-ticks/anaplasmosis/">http://labs.russell.wisc.edu/wisconsin-ticks/anaplasmosis/</a> Downloaded September 28, 2013.<br />
Kramer V L, Randolph M P, Hui L T, Irwin W E, Gutierrez A G, Vugia D J. Detection of the agents of human ehrlichioses in ixodid ticks from California. Am J Trop Med Hyg. 1999; 60:62–65.<br />
Piesman J., Hicks T. C., Sinsky R. J., Obiri G. Simultaneous transmission of Borrelia burgdorferi and Babesia microti by individual nymphal Ixodes dammini ticks. J. Clin. Microbiol. 1987; 25:2012–2013.<br />
Piesman J., Spielman A. Human babesiosis on Nantucket Island: prevalence of Babesia microti in ticks. Am. J. Trop. Med. Hyg. 1980; 29:742–746.<br />
Colville, J. L., and D. L. Berryhill. Rocky Mountain Spotted Fever, Handbook of Zoonoses, Mosby, Saint Louis, 2007, Pages 150-154.<br />
Ebel GD, Kramer LD. Short report: duration of tick attachment required for transmission of Powassan virus by deer ticks. AmJTrop Med Hyg. 2004; 6:268–271. <br />
Tickborne Encephalitis Centers for Disease Control & Prevention, 2009. <br />
Lindquist L, et al. Tick-borne encephalitis. Lancet. 2008; 371(9627):1861-71.<br />
<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a> <br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> </small><br />
<small> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons Attribution- </a></small><br />
<small><a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com13tag:blogger.com,1999:blog-4073397588746430486.post-18676741325144787782013-05-28T05:02:00.001-10:002013-08-17T19:41:36.116-10:00Persistence and Politics In Chronic Lyme Disease Research<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgcRQXBBfQocpAhqsHX2mR-1aXXygCq_AQ0YsjL_UD7k4FG7cip7nU7WkjIU_Rk4MTHfpy4ke9k6TNIuTkmXtzOa4V0LJfXc2LcpUEeCPVelmcZRGKrAPwssNrr3lxyCjqx-KU6Oi2RfQUD/s1600/Ixodesticks.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgcRQXBBfQocpAhqsHX2mR-1aXXygCq_AQ0YsjL_UD7k4FG7cip7nU7WkjIU_Rk4MTHfpy4ke9k6TNIuTkmXtzOa4V0LJfXc2LcpUEeCPVelmcZRGKrAPwssNrr3lxyCjqx-KU6Oi2RfQUD/s1600/Ixodesticks.jpg" /></a></div>
The story of the controversy over Lyme disease research and treatment guidelines seems so strange to me, I wouldn't have believed it if I hadn't gotten Lyme disease and ended up looking into it myself. <br />
<br />
I really thought when I first got bitten by a tick, got a rash, and got sick that it was going to be easy: take 2-3 weeks of antibiotics, get better, and go back to work. I had no idea at the time that one tick bite was going to change my life forever, and lead me down the path to learning about some controversy I previously knew nothing about. <br />
<br />
And as much as I've learned about the Lyme disease controversy in several years, <i>I still don't understand it.</i><br />
<br />
A recent set of articles published by <i>The Poughkeepsie Journal</i> about emails requested under the Freedom of Information (FOI) Act - emails exchanged between members of the Infectious Disease Society of America (IDSA), Centers for Disease Control (CDC), and others - inspired me to write, but these, too, do not help me make any more sense of the controversy.<br />
<br />
<b>A Primer On The Lyme Disease Controversy</b><br />
<br />
Before I proceed, for the uninitiated, here's the controversy in Lyme disease in a nutshell: <br />
<br />
Many patients and some doctors believe that three weeks of antibiotic treatment is not enough and some patients need longer term antibiotic treatment. They think the bacteria, Borrelia <i>burgdorferi</i>, which causes Lyme disease can survive the recommended amount of antibiotics advised in the IDSA's guidelines. The IDSA and other organizations think that the recommended amount of antibiotics is adequate in the vast majority of cases, and giving patients longer courses of antibiotics is generally regarded as a bad idea. They have stated that chronic Lyme disease* is most likely a post-Lyme syndrome which is autoimmune in nature. The IDSA Lyme disease panelists view these patients' doctors as acting irresponsibly and taking unfair advantage of people who are most likely sick with something other than Lyme disease. The doctors and their patients disagree vehemently with the IDSA panel's position. It has become very heated from there.<br />
<br />
<span style="font-size: x-small;">* It should be noted that the use of terms such as "chronic Lyme disease", "post-Lyme disease (syndrome)", and "post-treatment Lyme disease" are often used interchangeably and can cause confusion. "chronic Lyme disease" has been used in the past by American researchers to mean "chronic infection" and continues to be used by the NIAID in the US. In Europe, "chronic Lyme disease" is used to mean "late stage infection". In America today, "chronic Lyme disease" has been used by the Lyme disease patient community to mean a chronic infection with Lyme disease Borrelia bacteria - where the patient has received at least some antibiotic treatment yet continues to have symptoms. "Post-Lyme disease (syndrome)" has been used by the IDSA Lyme disease panel and its colleagues to denote a presumed autoimmune-like condition that patients can develop after having a bonafide case of Lyme disease. "Post-treatment Lyme disease" is used by some doctors and researchers as a form of "non-partisan" terminology that tries to side-step the infection/autoimmunty debate for causation. </span><span style="font-size: x-small;">(Sorry for any confusion. I'm confused too sometimes.)</span><br />
<br />
Now that you have the controversy in a nutshell, getting back to those articles on those emails requested under the FOI…<br />
<br />
<b>Journalist Publishes Lyme Disease Academic Physician Emails Released Under Freedom Of Information Act</b><br />
<br />
Mary Beth Pfeiffer, journalist working for <i>The Poughkeepsie Journal</i> wrote that <a href="http://ire.org/blog/transparency-watch/2013/05/20/foia-request-cdc-took-five-years-fulfill/">Kris Newby placed the FOI request for the emails five years ago and only recently had her request fulfilled</a>. Ms. Newby received copies of 3,000 individual emails under the FOI Act, of which several hundred were almost or entirely whited out, and shared them without condition with Ms. Pfeiffer for use in her articles.<br />
<br />
In the two articles I'm discussing, <a href="http://www.poughkeepsiejournal.com/interactive/article/20130517/WATCHDOG/305160051/INTERACTIVE-Lyme-ties-bind">"Interactive: Lyme, the ties that bind"</a> and its companion article, <a href="http://www.poughkeepsiejournal.com/article/20130519/NEWS01/305190007/VIDEO-Chronic-Lyme-disease-real-">"Chronic Lyme disease: Is it real?"</a> - and <a href="http://www.aldf.com/Poughkepse_Journal_Letter_to_the_Editor.pdf">one editorial letter</a> in response to them by Dr. Phil Baker, Executive Officer of the American Lyme Disease Foundation (ALDF) - different sides of the debate are touched upon.<br />
<br />
While Ms. Pfeiffer's position in her articles is that these FOI emails provide evidence of a possible unethical relationship between the Infectious Disease Society of America (IDSA) and their colleagues, the Centers for Disease Control (CDC), and the National Institute of Health (NIH), my focus here is not going to be on speculation about those relationships but instead are going to be about the need for clinical trials, how funding for Lyme disease is prioritized, patient relations, stagnation in science research, and questionable scientific conduct.<br />
<br />
I'm going to be taking a few excerpts from Ms. Pfeiffer's articles, the FOI emails to which they refer, and Dr. Baker's editorial letter, and making comments about them. <br />
<br />
But even more so? I'm going to be asking questions about them. Lots of questions - because to be frank, these emails and the content within them underscore the reasons why I don't want to get in the middle of the Lyme disease controversy and would much rather read about <i>Borrelia spp.</i> microbiology and immunology.<br />
<br />
To me, learning about the science directly from research makes sense. The Lyme disease controversy? <i>It doesn't make sense. </i>And over a number paragraphs, I'll explain why - and tie these articles, emails, and Dr. Baker's letter in with information from other sources.<br />
<br />
<b>ILADS Should Conduct Clinical Trials Based On Clear Patient Criteria And Their Own Treatment Approaches - But Can They?</b><br />
<br />
One notable passage from Dr. Phil Baker's editorial letter in response to Ms. Pfeiffer's articles got me to thinking:<br />
<br />
<blockquote class="tr_bq">
"I stated that the ILADS guidelines were deficient in that they: (a) did not provide a precise definition of “chronic Lyme disease” as a clinical entity, so that it could be distinguished from other non-infectious medical conditions (e.g., chronic fatigue syndrome, fibromyalgia, etc.) with similar symptoms; (b) failed to provide unequivocal clinical evidence to indicate that patients suspected of having “chronic Lyme disease” actually have a persistent borrelial infection that justifies antibiotic therapy; and (c) failed to demonstrate, from the results of published, peer-reviewed, randomized, placebo-controlled trials, that extended antibiotic therapy is not only beneficial but also safe for the treatment of “chronic Lyme disease”.</blockquote>
While I do not like the same things other patients have complained about which Dr. Baker said within the FOI released emails - including his referring to patients as "Lyme loonies" (and I think he owes patients an apology for that) - I think it's important to examine this editorial comment because it is worth further discussion. And it lead to me ask the question, "Why doesn't ILADS conduct clinical trials?"<br />
<br />
I asked, looking at the bigger picture and realized once I did, I could see where it would lead:<br />
<br />
If you ask the vast majority of doctors and scientists who have no ties to the IDSA, they will tell you they, too, would be more comfortable using treatments which have been shown to be effective in clinical trials - and would likely refrain from making most treatment decisions without such evidence.<br />
<br />
But beyond this, if ILADS conducted their own clinical trials based on patient criteria that they clearly define and treatment approaches they use in their own clinics, then once the evidence was provided which showed their effectiveness to others, many of the grievances patients have had about how chronic Lyme disease is handled would fade away:<br />
<ul>
<li>Primary care physicians across the country could treat chronic Lyme disease using ILADS' methods because they would be assured the methods are effective.<br /></li>
<li>Patients would not have to travel long distances to see a small number of doctors who specialize in treating chronic Lyme disease.<br /></li>
<li>Patients could see a doctor who is in-network under their insurance plan and have the cost of office visits covered or mostly covered.<br /></li>
<li>Insurance companies would stop denying coverage for specialized antibiotic treatments because they would have new data to rely on which supported new antibiotic regimens.</li>
</ul>
The situation as it currently stands is that patient advocacy organizations have petitioned individual states to pass laws which protect ILADS doctors (actually any doctor) from losing their license to practice solely because they administer long term antibiotics to patients with chronic Lyme disease. This legislation, which has been hard won by the efforts of many advocates and activists, hasn't changed the playing field in terms of increasing patient access to long term antibiotic treatment if that was one of the advocates' goals. In those states which pass such legislation, few new doctors prescribe antibiotics longer term.<br />
<br />
This reality means mostly only ILADS doctors continue to practice long term antibiotic treatment for chronic Lyme disease, which encourages an ongoing wave of criticism from various medical organizations, pundits in the media, and those skeptical about the existence of chronic Lyme disease as a persisting bacterial infection.<br />
<br />
The criticism is generally two-fold, and boils down to ILADS doctors taking unfair advantage of sick, vulnerable patients by operating concierge-style clinics where insurance is not accepted and concern about the growing problem of antibiotic resistance.<br />
<br />
Those who defend against this criticism - advocacy groups and patients - say ILADS doctors have saved their lives or at least changed them for the better.<br />
<br />
I would be one of them, too - my obvious EM rash went misdiagnosed as an allergic reaction to a tick bite and the doctor discarded the tick which had bitten me by tossing it in the trash without sending it to a lab. This when I had been bitten in a known endemic area by the state health department. The family physician I saw was practically useless, and I ended up at an ILADS doctor's office by referral after I had gotten so ill I could barely read and write, barely walk, and had trouble tracking conversations. (I'm better now, thankfully. Not normal - but better.)<br />
<br />
It was never my plan to end up in an ILADS doctor's office, any more than it was the plan for one woman I had talked to on Twitter to end up getting her best Lyme disease medical advice from a PhD at her local university because her own local MD had failed her. (Something is wrong when I tally up the number of times I've heard stories similar to ours. Why are family doctors missing what would be considered textbook presentations of Lyme disease?)<br />
<br />
This experience we share may be one reason Lyme disease advocacy groups and patients are not so proactive about pushing for clinical trials by the doctors who are helping them. If they've already had their diagnoses missed by family doctors who should be well informed about the symptoms and signs of early Lyme disease - and their infection went late stage - patients could have a lack of confidence in giving family and urgent care physicians the power to make medical decisions about chronic Lyme disease.<br />
<br />
Patients when asked will tell you they see ILADS doctors because they are already doing their best to take care of them and help them get better when nobody else would. And they support them, saying some members of ILADS have treated chronic Lyme disease since before ILADS even existed and have many years of clinical experience working with patients with tickborne diseases - diseases which other doctors have been either unable, unknowledgable about, or unwilling to treat. <br />
<br />
If ILADS seems to have a monopoly on treating chronic Lyme disease patients, how much of it is based on how poorly other doctors respond to patients with early cases of Lyme disease - such as my own case? How much of it is based on ILADS doctors developing a reputation for their treatment based on seeing patients who mostly have suffered from tickborne diseases - therefore having specialization in their practices? How much of it - critics have inquired - is because ILADS wants to hoard the care of such patients all to themselves in order to make a tidy profit?<br />
<br />
One of ILADS' more vocal doctors, Dr. Daniel Cameron, indicated he isn't interested in ILADS having a monopoly in treating chronic Lyme disease. <a href="http://www.mcall.com/health/mc-health-chat-lyme-disease,0,2438908.htmlstory">He made this remark on a Morning Call chat debate back in 2011 [12:38 mark]</a>, when he and Dr. Lawrence Zemel of the IDSA (a guidelines co-author) took questions from the audience:<br />
<blockquote class="tr_bq">
"We need many more physicians to diagnose and treat chronic Lyme disease. We will have less chronic LD if they are recognized early. Finally, more physicians will offer more options for patient within HMO's."</blockquote>
Dr. Cameron's desire seems to closely reflect those of what many chronic Lyme disease patients would like to see: access to more doctors who know how to diagnose and treat their condition, earlier diagnosis, and access to treatment options within the HMO system.<br />
<br />
This hardly sounds like a doctor who wants to monopolize the treatment of patients so he can make a buck. But those who spend any amount of time watching the Lyme wars scroll across their screen know that soon enough, someone will say he only made such a statement because politically it sounded good - not because he meant it with sincerity.<br />
<br />
And this is one strong example of why, by the way, I've gotten tired of reading and talking about Lyme disease when it comes to its sociopolitical aspect:<i> Everything anyone says, no matter which side of the Lyme disease treatment debate you are on isn't to be trusted.</i> This is, after all, a Lyme war and there are whisper campaigns, there are rumors; there are truths and half-truths - and good luck sorting them all out along with who really said what from your armchair at home.<br />
<br />
But I digress.<br />
<br />
I think that if Dr. Cameron and his colleagues want to see more doctors diagnose and treat chronic Lyme disease the way he does, he is going to have to find a way to conduct clinical trials in order to provide HMOs with an incentive to change their approach on how they diagnose and treat chronic Lyme disease.<br />
<br />
An important issue, of course, is whether or not Dr. Cameron and his colleagues at ILADS would be in any position to conduct the kind of clinical trials they would like to have based on their own treatments.<br />
<br />
Over the years, I've heard a few Lyme disease researchers complain that certain kinds of Lyme disease projects get selected for grants, again and again, and few projects are novel and bring in new talent.<br />
<br />
This issue was briefly touched upon by Ms. Pfeiffer in her articles as well:<br />
<br />
Ms. Pfeiffer reported that one Lyme disease researcher said to her:<br />
<blockquote class="tr_bq">
"How many studies have we got on coronary disease and cholesterol in the last 30 years? Thousands. We’ve got five with Lyme disease.” <span style="font-size: x-small;">(Editor's note: The "five" refers to antibiotic treatment trials only - there is a lot of Lyme disease related research.)</span></blockquote>
The scientist did not “want to be identified with either side of the controversy,” and, like others, said it was difficult to obtain government research funding for scientists with alternate theories.<br />
<br />
Dr. Stephen Barthold, a Lyme disease researcher from UC Davis <a href="http://archives.republicans.foreignaffairs.house.gov/112/HHRG-112-FA16-WState-BartholdS-20120717.pdf">stated at a House subcommittee hearing last July</a>:<br />
<blockquote class="tr_bq">
"Because of firmly entrenched opinion within the medical scientific community, evidence of persisting <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1574-6976.2009.00200.x/full">viable but non-cultivable</a> spirochetes is slow to be accepted and research proposals submitted to NIH that feature persistence following treatment are likely to receive prejudicial peer review in the contentious environment of Lyme disease*. Negative comments by peer reviewers of grant applications in the current financially austere NIH climate result in unfundable scores, if they are scored at all (triaged). I have no personal stake in this issue any more, as I am retiring within a year. </blockquote>
<blockquote class="tr_bq">
In my opinion, for such important and controversial studies to go forward, NIH will need to publish a specific call for applications, known as a “Request for Applications” (RFA), that requests research on the biological significance of persisting spirochetes following antibiotic treatment.<br />
________________________________________<br />
<span style="font-size: x-small;">
* a major weakness cited by a peer reviewer in a recent unfunded R01 application:<br />
“The lay public that has so far denied the validity of scientific data will misunderstand the significance of…[persisting non-cultivable Borrelia burgdorferi]…and use it as additional evidence to support the idea of treatment-resistant Lyme disease.</span>”</blockquote>
My thoughts on that footnote on Dr. Barthold's submitted testimony is that if the lay public has a misunderstanding of the significance of persisting non-cultivable Borrelia burgdorferi and how it does or does not support the idea of treatment-resistant Lyme disease, then researchers and science journalists who report the significance of such findings need to improve how they communicate with the public about them.<br />
<br />
Another goal I think they should have is to communicate the science clearly while also giving the patient community reasonable hope and evidence that projects are in the pipeline which will help them based on such findings.<br />
<br />
Right now, neither seems to appear to be happening as often as it should - and further educational outreach and positive patient engagement is in order.<br />
<br />
Separately, Dr. Baker has <a href="http://lymedisease.org/news/lymepolicywonk/lymepolicywonk-was-this-important-lyme-study-hidden-for-12-years.html#comment-3897">exchanged comments with me on the issue of more antibiotic treatment trials last February on lymedisease.org</a>, and informed me that the NIH-NIAID will most likely never do any long-term antibiotic treatment studies for chronic Lyme disease again:<br />
<br />
<blockquote class="tr_bq">
"Since I have retired from the NIH, I don’t know what their plans are for future research on Lyme disease. But, I can tell you that about 90% of the research that NIH supports is driven by proposals submitted as investigator initiated grant applications — the RO1 grants. So, if anyone has any good ideas, they are always welcome to submit a grant application, although competition for grants is very keen and only about 25% of all applications submitted are funded. One has to be persistent as most of my colleagues are to make it in science. Although I am not opposed to conducting another clinical trial, the odds for such a proposal getting funded are rather slim, especially since NIH has already supported 4 trials indicating that extended antibiotic therapy is not beneficial. Obviously, I would like to see more work done on whether the “persistors” [sic] Bockenstedt and Barthold noted in mice are infective and can cause disease, as well as whether they can stimulate a local inflammatory response. But, I think we would be making a big mistake by not considering other possibilities as I’ve mentioned in a recent article."</blockquote>
He thought chronic Lyme disease studies should be conducted working from different perspectives (which I agree with in principle) but I have yet to witness any of such studies actually occurring which apply to treatment - nor are any listed on clinicaltrials.gov - and I check periodically.<br />
<br />
Given that the NIH-NIAID is now suffering under the burden of sequestration, cuts have been made to research - including in areas which were already struggling for funding. I have a difficult time seeing how anyone doing research on Lyme disease is going to meet their projected goals for the future - whether their research is about long term antibiotic treatment or immunological factors involved in chronic Lyme/post treatment Lyme disease. <br />
<br />
With this current state of affairs it's the patients who are going to suffer the most.<br />
<br />
<b>What Does The IDSA Lyme Disease Guidelines Panel Think Chronic Lyme Disease Is, Anyway?</b><br />
<br />
Here are a few quotes from the IDSA Lyme disease guidelines panel members/colleagues' FOI emails from 2007 Ms. Pfeiffer published, stating they don't really know what chronic Lyme disease is:<br />
<blockquote class="tr_bq">
"I believe that it (CLD) is primarily psychological (but there must be biochemical correlates) and I think it is a bit like post-traumatic stress disorder…One other post infectious syndrome that might be comparable is <a href="http://pandasnetwork.org/">PANDAS</a>." - Dr. Eugene Shapiro </blockquote>
<blockquote class="tr_bq">
"The functional somatic syndromes is an excellent reference. I don't think I would mention <a href="http://pandasnetwork.org/">PANDAS</a>." - Dr. Henry Feder </blockquote>
<blockquote class="tr_bq">
"I doubt very much that autoimmunity or molecular mimicry has anything to do with post-Lyme disease syndrome. It is most like chronic [fatigue syndrome]." - Dr. Allen Steere</blockquote>
None of them think chronic Lyme disease is caused by a persisting bacterial infection that survives 2-3 weeks of antibiotic treatment - at least not in these specific emails which Ms. Pfeiffer has made public. <br />
But neither are they in agreement about what exactly chronic Lyme disease is, either. One additional statement which has been made publicly by IDSA Lyme disease guidelines members was the possibility that post-Lyme disease syndrome is an autoimmune-like disorder.<br />
<br />
Six years have passed since the emails' authors shared their ideas of what chronic Lyme disease is or isn't. Has anything changed since then that we can find on record? For that matter - <i>has anything changed since 1982? </i><br />
<br />
Lyme disease's causative agent, Borrelia <i>burgdorferi</i>, was discovered in 1982 and it wasn't long after that that doctors began noticing patients didn't always get better after having one course of antibiotics. Or even two courses. Unlike other conditions which have been labeled by others as "being invented by the internet", the same cannot be said about chronic Lyme disease. Patients who continue to have symptoms after early or delayed antibiotic treatment have been around for a long time, and over 100 Lyme disease support groups were already in existence by 1992. <br />
<br />
One major advocacy group had <a href="http://www.cs.cmu.edu/afs/cs.cmu.edu/user/jake/mosaic/lymenet-l/9">an electronic newsletter distributed from Lehigh University</a> and no web sites; only 6,000 people knew this list existed - far fewer than the number of people who have heard of Lyme disease and chronic Lyme disease today. This was before Lyme disease cases greatly escalated in number (and by extension, more patients with persisting symptoms as well).<br />
<br />
If Lyme disease has been easy to diagnose and treat, why did we have over 100 Lyme disease support groups back in 1992? Good question. And it's a good question to ask what has happened since then, and why there are even more support groups today, multiple advocacy organizations, protests, rallies, pushes for legislation, and controversial films like <i>Under Our Skin</i> being produced.<br />
<br />
When I read a transcript of a Senate subcommittee hearing on Lyme disease held back in 1993 - that's twenty years ago - it's apparent <i>the same sort of issues doctors, patients, and researchers had back then are the same ones they have today</i> (Copies of original hearing transcripts with commentary here: <a href="http://campother.blogspot.com/2011/03/1993-senate-testimony-on-lyme-disease.html">part one</a> and <a href="http://campother.blogspot.com/2011/03/1993-senate-testimony-on-lyme-disease_21.html">part two</a> ).<br />
<br />
And when I see Ms. Pfeiffer write about the amount of NIH grant money that has been going to the same small group of researchers over and over, year after year, and they happen to be the same people (or their colleagues) who make statements about what chronic Lyme disease is or isn't, I have to wonder why they didn't put more money towards researching this chronic condition years ago? <br />
<br />
And if they did put some money towards it - why it has been so non-productive an enterprise from the patients' perspective?<br />
<br />
<span style="font-style: italic;">Why are we still stuck?</span><br />
<br />
One reason why I am invested in answering these questions is apparent and biased: I'm a patient. But the other reason I am invested is that I'm genuinely curious why there has been no obvious progress on my condition and the development of more treatment studies.<br />
<br />
The entire scene seems particularly illogical when you realize the one point of agreement IDSA Lyme disease guidelines panelists' share with most doctors in practice now - including even ILADS doctors: <br />
<blockquote class="tr_bq">
Lyme disease which is treated with antibiotics early leads to a positive outcome. In terms of helping people with this disease, those who get an erythema migrans rash (the bull's-eye) and flu-like illness are treated early and go on to feel better, return to work, and go back to school. They don't NEED any further help from a doctor. They're fine.</blockquote>
It seems to me the sticking point - and the issue which needs more attention - are those patients who are NOT fine, and do NOT go on to be fine. Shouldn't they be the ones who should be getting the lion's share of research, to try to understand why they are not doing well and their symptoms persist?<br />
<br />
When it came to patients enrolled in the Klempner clinical trial (a long term antibiotic clinical trial for chronic Lyme disease patients conducted over 10 years ago), researchers said <a href="http://www.nih.gov/news/pr/jun2001/niaid-12.htm">the condition could be equally disabling as congestive heart failure and osteoarthritis</a>. <br />
<br />
Knowing this, you would think the IDSA Lyme disease guidelines panelists would make it a priority to help such patients get better - or at the minimum, write guidelines which acknowledged the range of severity of their condition based on hard data and made actionable suggestions as to how to improve patients' quality of life. Instead, the 2006 guidelines state that the percentage of patients with this condition that suffer from pain is no higher than that found in the population at large and there is no suggested treatment advice.<br />
<br />
When the Klempner trial was discontinued in 2001, <a href="http://www.nih.gov/news/pr/jun2001/niaid-12.htm">Dr. Phil Baker said</a>:<br />
<blockquote class="tr_bq">
"The antibiotic treatment component is <i>only one piece</i> of NIAID's comprehensive clinical studies on chronic Lyme disease. These studies have yielded a considerable amount of new information. We intend to characterize the patients enrolled in the study as thoroughly as possible to learn more about the mechanisms involved in chronic Lyme disease," Dr. Baker adds. "The knowledge obtained from such studies should be of immense value in developing new, more promising approaches for treating this disease."</blockquote>
It's been twelve years since Dr. Baker made that statement. <i>Twelve.</i> Where are the "new, more promising approaches for treating this disease"? <br />
<br />
<b>Where Are The Immune-Mediated Treatment Studies For Patients Who Cannot Take More Antibiotics?</b><br />
<br />
While some patients have given ILADS high accolades for saving their lives and changing them for the better due to longer term antibiotic treatment, other patients have not been as successful following the same plan. Those who support the outcomes of clinical trials done to date on long term antibiotic use for chronic Lyme disease would say hearing this is not surprising - though many patients would argue that the outcomes of those trials are not the full picture.<br />
<br />
Regardless of whichever side of the debate you are on when it comes to long term antibiotic use, the truth is there are patients who either have not experienced much improvement on long term antibiotics or they could no longer take them due to side effects, allergies, or contracting C. <i>difficile</i>. These patients continue to experience symptoms of varying severity, and for them there must be other treatment options. So far, antimicrobial herbal tinctures are their first remedy to try, followed by increasingly ineffective and unproven treatments including amongst other things, Rife machines. <br />
<br />
Is this the best that can be done for them? <i>What about more evidence-based treatments?</i><br />
<br />
If the IDSA Lyme disease guidelines panel and their colleagues think they have more evidence to support patients' persisting symptoms being caused by an autoimmune-like condition rather than a chronic infection, then where has their involvement and dedication been when it comes to the patient subgroup mentioned above?<br />
<br />
Why hasn't the IDSA Lyme disease guidelines panel or their colleagues applied for grant money to do research on treatments which involve immune mediation or addressing autoimmune disease caused by Lyme disease?<br />
<br />
The irony in Lyme disease research now is that a Lyme disease advocacy group - the kind of group which is typically reported about by many in the media as pushing for legislation to protect ILADS doctors and force insurers to cover long term antibiotics - has invested grant money in the development of the first novel immunological treatment for chronic Lyme disease, <a href="http://campother.blogspot.com/2012/04/viral-genetics-vgv-l-candidate-for.html">VGV-L</a>. <a href="http://www.vglifesciences.com/development/lyme-disease.php">VGV-L is a targeted peptide therapy developed by VG Life Sciences, Inc</a>. which has already met pre-IND requirements of the FDA and is expected to enter clinical trial stage later this year.<br />
<br />
The development of VGV-L has been funded by the <a href="http://www.lymeresearchalliance.org/research_new_active_projects.html">Lyme Research Alliance</a>, a patient advocacy group - and not Dr. Baker and his colleagues at the IDSA. And yet, VGV-L addresses immune dysregulation in Lyme disease - research he should be able to support as someone who does not think chronic Lyme disease is caused by ongoing infection.<br />
<br />
Yet there has been not a peep, not a press release, not one scientific article or review from Dr. Baker and his colleagues at the ALDF or the IDSA about VGV-L and how based on the scientific understanding of chronic Lyme disease to date, it might or might not work.<br />
<br />
And if Dr. Baker and his colleagues think that chronic Lyme disease is similar to fibromyalgia and chronic fatigue syndrome then why haven't they conducted clinical trials for chronic Lyme disease on low dose naltrexone - similar to <a href="http://snapldev.stanford.edu/research/completed-research-studies/">the successful Stanford University studies using low dose naltrexone for fibromyalgia</a>? Even now, some chronic Lyme disease patients are being prescribed low dose naltrexone off-label to help with managing pain - and some are reporting improvement.<br />
<br />
There has been no positive engagement between the IDSA Lyme disease guidelines panel and Lyme disease patients for years - even with just this subgroup of chronic Lyme disease patients who either cannot handle additional antibiotic treatment or for whom there is evidence their symptoms may actually be more immune-mediated. <br />
<br />
If I as a patient want to know more about post-treatment Lyme disease and how to treat it, and my doctor and I actually think my remaining symptoms are due to post-infection damage instead of persisting infection, there is no obvious resource for us to turn to.<br />
<br />
There simply isn't enough research being done by anyone that addresses this condition. We are driving blind, and making it up as we go based on trial and error and models of other neuroimmune and neurological conditions, and by talking to other doctors and patients who are navigating the same issues.<br />
<br />
<b>Why ILADS And The IDSA Lyme Disease Guidelines Panel Can't - Or Won't - Meet In The Middle?</b><br />
<br />
While I have wondered why the IDSA Lyme disease treatment panel dismisses the idea of persistent infection when it comes to Lyme disease - I've also wondered why a number of ILADS doctors and patients dismiss there being an element of immune dysregulation and autoimmune response where Lyme disease is concerned?<br />
<br />
And it seems no one has considered the possibility except for a few researchers - or it's at least not discussed online much - that infection and immune dysregulation in Lyme disease could occur concurrently.<br />
<br />
One possible combination treatment which could address both infection and immune regulation which could be used in clinical trials that both ILADS and the IDSA Lyme disease guidelines panel may want to consider is the use of IV ceftriaxone and <a href="http://en.wikipedia.org/wiki/Filgrastim">filgrastim</a> to treat Lyme disease patients who have persisting symptoms past initial treatment. <br />
<br />
Dr. Isabel Diterich has <a href="http://kops.ub.uni-konstanz.de/bitstream/handle/urn:nbn:de:bsz:352-opus-9814/Diss_formated_ENDVERSION.pdf?sequence=1">used both filgrastim and ceftriaxone to treat a stubborn case of late stage Lyme disease, and the patient completely recovered and reported no relapsing symptoms in the following eight years</a>. Additional studies were completed in animal models which showed some promise.<br />
<br />
Such studies would involve a shorter total antibiotic treatment than any of the clinical trials for chronic Lyme disease conducted to date at the NIAID. Yet no one that I know of outside of Dr. Diterich and <a href="http://www.icepha.de/profile/managing-director-prof-dr-albrecht-wendel.html">Dr. Albrecht Wendel</a> has commented on this potential treatment - and neither ILADS nor the IDSA Lyme disease panel has mentioned it to my knowledge.<br />
<br />
It's not as if getting more testing of this combination hasn't been tried before, either. Like those in the chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) community, with patients and doctors who lobbied hard <a href="http://www.biomedcentral.com/1471-2377/9/28">to conduct clinical trials on rituximab for CFS/ME patients</a>, Dr. Wendel tried to encourage Amgen to get involved in clinical trials to treat chronic Lyme disease patients using filgrastim alongside ceftriaxone. Amgen responded that they were not interested because the market for the drug was too small.<br />
<br />
As time goes on, I wonder with each passing year that Lyme disease cases rise if this will continue to be the case. I don't know.<br />
<br />
Both the IDSA Lyme disease guidelines panel and ILADS could have investigated this treatment approach, combining both antibiotics and immune mediation to see if it improved treatment outcomes for a higher percentage of patients. Instead, we're left with this ongoing debate between the ILADS promotion of long term antibiotic treatment because chronic Lyme disease is caused by infection versus the IDSA guidelines which have no advice for how to treat chronic Lyme/Post Lyme disease at all (and lots of verbiage on <a href="http://cid.oxfordjournals.org/content/43/9/1089/F8.expansion.html">how NOT to treat it)</a>.<br />
<br />
But even if this were a treatment trial which both ILADS and members of the IDSA Lyme disease guidelines panel could theoretically agree to, due to the history between members of both and contentious accusations shared in personal communications and in the media between advocacy organizations and anyone from the IDSA Lyme disease panel, this possibility looks slim. There is too much water under the bridge there.<br />
<br />
The most recent accusation against members of the IDSA Lyme disease guidelines panel comes from ILADS member Dr. Ken Liegner, one of the most experienced Lyme disease specialists who has been dealing with the controversy pretty much since it began. <a href="http://lymedisease.org/news/lyme_disease_views/leigner-nyc-lyme-rally.html">Dr. Liegner spoke to a crowd of chronic Lyme disease patients at a rally in New York City recently, accusing Dr. Dattwyler of scientific misconduct and withholding scientific information</a> that could prevent chronic disease and save lives:<br />
<br />
<blockquote class="tr_bq">
"In the year 2000, due to fortuitous circumstances, and unbeknownst to Dr. Dattwyler, I gained access to CDC-funded experimental methods in his research laboratory for more than 140 specimens of frozen cerebrospinal fluid on my patients.<br />
<br />
Whereas only 2% of specimens tested positive on standard spinal fluid tests, some 62 % of specimens tested positive on one or more of the four experimental assays used. Ironically, Vicki Logan’s CSF tested more than 7 times higher than the positive cut-off for detection of Outer surface protein C antigen, in the very laboratory of Empire Blue Cross & Blue Shield’s own expert consultant. </blockquote>
<blockquote class="tr_bq">
I asked Laboratory Supervisor, Priscilla Munoz, how they knew these methods were valid. She replied that the three collaborating research laboratories shared aliquots of samples and found excellent reproducibility between the three labs.The results of these CDC-funded studies on direct detection of OspA and OspC antigen and IgG and IgM borrelia-specific immune complexes in spinal fluid have never been published. </blockquote>
<blockquote class="tr_bq">
Why not? Did someone at CDC “deep six” the results of this research project? If so, who made this decision, and why? </blockquote>
<blockquote class="tr_bq">
I demand the “raw data” from these CDC-funded research studies, which have never seen the light of day, be made public immediately. </blockquote>
<blockquote class="tr_bq">
Thomas Frieden, as Director of CDC can ‘set the tone’ for the agency. I call on him, to ‘step up to the plate’ and fix the mess created by CDC. Dr. Frieden can ‘redeem’ the reputation of CDC, which is composed of fine physicians and scientists. Dissociate CDC from the disgraced IDSA Lyme disease guidelines. Otherwise, step down!"</blockquote>
In the Lyme wars, ILADS' critics would say Dr. Liegner is only making up stories in order to smear the reputations of those who challenge his livelihood as a Lyme doctor and stir up patients' ire toward activism. <br />
<br />
On the other hand - if he's correct, this is a very serious accusation which cannot go ignored and his anger is understandable. I think even if I were a casual outside observer and not a patient, with an accusation of this nature a full investigation is in order.<br />
<br />
Dr. Liegner's accusations are only one of many coming from ILADS and its advocates side towards those involved with the IDSA Lyme disease guidelines panel and the CDC. On both sides of the fence, accusations of conflicts of interest and scientific misconduct fly when it comes to the Lyme wars, with the most recent volley from the IDSA and its colleagues being <a href="http://www.healthunit.org/hazards/documents/Advocacy_of_Lyme_Disease.pdf">a highly critical editorial against ILADS and patient advocacy groups which was published in <i>The Lancet</i></a>.<br />
<br />
<b>The Crazy Mixed-Up World Of Persisting Spirochetes</b><br />
<br />
The IDSA Lyme disease guidelines panel and its colleagues at the American Lyme Disease Foundation (ALDF) state that chronic Lyme disease is not caused by persisting spirochetes - but like most patients, we have yet to hear the reason why they think persisting spirochetes are not causing patients' symptoms - at least in some subset of patients who are most likely to respond positively to additional antibiotics.<br />
<br />
Dr. Phil Baker (mentioned earlier as the author of the editorial letter to Ms. Pfeiffer of <i>The Poughkeepsie Journal</i> in this post) is executive director of the ALDF, and has strong ties to the IDSA Lyme disease guidelines panel and also to the NIAID since he was a program officer for the Lyme disease research division there in the past. <br />
<br />
While he doesn't support additional long-term antibiotic studies for chronic Lyme disease patients, he does support additional research on persister cells related to the research <a href="http://www.aldf.com/about.shtml">one member of the ALDF's scientific advisory board</a>, Dr. Stephen Barthold, has been conducting. He also promotes similar research to that which was completed by Dr. Bockenstedt, who has stated in her own research published last year that spirochetal antigens may get trapped in patients' joints and that may be what causes their persisting symptoms.<br />
<br />
<i>
What has Dr. Stephen Barthold said specifically about the nature of these persistent spirochetes in the past?</i><br />
<br />
From <a href="http://www.blogger.com/%E2%80%AAhttp://www.news.ucdavis.edu/search/news_detail.lasso?id=8584%E2%80%AC">an article published at the University of California at Davis in 2008</a>, where Dr. Barthold does his work:<br />
<blockquote class="tr_bq">
In the case of Lyme disease, the research findings do not suggest that continued use of antibiotics would succeed in getting rid of the lingering bacteria. </blockquote>
<blockquote class="tr_bq">
"I suspect that if the initial round of antibiotics hasn't eliminated them, it's not likely that a longer regimen of antibiotics would be any more successful," Barthold said. "It's more likely that a completely different class of antibiotics would be needed to accomplish that. This laboratory mouse model will allow us to address those possibilities."</blockquote>
If Dr. Barthold's suspicion is correct, the reason why clinical trials using long term antibiotics to treat chronic Lyme disease haven't been entirely effective may be because the antibiotics which were used were inappropriate for treating the Borrelia <i>burgdorferi</i> infection patients had in the first place. They may have had some positive effect for some subset of patients - but clearly they did not improve all patients' symptoms. <br />
<br />
In other words: Patients with chronic Lyme disease could have chronic infections, but treating them with the kind of antibiotics we have now won't help much. (They might, however, help some patients who have unidentified confections.)<br />
<br />
Dr. Barthold has confused many patients with another hypothesis: <a href="http://thedianerehmshow.org/shows/2012-02-29/diagnosing-and-treating-lyme-disease/transcript">It isn't infection with the spirochetes which is the primary problem, given their low numbers - rather that it's their ongoing presence which causes patients' persisting symptoms</a> [11:21:11 mark].<br />
<br />
Later on, in 2012, in his testimony at a federal House subcommittee hearing, Dr. Barthold stated:<br />
<blockquote class="tr_bq">
"Because persistence of non-cultivable spirochetes has been shown to occur following treatment with several different classes of antibiotics, the phenomenon is likely explained by antimicrobial tolerance (in contrast to antibiotic resistance or inadequate antibiotic treatment), in which all classes of antibiotics fail to completely eliminate non-dividing or slowly-dividing subpopulations of a broad array of bacteria and fungi [44,45].<br />
<br />
A possible explanation for these attenuated antibiotic-tolerant spirochetes may be because of plasmid loss, in which spirochetes have lost critical genetic material that favors robust growth. It has been known for decades that during in vitro passage, B. burgdorferi is highly prone to plasmid loss [46,47,48], and therefore plasmid loss is likely to also occur during the course of infection and increase over time. This may explain why treatment success in humans [3,8] and laboratory mice [2,38] appears to be most effective during early infection.<br />
<br />
Treatment success is inversely correlated with spirochete populations, since spirochete burdens in mouse (and human) tissues are highest during early infection [49], when antibiotics work best. The biological (in contrast to medical) significance of attenuated spirochetes is probably insignificant, in that robustly dividing-, genetically-intact spirochetes would be selectively favored upon tick acquisition, transmission, and survival in reservoir hosts. The medical significance of attenuated persisting spirochetes is another matter, and compels further investigation."</blockquote>
For direct reference to the above citations, see full text here: <br />
<a href="http://archives.republicans.foreignaffairs.house.gov/112/HHRG-112-FA16-WState-BartholdS-20120717.pdf">http://archives.republicans.foreignaffairs.house.gov/112/HHRG-112-FA16-WState-BartholdS-20120717.pdf</a><br />
<br />
(As an aside, it is interesting to note that Dr. Isabel Diterich also <a href="http://iai.asm.org/content/71/7/3979">published research in 2003 about antibiotic tolerance and immunosuppression involving Borrelia <i>burgdorferi</i></a>.)<br />
<br />
Dr. Bockenstedt doesn't discuss lingering spirochetes in her most recent research which applies here - <a href="http://www.jci.org/articles/view/58813">she discusses lingering antigens</a> which might contribute to patients' persisting symptoms - rather than persister cells.<br />
<br />
Dr. Barthold's and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0029914">Dr. Monica Embers' research involving persistent spirochetes</a> have intrigued the Lyme disease community, and it has called upon a world expert on persister cells, <a href="http://www.northeastern.edu/biology/people/faculty/kim-lewis/">Dr. Kim Lewis</a>, to help. <br />
<br />
Dr. Lewis, Distinguished Professor and Director, Antimicrobial Discovery Center, Northeastern University, Boston, Massachusetts. Dr. Lewis, in collaboration with Brian Fallon, MD, MPH, Director of the Lyme and Tick-Borne Diseases Research Center at Columbia University, has recently been <a href="http://www.prweb.com/releases/prweb2013/5/prweb10758340.htm">awarded a grant from the Lyme Research Alliance to do research which will focus on persisters</a> and introduce a new, rapid method for determining antibiotic sensitivity. A particular variant of persisters will be studied to better understand chronic infection and several experimental compounds will be tested in an effort to eradicate persister populations.<br />
<br />
Only further research can determine exactly what is happening with the pathology of chronic Lyme disease, but this research demonstrates that chronic Lyme disease is <i>not</i> easily dismissed with a vague diagnosis of something "a bit like post-traumatic stress disorder".<br />
<br />
Something else is going on which is affecting patients and science help can determine what's behind patients' symptoms even if it takes longer to fully understand the process.<br />
<br />
I applaud Dr. Barthold, Dr. Embers, Dr. Lewis, and Dr. Bockenstedt for further investigating the cause of chronic Lyme disease even amid dissent and scientific uncertainty. This is the only way to get real answers and stop the decades-long argument about who is right - and who is wrong.<br />
<br />
<b>End point?</b><br />
<br />
What is the future of chronic Lyme disease (or post treatment Lyme disease, if that's your preferred term)? I don't know. My current hope is that research which is done with integrity by scientists who have no conflicts of interest and care about patients will be the focus of the next decade and not the kind of petty, low-minded handling my condition has received both in the media and behind the scenes.<br />
<br />
If it is confirmed patients have an infection with persister cells, this will spur a whole new generation of treatment development to address persisters. If it is confirmed that retained antigens are a problem, then perhaps a different treatment will be designed for that. But as it stands, no one gets anywhere if we keep fighting. And it seems that patients, their families, and advocates have to hope that Lyme disease advocacy organizations can get together enough of the funding they need to offer grants for research to look into the problem rather than hope and pray that one of a handful of projects patients see as important gets funded by an NIH-NIAID under sequestration.<br />
<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjAGgEYmmPV407KSZUHIGDADHGtcE_T-K_zkiBGiMkT5-rJbNX9OxP1XZhc5N1CzLwkE4xrzpkawAH0em1wtDUeSnbSaV7hFKcgyI7C6VXzMGWjlHkhQHSnHF-w21SgWeVZlyVNz3oZxfFs/s1600/chronicquestion.jpeg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjAGgEYmmPV407KSZUHIGDADHGtcE_T-K_zkiBGiMkT5-rJbNX9OxP1XZhc5N1CzLwkE4xrzpkawAH0em1wtDUeSnbSaV7hFKcgyI7C6VXzMGWjlHkhQHSnHF-w21SgWeVZlyVNz3oZxfFs/s1600/chronicquestion.jpeg" /></a></div>
<br />
<div style="text-align: center;">
<span style="color: #999999; font-size: x-small;"><i>And people wonder why I want some more scotch...</i></span></div>
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small><br />
<small><br /></small>
<div style="text-align: left;">
<span style="font-size: x-small;">[Minor edit August 17, 2013 - Changed "fourteen years" to "twelve years" due to basic miscalculation error.]</span></div>
</div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com9tag:blogger.com,1999:blog-4073397588746430486.post-348731617670836952013-03-28T22:45:00.002-10:002013-03-28T22:45:23.201-10:002009 Final Report's Proposed Changes to IDSA Lyme Disease Guidelines<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiiQxjFu6LD3Y58meVkudNQa9iuRz1DPB4YPAspIqTh62hGe3sKxoGkAlVnpeTibQ-gm3TZnhwsQjMn1Aw3XN5F0qAYgIVRwNRWcCH6Ao6bPxEyk1hgEWj1R8QqqKZVrEIrguedEWx0EOzh/s1600/LDreviewpanel.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiiQxjFu6LD3Y58meVkudNQa9iuRz1DPB4YPAspIqTh62hGe3sKxoGkAlVnpeTibQ-gm3TZnhwsQjMn1Aw3XN5F0qAYgIVRwNRWcCH6Ao6bPxEyk1hgEWj1R8QqqKZVrEIrguedEWx0EOzh/s1600/LDreviewpanel.jpg" /></a></div>
I decided to take a break from discussing <i>The Lancet</i> antiscience letter and highlight a few items of note about proposed upcoming changes to the Infectious Disease Society of America's 2006 guidelines for the treatment of Lyme disease.<br />
<br />
Below is a list of some Lyme disease guideline items and recommendations for their revision taken from the <a href="http://www.idsociety.org/uploadedFiles/IDSA/Topics_of_Interest/Lyme_Disease/IDSALymeDiseaseFinalReport.pdf">2009 Final Report [.pdf]</a> that the Infectious Disease Society of America (IDSA) review panel wrote in response to Senator Blumenthal's antitrust investigation of the IDSA a few years ago.<br />
<br />
In this report, an independent review panel came to the conclusion that several changes needed to be made to the 2006 guidelines which would be included in the next version of the guidelines (which has <i>yet </i>to be published).<br />
<br />
I have provided a table from the original final report which outlines what the quality of the evidence is which supports each recommendation and the strength of each recommendation, based on the IDSA review panel's judgment.<br />
<br />
Following that table, I have provided a more detailed table which takes portions of the original 2006 Lyme disease diagnosis and treatment guidelines (which are more or less identical to the IDSA's 2000 treatment guidelines for Lyme disease with few exceptions) alongside the recommendations of the 2009 panel for the next version of the IDSA guidelines.<br />
<br />
I provide this information, along with a few questions for readers:<br />
<ol>
<li>The state of the science in Lyme disease has been moving along at a fair clip, and with more cases, more doctors are also getting a fair amount of clinical experience in treating Lyme disease (as well as other tickborne infections which are on the rise). <b>Why is it that now, in 2013, doctors are referring to guidelines based on data from 2000 and not recommendations made from 2009?</b> Is it the view of most doctors that they won't change their practice concerning Lyme disease until the IDSA's official guidelines are updated to include the changes in this 2009 report? <i>Why wait?<br />
<br />
</i></li>
<li>A number of proposed changes which the panel highlighted - such as measuring elevated liver enzymes and looking for signs of disseminated disease - are old news to patients who were treated by LLMDs during the past decade. <b>If LLMDs found these tests and diagnoses of value in helping patients earlier, couldn't their clinical experience have been incorporated into changes to guidelines sooner?</b> Or, is the case that because there are some LLMDs who are viewed with suspicion by mainstream medical professionals that all of their experience is of no value and cannot be validated - therefore their clinical approach would not be considered in new guidelines? Or, is it the case that LLMDs were doing something some infectious disease doctors already had been doing - but none of their clinical ideas were being integrated into new guidelines anyway? <i>What happened?<br />
<br />
</i></li>
<li>If one were to write out a table such as the one below with the strength of the recommendation and quality of evidence <i>for each of the ILADS'guidelines</i>, how would they compare to the revised guidelines with the included changes below?<br /><br />
</li>
</ol>
<hr height="1" />
<br />
<b>Table 1 - Infectious Diseases Society of America-US Public Health Service Grading System for ranking recommendations in clinical guidelines:</b><br />
<br />
Category, grade <br />
Strength of Recommendation:<br />
<br />
A - Strongly in favor<br />
B - Moderately in favor<br />
C - Optional<br />
D - Moderately against<br />
E - Strongly against<br />
<br />
Ranking of Quality of the Evidence:<br />
<br />
I - Evidence from >1 properly randomized, controlled <i>trial </i><br />
II - Evidence from >1 well-designed clinical <i>trial</i>, without randomization; from cohort or <i>case-controlled analytic studies</i> (preferably from >1 center); from <i>multiple time series studies</i>; or from dramatic results from <i>uncontrolled experiments </i><br />
III - Evidence from <i>opinions of respected authorities</i>, based on clinical <i>experience</i>, <i>descriptive studies</i>, or <i>reports</i> of expert committees<br />
<br />
Please take note of the category AND quality of the evidence ranking for each item below. In particular, note items marked with a Level III evidence ranking, and those of Level I ranking which were considered by panel members to be too high.<br />
<br />
<b>Table 2 - Old 2006 Guidelines Versus Recommended Changes For New Guidelines:</b><br />
<br />
<table border="1" cellpadding="10" cellspacing="3"><tbody>
<tr> <td><b>Item - Tick Bite Prophylaxis Judgment</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">(p. 6) A single dose of doxycycline may be offered to adult patients (200 mg dose) and to children >8 years of age (4 mg/kg up to a maximum dose of 200 mg)<b> (B-I) </b>when all of the following circumstances exist: (a) the attached tick can be reliably identified as an adult or nymphal I. <i>scapularis</i> tick that is estimated to have been attached for >36 h on the basis of the degree of engorgement of the tick with blood or of certainty about the time of exposure to the tick; (b) prophylaxis can be started within 72 h of the time that the tick was removed; (c) ecologic information indicates that the local rate of infection of these ticks with B. <i>burgdorferi </i>is >20%; and (d) doxycycline treatment is not contraindicated. The time limit of 72 h is suggested because of the absence of data on the efficacy of chemoprophylaxis for tick bites following tick removal after longer time intervals. Infection of >20% of ticks with B. burgdorferi generally occurs in parts of New England, in parts of the mid-Atlantic States, and in parts of Minnesota and Wisconsin, but not in most other locations in the United States. Whether use of antibiotic prophylaxis after a tick bite will reduce the incidence of HGA or babesiosis is unknown.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, <b>the Review Panel recommends the careful consideration of the grading for quality of evidence. One panel member thought the quality of evidence assigned to the recommendation (I) might be too high.</b></td></tr>
<tr> <td><b>Item - Doxycycline Use, Pregnant Women and Young Children</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">(p. 7) Doxycycline is <b>relatively contraindicated</b> in pregnant women and children less than 8 years old. The panel does not believe that amoxicillin should be substituted for doxycycline in persons for whom doxycycline prophylaxis is contraindicated because of the absence of data on an effective short-course regimen for prophylaxis, the likely need for a multiday regimen (and its associated adverse effects), the <b>excellent efficacy</b> of antibiotic treatment of Lyme disease if infection were to develop, and the extremely low risk that a person with a recognized bite will develop a serious complication of Lyme disease (<b>D-III</b>).</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel recommends <b>removal of the modifiers “relatively” contraindicated and “excellent” efficacy</b>.</td></tr>
<tr> <td><b>Item - Need For Doctors To Identify Tick & Engorgement Degree</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">(p. 7) To prescribe antibiotic prophylaxis selectively to prevent Lyme disease, health care practitioners in areas of endemicity should learn to identify I. <i>scapularis</i> ticks, including its stages (figure 1), and to differentiate ticks that are at least partially engorged with blood (figure 2A and 2B) <b>(A-III)</b>.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel recommends the careful consideration of the strength of recommendation. <b>Although a subjective measure, two Review Panel members thought that the strength assigned to this recommendation (A) might be too high.</b></td></tr>
<tr> <td><b>Item - Specifics On Monitoring Tickborne Coinfections & Disseminated Lyme Disease</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">(p. 8) Health care practitioners, particularly those in areas of endemicity, should become familiar with the clinical manifestations and recommended practices for diagnosing and treating Lyme disease, HGA, and babesiosis <b>(A-III)</b>.<br />
Persons who have removed attached ticks from themselves (including those who have received antibiotic prophylaxis) should be monitored closely for signs and symptoms of tickborne diseases for up to 30 days; in particular, they should be monitored for the development of an expanding skin lesion at the site of the tick bite (erythema migrans) that may suggest Lyme disease. Persons who develop a skin lesion or viral infection–like illness within 1 month after removing an attached tick should promptly seek medical attention to assess the possibility of having acquired a tickborne infection.</td><td style="vertical-align: top;">The Review Panel determined that this recommendation is medically/scientifically justified in light of all of the evidence and information provided (8-0). When the 2006 Lyme Guidelines are next updated, <b>the Review Panel recommends that consideration be given to specifying what constitutes “monitoring” and to providing anticipatory guidance for patients about possible manifestations of disseminated Lyme disease (e.g., arthritis, meningitis).</b></td></tr>
<tr> <td><b>Item - Treatment of Early Lyme Disease</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">(p. 9) Doxycycline (100 mg twice per day), amoxicillin (500 mg 3 times per day), or cefuroxime axetil (500 mg twice per day) for 14 days (range, 10–21 days for doxycycline and 14–21 days for amoxicillin or cefuroxime axetil) is recommended for the treatment of adult patients with early localized or early disseminated Lyme disease associated with erythema migrans, in the absence of specific neurologic manifestations (see Lyme meningitis, below) or advanced atrioventricular heart block <b>(A-I)</b>. <b>Ten days of therapy is sufficient if doxycycline is used; however, given the much shorter half-life of ß-lactam drugs, such as amoxicillin or cefuroxime axetil, it is unclear whether a 10-day course of these drugs would be as effective.</b> Therefore, for uniformity, a 14-day course of therapy is recommended for all of the first-line oral agents. Each of these antimicrobial agents has been shown to be <b>highly effective for the treatment </b><b>of erythema migrans</b> <b>and associated symptoms</b> in prospective studies. Doxycycline has the advantage of being effective for treatment of HGA (but not for babesiosis), which may occur simultaneously with early Lyme disease. Doxycycline is <b>relatively contraindicated</b> during pregnancy or lactation and in children less than 8 years of age.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel suggests<b> removal of the modifiers “highly” and “relatively.”</b></td></tr>
<tr> <td><b>Item - Choice of Treatment Modality</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">(p. 10) Because of a lack of biologic plausibility, lack of efficacy, absence of supporting data, <b>or</b> the potential for harm to the patient, the following are not recommended for treatment of patients with any manifestation of Lyme disease: first-generation cephalosporins, fluoroquinolones, carbapenems, vancomycin, metronidazole, tinidazole, amantadine, ketolides, isoniazid, trimethoprim- sulfamethoxazole, fluconazole, benzathine penicillin G, combinations of antimicrobials, pulsed- dosing (i.e., dosing on some days but not others), long-term antibiotic therapy, anti-Bartonella therapies, hyperbaric oxygen, ozone, fever therapy, intravenous immunoglobulin, cholestyramine, intravenous hydrogen peroxide, specific nutritional supplements, and others (see table 4) (<b>E-III)</b>.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, <b>the Review Panel suggests that “lack of biological plausibility, lack of efficacy” be replaced with “lack of demonstrated efficacy in controlled studies.”</b><br />
<br />
There are data demonstrating that the following are ineffective in the treatment of Lyme disease: first-generation cephalosporins, fluoroquinolones, carbapenems, vancomycin, metronidazole, tinidazole, ketolides, isoniazid, trimethoprim-sulfamethoxazole, fluconazole, benzathine penicillin G and combinations of antimicrobials. There are also data demonstrating that the following are <b>potentially harmful</b>: combinations of antimicrobials, pulsed-dosing (i.e., dosing on some days but not others), and long-term antibiotic therapy (e.g., more than 4 weeks). There is<br />
a paucity of data regarding the safety and effectiveness of the use of the following in the treatments for Lyme disease: hyperbaric oxygen, ozone, fever therapy, intravenous immunoglobulin, cholestyramine, intravenous hydrogen peroxide, and specific nutritional supplements, but <b>some</b> of these are likely to be harmful to the patient. Many of these examples, such as fever therapy and hydrogen peroxide, carry considerable risk of harm to the patient.</td></tr>
<tr> <td><b>Item - Diagnosing Tickborne Coinfections</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">Coinfection with B.<i> microti</i> or A. <i>phagocytophilum</i> or both may occur in patients with early Lyme disease (usually in patients with erythema migrans) in geographic areas where these pathogens are endemic. <b>Coinfection should be considered in patients who present with more- severe initial symptoms than are commonly observed with Lyme disease alone, especially in those who have high-grade fever for >48 h, despite receiving antibiotic therapy appropriate for Lyme disease, or who have unexplained leukopenia, thrombocytopenia, or anemia</b> <b>(A-III)</b>.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated,<b> the Review Panel recommends that abnormal hepatic transaminases (AST and ALT), lactate dehydrogenase, or bilirubin should also prompt evaluation for coinfection with B. <i>microti</i> or A.<i> phagocytophilum</i>.</b></td></tr>
<tr><td>(p. 11) Coinfection <b>might</b> also be considered in the situation in which there has been resolution of the erythema migrans skin lesion, but either no improvement or worsening of viral infection like symptoms <b>(B-III)</b>.</td><td style="vertical-align: top;"><b>When the 2006 Lyme Guidelines are next updated, the Review Panel recommends that consideration be given to changing “might” to “should.”</b></td></tr>
<tr> <td style="vertical-align: top;"><b>Item - Early Acute Neuroborreliosis Treatment </b></td><td><b>Recommendation</b></td></tr>
<tr><td>For adult patients with early Lyme disease and the acute neurologic manifestations of meningitis or radiculopathy, the use of ceftriaxone (2 g once per day intravenously for 14 days; range, 10–28 days) in early Lyme disease is recommended for adult patients with acute neurologic disease manifested by meningitis or radiculopathy <b>(B-I)</b>.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel recommends that consideration be given to the emerging data supporting the use of oral doxycyline as first line therapy in <i>selected patients</i> with neurologic manifestations of Lyme disease, such as those with hypersensitivity to beta lactam antibiotics.</td></tr>
<tr> <td><b>Item - Lyme Arthritis Without Neurological Disease</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">(p. 14) <b>Lyme arthritis</b> can usually be treated successfully with antimicrobial agents administered orally. Doxycycline (100 mg twice per day) <b>(B-I)</b>, amoxicillin (500 mg 3 times per day)<b> (B-I)</b>, or cefuroxime axetil (500 mg twice per day) <b>(B-III)</b> <b>for 28 days is recommended for adult patients without clinical evidence of neurologic disease.</b></td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel suggests that careful consideration be given to the current quality of evidence for amoxicillin. <b>Two Review Panel members thought that the quality of evidence assigned to doxycycline in this recommendation (I) might be too high</b> based on the available evidence.</td></tr>
<tr> <td><b>Item - Lyme Arthritis in Children</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">For children amoxicillin (50 mg/kg per day in 3 divided doses [maximum of 500 mg per dose]) <b>(B-I)</b>, cefuroxime axetil (30 mg/kg per day in 2 divided doses [maximum of 500 mg per dose]) (B-III), or, if the patient is >8 years of age, doxycycline (4 mg/kg per day in 2 divided doses [maximum of 100 mg per dose]) <b>(B-I)</b> is recommended. Oral antibiotics are easier to administer than intravenous antibiotics, are associated with fewer serious complications, and are considerably less expensive.<br />
However,<b> it is important to recognize that a small number of patients treated with oral agents have subsequently manifested overt neuroborreliosis, which may require intravenous therapy with a ß-lactam antibiotic</b> for successful resolution. Further controlled trials are needed to compare the safety and efficacy of oral versus intravenous therapy for Lyme arthritis.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel suggests that careful consideration be given to the current quality of evidence for amoxicillin. <b>Two Review Panel members thought that the quality of evidence assigned to this recommendation (I) might be too high based on the available evidence.</b></td></tr>
<tr> <td><b>Item - Diagnosis and Treatment of Neurological Disease</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;">Neurologic evaluation that may include lumbar puncture should be performed for patients in whom there is a clinical suspicion of neurologic involvement.<br />
Adult patients with arthritis and<b> objective</b> evidence of neurologic disease should receive: parenteral therapy with ceftriaxone <b>(A-II)</b> for 2-4 weeks. Cefotaxime or penicillin G administered parenterally is an acceptable alternative <b>(B-II)</b>.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel suggests consideration of specifying neurological issues that should be included/excluded. In addition,<b> the Review Panel suggests that “evidence of neurologic disease” be defined and that the adjective “objective” be deleted. </b><b>Clarifying the language to indicate that penicillin is inferior to cefotaxime in this clinical setting should also be considered when the guideline is next updated.</b></td></tr>
<tr><td style="vertical-align: top;">For children intravenous ceftriaxone or intravenous cefotaxime is recommended <b>(B-III)</b>; penicillin G administered intravenously is an alternative <b>(B-III)</b>.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel suggests that consideration be given to clarifying the language to indicate that penicillin is inferior to cefotaxime.</td></tr>
<tr><td style="vertical-align: top;">Adult patients with late neurologic disease affecting the central or peripheral nervous system should be treated with intravenous ceftriaxone for 2 to 4 weeks <b>(B-II)</b>.<br />
Cefotaxime or penicillin G administered intravenously is an alternative <b>(B-II)</b>. <b>Response to treatment is usually slow and may be incomplete. Re-treatment is not recommended unless relapse is shown by reliable objective measures.</b></td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel suggests that consideration be given to <b>adding a rating for strength of recommendation and level of evidence </b>to the last part of this recommendation. Consideration should also be given to providing examples of <b>reliable “objective measures.”</b></td></tr>
<tr> <td><b>Item - Post (-Treatment) Lyme Disease Syndrome</b></td><td><b>Recommendation</b></td></tr>
<tr><td style="vertical-align: top;"><br />
There is no well-accepted definition of post–Lyme disease syndrome. This has contributed to confusion and controversy and to a lack of firm data on its incidence, prevalence, and pathogenesis. In an attempt to provide a framework for future research on this subject and to reduce diagnostic ambiguity in study populations, a definition for post–Lyme disease syndrome is proposed in these guidelines. Whatever definition is eventually adopted, having once had <b>objective evidence</b> of B. burgdorferi infection must be a condition <i>sine qua non</i>. Furthermore, when laboratory testing is done to support the original diagnosis of Lyme disease, it is essential that it be performed by well-qualified and reputable laboratories that use recommended and appropriately validated testing methods and interpretive criteria. Unvalidated test methods (such as urine antigen tests or blood microscopy for Borrelia species) should not be used.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, the Review Panel suggests that the sentence that begins with “Whatever definition” be modified as follows: “Whatever definition is eventually adopted, having once had <b>objective clinical or laboratory evidence</b> of B. <i>burgdorferi </i>infection must be a condition <i>sine qua non</i> until a syndrome is formally defined.”</td> </tr>
<tr><td style="vertical-align: top;">To date, there is no convincing biologic evidence for the existence of symptomatic chronic B. <i>burgdorferi</i> infection among patients after receipt of recommended treatment regimens for Lyme disease.</td><td style="vertical-align: top;">When the 2006 Lyme Guidelines are next updated, <b>the Review Panel suggests that consideration be given to changing the phrase “no convincing biologic evidence” to something more specific, such as “Reports purporting to show the persistence of viable B. <i>burgdorferi </i>organisms after treatment with recommended regimens for Lyme disease have not been conclusive or corroborated by controlled studies.”</b> It has been proposed by some that there are hardy, drug-tolerant reservoirs of B. <i>burgdorferi</i>, including intracellular cystic forms. To date, this has not been shown to correlate with symptom persistence, nor has eradication of these forms been shown to correlate with symptom improvement.</td></tr>
<tr><td style="vertical-align: top;">Antibiotic therapy has not proven to be useful and is not recommended for patients with chronic (>6 months) subjective symptoms after recommended treatment regimens for Lyme disease <b>(E-I)</b>.</td><td style="vertical-align: top;">Panel determination summary: [...] in the case of Lyme disease, there has yet to be a single high quality clinical study that demonstrates comparable benefit to prolonging antibiotic therapy beyond one month. Therefore, <b>the Review Panel concluded that in the case of Lyme disease inherent risks of long-term antibiotic therapy were not justified by clinical benefit.</b><br />
<br />
[...] This conclusion was reached despite the large volume of case reports, case series, anecdotes, and patient testimonials reviewed that attested to perceived clinical improvement during antibiotic therapy. <br />
<br />
In the end, <b>such sources of evidence were felt to be fertile material for hypothesis- generation, but intrinsically incapable of hypothesis-testing. </b>By contrast, the prospective, randomized, controlled trials were formal hypothesis tests with strict recruitment criteria, prospectively defined outcome measures, and independent oversight.<br />
<br />
The Panel’s conclusions, which are consistent with those reached by guidelines panels from the IDSA as well as other societies, represent the state of medical science at the time of writing. <b>Only high-quality, prospective, controlled clinical trial data demonstrating both benefit and safety will be sufficient to change the current recommendations.</b></td></tr>
</tbody></table>
<br />
<br />
These proposed changes to some of the guidelines look like a case of updating them to reflect a reality those of us who have been ill already knew <i>years ago</i> based on testing and experience. In particular:<br />
<ul>
<li><b>It appears antibiotics used to treat Lyme disease in its early acute stage are not as effective as they were originally thought to be. </b></li>
<li><b>It appears that objective evidence of neurological involvement isn't the only reason to consider more intense antibiotic treatment - subjective neurological symptoms may be considered, too - provided they are well-characterized and defined.</b></li>
<li><b>Abnormal liver panels can be used to indicate the presence of coinfections.</b></li>
<li><b>Coinfections should always be considered when symptoms are severe and/or persist after initial antibiotic treatment for Lyme disease.</b></li>
<li><b>A single 200 mg dose of doxycycline as prophylaxis may not have the originally stated quality of evidence to back its use. </b></li>
</ul>
The IDSA has stated repeatedly that its current 2006 guidelines are evidence-based and are the best science has to offer. But it seems that the current guidelines are already outdated and have been, and do not reflect the state of the science nor clinical experience. They need to be updated, even within the most conservative perspective of how Lyme disease should be viewed and treated.<br />
<br />
It should be noted that in a number of cases, items with Level I evidence ratings were considered to be rated too high according to some members of the review panel.<br />
<br />
One thing I question is what the state of the science is and level of transparency on any recommendation which is labeled with an evidence level of "III". Those who wrote the guidelines used their expertise and unpublished information to determine that recommendation, with no external validation as to which data they relied upon and how they drew their conclusions about that recommendation based on that data. Level III recommendations are about opinion - not double blind, random controlled trials or observational studies on patients, which are a higher level of evidence.<br />
<br />
If anyone is an investigative reporter or researcher on Lyme disease - let alone a patient suffering from it - wouldn't you like to know more about how the experts came to their conclusions about such recommendations in the first place?<br />
<br />
While the debate rages on about chronic Lyme disease or Post-treatment Lyme Disease Syndrome, and the reviewers of these guidelines stated that there isn't evidence to support the use of long term antibiotics for patients with persisting symptoms - the reviewers do not offer any alternative treatment methods or recommendations, either. This is a long outstanding issue which strongly needs to be addressed.<br />
<br />
Either doctors who are using long term treatments and having success with their patients will be asked to produce evidence of that success outside of testimonials and case studies - or longer clinical trials using antibiotic regimens other than those already used in double blind clinical trials will need to be conducted.<br />
<br />
But even before one gets there, one has to ask this question: <i>How adequately have early stage Lyme disease cases been treated based on some of the above proposed changes to the guidelines? </i><br />
<i><br /></i>
And whether patients agree or not with the proposed changes to guideline recommendations, <i>why is anyone still waiting for these proposed changes to be included and published 3 YEARS after the 2009 report</i>?<br />
<br />
<i>Has any research been completed in the past 3 years which challenges the content in these guidelines?</i><br />
<br />
<div align="center">
<a href="http://www.idsociety.org/uploadedFiles/IDSA/Topics_of_Interest/Lyme_Disease/IDSALymeDiseaseFinalReport.pdf"></a><br />
<div class="separator" style="clear: both; text-align: center;">
<a href="http://www.idsociety.org/uploadedFiles/IDSA/Topics_of_Interest/Lyme_Disease/IDSALymeDiseaseFinalReport.pdf"></a><a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license" style="margin-left: 1em; margin-right: 1em;"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0px;" /></a></div>
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <br />
<a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons Attribution-NonCommercial-<br />
ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com2tag:blogger.com,1999:blog-4073397588746430486.post-755556816874035192013-03-26T00:05:00.000-10:002013-10-14T12:04:39.271-10:00Lyme disease pseudoscience and science: The antiscience letter<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjBTuCYLt9MGo98loeLAtPuyH9oPP-3-14x_mBQqEWF3Bxmr3d8lFk0owE_46I-_0tJ6sXAvphDVoh8-O2ml12jwSBGvtI-icjgXvuQPo462T58F1NRoIp8bP0xu6vlJNzSUIrq6eGJPgwp/s1600/Disappointment.gif" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="138" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjBTuCYLt9MGo98loeLAtPuyH9oPP-3-14x_mBQqEWF3Bxmr3d8lFk0owE_46I-_0tJ6sXAvphDVoh8-O2ml12jwSBGvtI-icjgXvuQPo462T58F1NRoIp8bP0xu6vlJNzSUIrq6eGJPgwp/s200/Disappointment.gif" width="200" /></a></div>
When I first read this Personal View paper, "<a href="http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(11)70034-2/abstract">Antiscience and ethical concerns associated with advocacy of Lyme disease</a>", a truncated version was making the rounds between patient mailing lists and online groups. I didn't yet know what the full version contained, and given that the truncated version was high on accusation and negative characterization of Lyme disease advocates and low on science and attribution, I could do nothing but rant at it.<br />
<br />
The full text was (and continues to be) officially behind a paywall, so most patients have not seen the full version unless they sought out alternative links, such as this <a href="http://www.healthunit.org/hazards/documents/Advocacy_of_Lyme_Disease.pdf">site's copy (pdf) posted by Dr. Susan O'Connell</a>, who was a co-author of the letter.<br />
<br />
One of my ongoing complaints about paywalls is that disabled and often financially challenged patients cannot afford to pay for 24 hours access to a paper about an issue which concerns them or is about their medical condition. Another issue is some patients have cognitive issues including short term memory problems, so even if they have the money, they need more than 24 hours access to a paper. But when it comes to this particular paper, I think most Lyme disease patients would give it a pass when they read it and realize that the authors' focus is on criticizing the organizations which have served and represented them for years. <br />
<br />
But I digress… Now that I've read the full text more than once, I'm left in a difficult position in how to respond to this paper as a patient who has persisting symptoms related to Lyme disease and is also skeptical.<br />
<br />
First of all, when you read the first paragraph and find that advocates and activists around your disease are being equated with AIDS denialists and antivaccine campaigners, you know you're off to a bad start. It angers me, because making such comparisons has a tendency to stereotype and label all Lyme disease advocates and activists as being analogous to these groups. <br />
<br />
Reading this made me feel defensive because I'm not an AIDS denialist and I support vaccine development - but I have ground to cover, and I am going to work on addressing the core content of this letter over a series of entries in <strike>the weeks</strike> future entries to come. I don't want to get too caught up in how certain comparisons or portrayals by the authors inflame me for now - I want to focus more on the substance.<br />
<br />
Many of the authors' criticisms and concerns were ones I was familiar with before - I just had never seen them concentrated all in one place until now, serving as a sort of beacon which informs the readers of <i>The Lancet </i>just how dreadful they think Lyme disease advocates and activists are. And a lot of the criticisms are not even about advocates and activists themselves.<br />
<br />
I'm not naive - a number of these issues are ones of which I as a patient am also critical. Bad things have happened in regards to how some medical professionals have treated Lyme disease patients. There are charlatans out there without medical degrees who have taken advantage of patients who are sick and vulnerable. There was a self-defined Lyme disease expert who killed a patient with an injection of bismuth. There was some man who pretended to be a doctor in California who <a href="http://blog.sfgate.com/crime/2011/06/14/doctors-prescription-eat-watermelon-in-a-hot-tub/">told a woman to sit in a hot tub with a watermelon to help her kidneys and misdiagnosed her mother with Lyme disease when she had MS</a>. There are some doctors and laboratories who may have conflicts of interest, and that's something which would require a full investigation if it is going on. I also know that some advocates and activists hold unsubstantiated beliefs about Lyme disease, too - and hope that by having this blog and referring to scientific source material that they will leave here more informed.<br />
<br />
So I'm not ignorant of the statements and criticisms the authors are emphasizing in their letter to The Lancet. <i>Not at all.</i> Some of the accusations and concerns voiced are based on situations which happened over twenty years ago, and notably, some of them deserve more than the quick soundbite the authors devoted to them because of the complex issues surrounding them.<br />
<br />
Soundbite is what we get, though, and the letter's intent isn't to persuade anyone things are going well. It is a charge against all the authors see as erroneous, flawed, and egregious, without subtleties; without digging deeper or giving readers a wide angle view.<br />
<br />
Reading this paper was difficult for me because it's a tired trope that's been pulled out before, again and again, in similar editorials and letters about chronic Lyme disease - in some cases from some of the same authors who wrote this one. I begin to think, <i>"Don't you guys have anything new to say?"</i><br />
<br />
And I'm not saying that to be dismissive of everything they wrote. It's just that it's no surprise when I've seen it before.<br />
<br />
I want to start with focusing on one aspect of the letter which criticized Lyme disease patient advocacy groups and activists for supporting pseudoscience and funding Lyme disease research and publications which fall into a parallel universe.<br />
<br />
The authors state on page one:<br />
<blockquote>
"As with other antiscience groups, some Lyme disease activists have created a parallel universe of pseudoscientific practitioners, research, publications, and meetings, arranged public protests and made accusations of corruption and conspiracy, used harassment and occasional death threats, and advocated legislative efforts to subvert evidence-based medicine and peer-reviewed science."</blockquote>
They also later state:<br />
<blockquote>
"Activists have organised their own scientific meetings, published their own journal, and funded research by LLMDs <span style="font-size: x-small;">58,59</span> All this activity has led to the creation of a cadre of doctors and activists with their own institutions, research, and conferences, a dedicated pool of patients, and unorthodox, alternative views of microbiology, immunology, and pharmacology."</blockquote>
(That's a pretty heavy indictment of these activists in the paragraph above - of which I'm certain only a very few engage in harassment or make threats. I don't endorse such behavior, and unfortunately in any group where there are empassioned activists, a few might step over the line that most of us won't.)<br />
<br />
Anyway, when you examine citations #58 and #59, the institutions and research grants the authors are mentioning are none other than Columbia University's Lyme and Tickborne Diseases Research Center and many grants which the Lyme Disease Association have given toward research. <br />
<br />
So it would seem that the authors think that Columbia University and the many researchers who were awarded grant money by the LDA are engaged in a parallel universe of pseudoscientific research, publications, and meetings? <br />
<br />
If so, <i>where are these pseudoscience-laiden research projects and publications?</i><br />
<ul>
<li>The Lyme Disease Association <a href="http://www.lymediseaseassociation.org/index.php?option=com_content&view=article&id=957:lda-awards-94-research-grants-since-1992&catid=186:research&Itemid=664">awarded 94 research grants to researchers in 14 states between 1992 and 2012</a>. A list of the grants can be found at the preceding link.<br />
<br />
</li>
<li>The above research led to the publication of 28 peer-reviewed papers in such journals as PLoSONE, Journal of Bacteriology, Genetics, Journal of Medical Entomology, Neurobiology of Disease, Gene, Emerging Infectious Diseases, Neurology, Infection and Immunity, JAMA, and others.<br />
<br />
</li>
<li>Research covers a wide range of Lyme disease related topics such as surveys of tick populations, comparative genomics of Borrelia <i>burgdorferi </i>plasmids, proteomic studies of cerebral spinal fluid of patients, investigation into Lyme disease and other tickborne diseases in the southern US, examination of the humoral response to Borrelia <i>burgdorferi</i>, and many other topics.<br />
<br />
</li>
<li>One project resulted in data used to apply for/receive $4.7 million NIH grant. Significant genome mapping initially funded by the LDA has shown that different strains of Borrelia have the ability to exchange genetic material among themselves.<br />
<br />
</li>
<li>The Lyme Disease Association's 2013 Conference in June <a href="http://www.lymediseaseassociation.org/index.php?option=com_content&view=article&id=1111:2013-lda-conference-agenda&catid=204:lda-conf-2013&Itemid=712"> will have a wide range of scientific researchers and a few doctors</a> who have experience treating Lyme disease giving presentations.<br />
<br />
</li>
<li>The biographies of those researchers and doctors who attended the Lyme Disease Association's 2012 Conference cover a wide range of tickborne disease related specialists, <a href="http://www.lymediseaseassociation.org/index.php?option=com_content&view=article&id=1056:2012-conference-speaker-biographies&catid=176:lda-conf-2012&Itemid=624">none of whom seemed to support pseudoscience.</a><br />
<br />
</li>
<li>The Lyme Disease Assocation and Lyme Research Alliance, in collaboration with the trustees of Columbia University helped established the <a href="http://www.columbia-lyme.org/">Lyme and Tickborne Diseases Research Center</a> at the university. Here's an overview from the LRA of what the Center does: <a href="http://www.lymeresearchalliance.org/research_new_columbia.html">Columbia Lyme disease research summary</a>.<br />
<br />
</li>
<li>The Lyme Research Alliance has a list of <a href="http://www.lymeresearchalliance.org/research_new_active_projects.html">currently active projects</a>: research on vertebrate reservoirs for tick-borne diseases in central US, identification of better diagnostic tests and better treatments for people with chronic persistent symptoms, strain virulence characterization from EM rashes, research on antineuronal antibodies in patients with persistent symptoms, exploration of potential biomarkers for persisting brain and nervous system symptoms, and investigation into autoimmunity treatment for chronic Lyme disease.<br />
<br />
</li>
<li>The Tickborne Disease Alliance and X Prize Foundation created a <a href="http://tbdalliance.org/press/118-announcing-x-prize">diagnostic X Prize global competition</a> to develop a fail-safe diagnostic tool for Lyme and tick-borne diseases.<br />
<br />
</li>
<li>Although there is no detailed list of projects provided, Lymedisease.org (formerly CALDA) states on its website that it "funds research projects at Stony Brook University (NY), the University of California at Davis, Stanford University, Johns Hopkins University, and the University of New Haven (CT)" and awards grants which "average between $15,000 and up to $50,000 for research projects up to 2 years."<br />
<br />
</li>
<li>Of historical significance, it's important to remember that the <a href="http://www.lyme.org/">Lyme Disease Foundation</a> (which is retired) originally supported development of an effective vaccine to prevent Lyme disease. It also supported a number of scientific conferences and projects, and partnered with the NIH's Rocky Mountain Labs, Tulane University, Texas A & M, Connecticut Agricultural Experiment Station, and many others.</li>
</ul>
I think that many patients, researchers, and members of the public will look at the above list and wonder just which of these researchers, organizations, and universities are supporting pseudoscience. The authors of <i>The Lancet</i> letter never spell out the particulars of what research has been done which comes from a parallel universe or which publications they consider to be pseudoscience. <br />
<br />
To add to the confusion I have about <i>The Lancet</i> antiscience letter, it also seems as if leaves open the potential for the authors' statements to shoot themselves in the foot. One of the researchers who is part of the IDSA and CDC-endorsed American Lyme Disease Foundation's (ALDF) science advisory board is also a member of a Lyme disease patient advocacy science advisory board. Dr. Robert S. Lane is a science advisor to both <a href="http://lymedisease.org/calda/directors.html">Lymedisease.org/CALDA's science advisory board</a> and the <a href="http://www.aldf.com/about.shtml">ALDF's science advisory board</a>. Dr. Stephen Barthold, who is often called upon by Lyme disease advocacy groups to discuss his research at conferences and in interviews and was a recipient of an LDA grant - is also a member of the ALDF's science advisory board and has served on ad hoc committees for the <a href="http://www.nrftd.org/">National Research Fund for Tick-Borne Diseases, Inc</a>.<br />
<br />
Any of a number of the researchers who have attended and given presentations at major Lyme disease advocacy organization conferences and events and were awarded grant money by Lyme disease advocacy organizations were at times affiliated with (either directly or indirectly) the authors of the antiscience letter in <i>The Lancet.</i> It would be strange if they found their research to come from a parallel universe - but if it did, at least part of it would be coming from their own.<br />
<br />
<u><b>Next installment on Lyme disease pseudoscience and science:</b></u> Discussing what constitutes the facts about Lyme disease in relation to the antiscience paper. Stay tuned...<br />
<br />
<span style="color: #999999; font-size: x-small;">Animated gif credit: <a href="http://commons.wikimedia.org/wiki/File:Disappointment.gif">GRPH3B18</a></span><br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com4tag:blogger.com,1999:blog-4073397588746430486.post-33092416316188651592013-03-17T22:14:00.001-10:002013-03-17T22:14:12.465-10:00Introduction: Lyme Disease Science And PseudoscienceWhen I began this blog, part of it was in response to <i>The Chicago Tribune</i>'s article, "Chronic Lyme: A dubious diagnosis". And while I did <a href="http://campother.blogspot.com/2010/12/chicago-tribune-chronic-lyme-dubious.html">a fair deconstruction of it</a> of my own, I think Paul Raeburn's original comment on the piece pretty much captured my opinion, too:<br />
<blockquote>
"Again and again, Callahan and Tsouderos give far more space to advocates making questionable claims than they do to experts who refute those claims, allowing the serious case for chronic Lyme disease, whatever that might be, to be buried under the dubious claims of advocates.<br />
<br />
The reporters go on and on impuguning patients and advocates without ever telling us whether there is a debate among legitimate experts about whether Lyme disease might assume a chronic form."</blockquote>
Raeburn's remarks did not go without criticism from others. Orac, of Respectful Insolence blog, pointed out that Raeburn was demonstrating that he supported false balance in reporting - that as long as the evidence against chronic Lyme disease outweighed the evidence in favor of it, there was no way to give it equal time. (More on this in a later post.)<br />
<br />
Since reading the <i>Tribune</i> article, I've read a number of articles, blogs, and editorials which questioned if not denied the existence of chronic Lyme disease, such as Hoofnagle's Denialism blog entry on <a href="http://scienceblogs.com/denialism/2008/05/20/fake-diseases-part-deuxchronic/">chronic Lyme being a fake disease</a>; White Coat Underground's <a href="http://whitecoatunderground.com/2009/05/27/lyin-about-lyme/">"Lyin about Lyme"</a> entry; The Lippard Blog's <a href="http://lippard.blogspot.com/2009/07/science-based-medicine-conference-part_15.html">"Science-based Medicine Conference, part 5: Chronic Lyme"</a>; <a href="http://www.nejm.org/doi/full/10.1056/NEJMra072023">"A Critical Appraisal of Chronic Lyme Disease"(NEJM)</a>; <a href="http://www.fasebj.org/content/24/11/4175.full">"Chronic Lyme disease: In defense of the scientific enterprise"(FASEBJ)</a>; "<a href="http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(11)70034-2/abstract">Antiscience and ethical concerns associated with advocacy of Lyme disease</a>"- and more.<br />
<br />
I read them because wanted to find out why people had doubts about chronic Lyme disease - and what, if anything, they would say about an alternative hypothesis for patients with persisting symptoms - namely post-Lyme disease syndrome, an autoimmune-like disorder triggered by Lyme disease.<br />
<br />
Far as I could see, most blog posters and many of their commenters made no mention of the scientific evidence that some patients who contract Lyme disease do in fact go on to experience persisting symptoms - while many editorials and journal publications at least acknowledged this fact.<br />
<br />
To quote Dr. Paul Lantos of Duke University, who wrote about chronic Lyme in "<a href="http://www.expert-reviews.com/doi/abs/10.1586/eri.11.63">Chronic Lyme disease: The controversies and the science</a>"(<a href="http://www.aldf.com/pdf/Lantos_Chronic_LD_2011.pdf">full text here</a>):<br />
<blockquote class="tr_bq">
"It is well-established that some patients experience prolonged somatic or neurocognitive symptoms during convalescence from Lyme disease, and a subset suffer significant functional impairment. Whether this phenomenon occurs frequently or rarely, and whether it is caused by persistent infection with B. burgdorferi, lie at the heart of the often acrimonious controversy over what has been termed ‘chronic Lyme disease’."</blockquote>
<i>This is me.</i> I am part of "some patients". I had a tick bite, developed an erythema migrans or bull's eye rash, and a positive blood test for Lyme disease. I have a history of being significantly functionally impaired. I have taken antibiotics - and even took more than was advised under the IDSA's treatment guidelines. I have tried prescription pain medicine and other treatments for my symptoms. <br />
<br />
Yet I still suffer, and as a patient one of the problems I face is that a lot of negative media press, blogs, and articles not only deny chronic Lyme disease's existence but also neglect to mention that there <i>is</i> scientific evidence that some patients who contract Lyme disease develop prolonged symptoms after initial treatment. <br />
<br />
To give Orac on his Respectful Insolence post some credit, when <a href="http://scienceblogs.com/insolence/2010/12/20/the-chicago-tribune-chronic-lyme-disease/">he wrote about the dubious diagnosis article</a> in <i>The</i> <i>Chicago Tribune</i> he did say:<br />
<blockquote>
"Don’t get me wrong. Lyme disease is real. There does even appear to be a post-Lyme disease syndrome, which is seen in patients who had Lyme disease and now have chronic symptoms (such as fatigue, various pains, and difficulty concentrating) after having been treated. Indeed, this is even referred to as category 4 Lyme disease. What causes this syndrome is a mystery, and there is no doubt that there are patients out there with debilitating symptoms after being treated for Lyme disease, but current scientific and clinical evidence does not support the idea that these symptoms are due to a chronic ongoing infection or that prolonged courses of antibiotics do any good."</blockquote>
And a commenter on that post, Kyle, also said something which hit home for me:<br />
<blockquote>
"When it comes to the advocacy surrounding the disease, it can be difficult to separate those that are truly sick with tick-borne disease, and those that seek the diagnosis of Lyme disease to explain their symptoms. Unfortunately, for this reason, I believe the truly ill may be simply ignored.<br />
<br />
We also have to take in account that there are many other pathogens that can be transmitted from a tick that have symptoms that resemble that of Lyme disease, and it’s not uncommon for an infected individual to receive multiple infections at the same time."</blockquote>
These two at least acknowledge that yes, there are patients with tickborne diseases who suffer from them and also those who suffer with persisting symptoms after initial treatment - though unlike most patients and their advocates, they disagree that symptoms can arise from a chronic infection.<br />
<br />
But getting back to it: Let's say for the sake of argument here it's firmly established I'm an individual who became truly sick with a tickborne disease, took antibiotics, and continue to have symptoms since the fateful day I was bitten.<br />
<i><br />
</i> <i>What now?</i><br />
<br />
The person in my situation is faced with a dilemma, when it comes to knowing what to do once the symptoms acquired during infection do not go away - especially after treatment. Not after a week. Not after a few months. And not after years.<br />
<br />
Given my history of being a skeptic, I initially hoped that reading what other skeptics had written would be useful. I thought it would challenge me to think and inform me with facts about Lyme disease and other tickborne diseases I hadn't known before.<br />
<br />
Surely, I thought, they would have gotten deep into an explanation of Lyme disease's pathogenesis and explained the mechanisms behind my condition and provided evidence as to why chronic infection wasn't a viable cause for my symptoms. And I thought they would have educated me and others on not only Lyme disease and chronic Lyme disease - but on Post Lyme Disease Syndrome and how it occurs.<br />
<br />
This is not how things turned out, though. I've read pretty much all the skeptics' blog posts and critical editorials on chronic Lyme disease that I can get my hands on, thinking I could learn something from them - only to realize three things about them:<br />
<ol>
<li>They don't typically offer enough detailed weighing of the data to show how those who do not support the existence of chronic Lyme disease came to their conclusion.</li>
<li>Most do not even mention the concept of post-treatment or post Lyme disease syndrome; those that do, do so briefly and offer no advice on how to handle it.</li>
<li>They don't help patients in my situation with ideas on how to get better.</li>
</ol>
When it gets down to it, the main reason these skeptical venues lacked value for me was that they <i>contain no useful, actionable information for me as a patient</i>. There is no helpful advice given. There is sometimes a verbal note of sympathy (see above) but that's as far as it goes.<br />
<br />
And from a scientific perspective, there has been little actual discussion from skeptics about which lines of research could be pursued next which could help someone in my shoes. There is little detailed discussion of the specifics of why precisely it is that the authors and commenters reject the idea that Borrelia <i>burgdorferi</i> - as well as any other Borrelia or tickborne pathogen - might persist in its host.<br />
<br />
The conversation never gets that far. I was hoping it would. But mostly, skeptical people have chosen not to engage me on this topic even though I myself have been a skeptic and question many things.<br />
<br />
There has been nothing to learn there, so I began my own line of inquiry and began doing my own research on my condition once my brain began working well enough to read again. And instead of skeptics, I have turned to other patients for support during my illness who commiserate with what I'm going through - patients who mostly support a model of chronic and persisting infection of Lyme disease - though a few also wonder if something immune-related or autoimmune might be contributing to their symptoms as well.<br />
<br />
I know when I talk to another patient that I will have someone in my corner who understands what I'm going through; it's one small consolation for dealing with a difficult condition. We can share ideas with each other about what kinds of treatment we've experienced and our outcomes, and sometimes there is a useful gem to be found there which when acted on will make our lives better.<br />
<br />
For those who are skeptical about having a chronic infection and/or truly think their situation is post-infectious, it should be noted that there are no "post Lyme disease syndrome" support groups. Googling "post Lyme disease support" will redirect you to any of a number of friendly and welcoming sites informing you about chronic Lyme disease. (To the skeptical, go ahead and open a new browser window and try it. I'll be waiting for you right here until you get back.)<br />
<br />
Given this, if you think dealing with chronic Lyme disease on its own is hard enough, when you think you have a newly acquired autoimmune condition that was triggered by Lyme disease it becomes even more challenging to find information and support. You might find your answers in a few isolated forum posts where patients bring up the issue of developing hypothyroidism or <a href="http://www.lymeneteurope.org/forum/viewtopic.php?f=7&t=4433&sid=afff74fabfe34ad6f194a0e1f0309dc7&start=100#p34230">a case</a> of <a href="http://www.nhlbi.nih.gov/health/health-topics/topics/aps/">antiphospholipid syndrome</a> after contracting Lyme disease.<br />
<br />
This situation is slowly changing, though, as more patients acknowledge that alongside infection, immune factors in general can play a role in their condition, and advocacy groups fund research on novel treatments for chronic Lyme disease such as <a href="http://campother.blogspot.com/2012/04/viral-genetics-vgv-l-candidate-for.html">VG LifeSciences VGV-L</a>.<br />
<br />
It seems to me that most patients give up on interacting with those who are skeptics of chronic Lyme disease and stick to mingling with those who do not question their condition in any way. It's understandable to withdraw and be self-protective when there is so much suffering - especially since all some skeptics seem to want to do is tell patients our symptoms are "all in our heads" without really knowing a damn thing about us. Since this is not the sort of feedback anyone needs when we are genuinely struggling with a chronic illness, those who deny the reality of our condition are usually avoided.<br />
<br />
However, I'm not fully avoidant. I'm more confrontational, and I've never been "most patients" because I've had one foot in the world of the skeptic and have continued to question the nature of my own condition. <i>Could what I have really be a chronic infection? Is it something else? Or is it a combination of things from which I suffer?</i> I periodically visit and revisit the writings of those who are skeptical of either the existence of chronic Lyme disease or its hypothetical cause to see if there is anything new to learn... <i>Something.</i> <i>Anything.</i><br />
<br />
In the end, I'm not always sure where to turn when coming from this space. I ask the questions many patients ask, such as, "What is the truth about Lyme disease?", "What exactly is the best thing for me to do as an individual, based on my condition?", and "Is there any external auditor who can look at all the information about Lyme disease that is out there and give me a straight answer about it?"<br />
<br />
I<i>n the end, are there any clear answers?</i><br />
<i><br /></i>
I offer all of the above as an introduction for what I plan to discuss in the coming days and weeks on this blog: The issue of skepticism around chronic Lyme disease, how the science and pseudoscience of Lyme disease has been discussed online and in journals, and a meta-discussion of how a patient approaches these discussions with the kinds of questions a patient like myself might be inclined to ask.<br />
<br />
This is no minor undertaking. As a patient, I am always drowning in information about tickborne diseases and trying to make sense of it while simultaneously having to understand and fend off criticism from individuals who and organizations which don't even know me and don't understand my condition. They treat me as some vague data point or offer up a two-dimensional stereotypical patient when I'm a real human being living a three-dimensional life full of daily struggles.<br />
<br />
Somehow, there has to be a way to address being in the situation in which I find myself. Somehow there has to be a way to break out of this box which has been imposed on me and add another dimension.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgs66p7XG1rUGs3vengZjZZgTlca44YPvoy2RXXPEF6oy0EODDwsYtkGiMGAxQAOr95gNVmw3bIO00QWci5mbI5qNY0PwN7rv5dR113KJFfF_xRp-zHjsNrE65OykZnT7aGoCNuBoXdPUsL/s1600/320px-Drowning_in_a_matelrialistic_world.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgs66p7XG1rUGs3vengZjZZgTlca44YPvoy2RXXPEF6oy0EODDwsYtkGiMGAxQAOr95gNVmw3bIO00QWci5mbI5qNY0PwN7rv5dR113KJFfF_xRp-zHjsNrE65OykZnT7aGoCNuBoXdPUsL/s1600/320px-Drowning_in_a_matelrialistic_world.jpg" /></a></div>
During my exploration of these issues, it's important to question and respond to the statements which are offered in editorial pieces such as "<a href="http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(11)70034-2/abstract">Antiscience and ethical concerns associated with advocacy of Lyme disease</a>" (<a href="http://www.healthunit.org/hazards/documents/Advocacy_of_Lyme_Disease.pdf">full text here</a>) because in a very real way, the statements within affect the way society not only looks at a condition such as chronic Lyme disease but also how it looks at and characterizes the patient population which is suffering from the condition.<br />
<br />
As a patient, I'd like to give a face to and a voice to a condition which - while hotly contested in terms of cause - is definitely real to me. And I intend to question and discuss the criticisms and skepticism offered in a logical and methodical way. Stay tuned to take that journey with me.<br />
<br />
<span style="color: #999999; font-size: x-small;">Photo credit: <a href="http://commons.wikimedia.org/wiki/User:Dorcha">Tim Houlihan</a></span><br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com2tag:blogger.com,1999:blog-4073397588746430486.post-83914926702669932552013-01-18T00:28:00.000-10:002013-01-19T11:39:27.169-10:00Questions on Borrelia Miyamotoi and Lyme Disease <div class="separator" style="clear: both; text-align: center;"><a href="http://upload.wikimedia.org/wikipedia/commons/thumb/2/25/Borrelia-theileri-cow.jpg/240px-Borrelia-theileri-cow.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="200" src="http://upload.wikimedia.org/wikipedia/commons/thumb/2/25/Borrelia-theileri-cow.jpg/240px-Borrelia-theileri-cow.jpg" width="200" /></a></div>I have been working diligently on a post about the pseudoscience and science of Lyme disease, in hopes of publishing it soon. However, given the recent news out of Yale University this week, I have decided to delay publication on that post because there is a lot to say about the research from Yale:<br />
<br />
<b>Yale research confirms Borrelia miyamotoi causing infection in US</b><br />
<br />
A tickborne disease caused by spirochetes more closely related to relapsing fever spirochetes than Lyme disease spirochetes was <a href="http://news.yale.edu/2013/01/16/so-new-it-doesn-t-have-name-yale-researchers-discover-tick-borne-infection">found in 18 patients in southern New England and New York</a>, according to research published in the <i>New England Journal of Medicine</i> <a href="http://www.nejm.org/doi/full/10.1056/NEJMc1215469">January 17</a>. <br />
<br />
The infection - caused by spirochetal bacteria known as Borrelia <i>miyamotoi</i> - was detected in 21 percent of 14 patients with unexplained summertime febrile illness, 3 percent of 273 patients with Lyme disease (or suspected Lyme disease), and 1 percent of 584 healthy people from areas endemic for Lyme disease.<br />
<br />
This study is one of a few which offer the indication that infection with Borrelia <i>miyamotoi</i> in North America is less common than its well-known more distantly related relative, Borrelia <i>burgdorferi</i>, the spirochete which causes Lyme disease.<br />
<br />
It's estimated 2-3,000 people* in the United States may be infected with Borrelia <i>miyamotoi</i> annually - but due to it being an emerging infectious disease which is difficult to diagnose, how common it is and will be in the future remains to be seen. <br />
<br />
In surveillance studies, anywhere from 1-16% of Ixodes scapularis ticks have been infected with Borrelia <i>miyamotoi</i>, depending on the region. This is about the same percentage range of Ixodes ticks which are infected with Borrelia <i>miyamotoi</i> in Russia and Western Europe.<br />
<br />
In North America, Ixodes ticks infected with Borrelia <i>miyamotoi</i> have been found in the northeastern US, midwest, west coast, and Canada.<br />
<br />
<b>How Borrelia miyamotoi infection differs from Lyme disease</b><br />
<br />
<b>Early symptoms</b><br />
<br />
Clinically speaking, an infection with B. <i>miyamotoi</i> has symptoms which overlap those of Lyme disease. They include fever, muscular aches and pains, joint aches, chills, sweats, vomiting (sometimes), headaches and fatigue, with a small portion also developing a rash such as with Lyme disease. Also, symptoms can be more severe than those found in Lyme disease and some patients may require treatment in a hospital.<br />
<br />
The two most striking differences between B. <i>miyamotoi</i> infections and Lyme disease?<br />
<br />
<b>Usually there isn't a rash - the exact opposite of Lyme disease. </b>One Russian study stated that more than 50% of patients documented with the disease did not have a characteristic rash. According to Dr. Peter Krause, only 10-15% of patients get a rash and it is usually smaller than those seen in Lyme disease.<br />
<br />
<b>Sometimes, people get cycling, spiking fevers.</b> Studies demonstrated that some patients had episodes of high spiking fevers which occurred days or one to two weeks apart. These cyclical fevers and the lack of a rash map closely to symptoms found in relapsing fever - a spirochetal disease which is usually transmitted by soft-bodied ticks.<br />
<br />
Here is an example of two patterns of fever and symptoms found in <a href="http://wwwnc.cdc.gov/eid/pdfs/10-1474-ahead_of_print.pdf">patients studied in Russia</a> [pdf]:<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="http://wwwnc.cdc.gov/eid/images/10-1474-F2.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="320" src="http://wwwnc.cdc.gov/eid/images/10-1474-F2.jpg" width="237" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Graph From: Humans Infected with Relapsing Fever<br />
Spirochete Borrelia miyamotoi, Russia<br />
<i>Emerg Infect Dis.</i> 2011;17:1816-1823 </td></tr>
</tbody></table><div class="separator" style="clear: both; text-align: center;"></div>Note that two patients' patterns of fevers and symptoms differed, but a spiking fever with periods of normal temperature between fevers is common in relapsing fever. (These two patterns are not representative of all patients - other patients may have their own variation on how the disease process unfolds.)<br />
<br />
<b>Later stages of infection</b><br />
<br />
Not much is known about later stages of infection with B. <i>miyamotoi</i>. This is because its study in human and animal hosts is relatively new, having been discovered only in 1995 in Japan.<br />
<br />
However, one could potentially extrapolate how B. <i>miyamotoi</i> will behave after initial infection by looking at research on its genetically closest living relatives which are also relapsing fever spirochetes. <br />
<br />
Borrelia <i>miyamotoi</i>'s closest living relatives appear to be Borrelia <i>hermsii</i> and Borrelia <i>lonestari</i>. <br />
<br />
<div class="separator" style="clear: both; text-align: center;"><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320305/bin/04-0236-F.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="289" src="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320305/bin/04-0236-F.jpg" width="320" /></a><br />
Image from: Typing of Borrelia Relapsing Fever Group Strains.<br />
Emerg Infect Dis. 2004 September; 10(9): 1661–1664.<br />
doi: 10.3201/eid1009.040236 </br></div><br />
<b>Testing for the presence of Borrelia miyamotoi</b><br />
<br />
From both the patient's and the doctor's point of view, one troubling aspect of being infected with Borrelia <i>miyamotoi</i> is that even if the patient has a history of a tick bite and has symptoms which seem similar to those found in Lyme disease - a blood test for Lyme disease will be <i>negative</i>.<br />
<br />
This is because Borrelia <i>miyamotoi</i> is genetically distant enough from Borrelia <i>burgdorferi</i> that the antibodies produced in response to <i>miyamotoi</i> seldom cross react with those of Borrelia <i>burgdorferi</i>. <br />
<br />
So how do you test for the presence of Borrelia <i>miyamotoi</i>? <br />
<br />
If you're a microbiologist and do not have access to antibody testing, have an acutely ill patient in front of you with a current flare up of symptoms including spiking fever, a blood smear and dark field microscopy might yield a positive result for Borrelia <i>miyamotoi</i> - as it does for other relapsing fever spirochetes. <br />
<br />
But most family physicians will likely want to order a blood test using PCR and/or an antibody test specifically designed for relapsing fever in order to detect infection. <br />
<br />
In a study of 47 Russian patients found to have infections with Borrelia <i>miyamotoi</i>, presence of infection could be detected using an ELISA (EUROIMMUN AG, Lübeck, Germany) for major Borrelia burgdorferi <i>sensu latu</i> genospecies found in Europe - but it could not discriminate (sort) specific antibodies against any of these species. <br />
<br />
Given that ELISA tests for Borrelia other than Borrelia burgdorferi <i>sensu strictu</i> are hard to come by in the US and Canada, the detection of Borrelia <i>miyamotoi</i> using standard Lyme disease ELISA may not work in North America.<br />
<br />
Instead of a standard North American Lyme disease ELISA or EUROIMMUN AG, an ELISA or Western Blot for relapsing fever which contains <a href="http://www.wikigenes.org/e/gene/e/916832.html">GlpQ protein</a> - an antigen which is non-reactive to Borrelia <i>burgdorferi</i> antibody - can be used to detect infection with Borrelia <i>miyamotoi</i>.<br />
<br />
This information should serve as a cautionary tale for the doctor: <br />
<br />
If a patient has been in an environment where ticks are found and has Lyme disease-like symptoms or a summer flu, consider relapsing fever as a differential diagnosis - especially if the patient does not recover as they would from a flu and has a negative Lyme disease ELISA. <br />
<br />
Blood tests and PCR are most likely to yield a positive result when a sample is taken during a patient's spiking fever and the height of symptoms because that is when spirochetemia is peaking. With each relapse of infection, the number of spirochetes in the blood is reduced - thus making it less likely to obtain positive test results the later it is during the course of infection.<br />
<br />
<b>Treatment</b><br />
<br />
So far, all the research points to the same antibiotics being used for Lyme disease as being effective for treating relapsing fever, and this extends to infections with Borrelia <i>miyamotoi</i>. In addition to amoxicillin, tetracycline, and doxycycline, relapsing fever has also been treated with chloramphenicol with success. Intravenous ceftriaxone may be required for more severe illness.<br />
<br />
If a patient with Borrelia <i>miyamotoi</i> is treated with antibiotics and continues to suffer from high spiking fevers and other symptoms, retreatment may be needed with intravenous antibiotics. Co-infections such as babesiosis and ehrlichiosis should be investigated as they can produce similar symptoms.<br />
<br />
In a 2011 study on Russian patients treated for Borrelia <i>miyamotoi</i> infection, this was the treatment and outcome:<br />
<br />
<blockquote>Therapy consisted of ceftriaxone, 2 g intravenously every 24 hours for 2 weeks (42 patients) or doxycycline 100 mg orally every 12 hours for 2 weeks (2 patients). Two patients received no antimicrobial drug while hospitalized; 1 later received doxycycline at home, and the other was readmitted to the hospital for relapse and received ceftriaxone.</blockquote><br />
<b>Outcome</b><br />
<br />
Some relapsing fever strains can cause severe illness, and without treatment these strains have a high rate of case fatality. So far, B. <i>miyamotoi</i> lies along a spectrum of illness which appears to range from mild to moderate severity, but even so, infection should be treated with antibiotics immediately to avoid complications.<br />
<br />
The good news is that most people who are infected with relapsing fever and are treated promptly with antibiotics go on to recover. The same will probably apply to infection with B. <i>miyamotoi</i> based on research published to date - but the true picture remains uncertain until more patients are diagnosed, treated, and proper follow-up is completed.<br />
<br />
<b>Complications</b><br />
<br />
Are the complications found in Borrelia <i>miyamotoi</i> infections going to be the same as those found in Lyme disease? Given that it is genetically closer to relapsing fever spirochetes and more distant to Borrelia <i>burgdorferi</i>, one could speculate that it may have characteristics and complications common to relapsing fever - but without further research, it is unclear.<br />
<br />
The risk for infected untreated pregnant women to pass on infection to the fetus in utero with a negative outcome (e.g. miscarriage; defects) might be more likely than it is in Lyme disease. Infection of the central nervous system may also occur more rapidly than it typically does in Lyme disease. But this is speculative, due to being based on research where there is variability in severity and outcome across relapsing fever strains.<br />
<br />
<b>Facts and uncertainties</b><br />
<br />
It is known that in many cases, Borrelia <i>miyamotoi</i> - unlike Borrelia <i>burgdorferi</i> - is transmitted transovarially in deer ticks. This means the female tick infects her offspring, which produces infected larvae. These larvae will go on to molt and become infected nymphs. (Transovarial infection is rare to nonexistent in Borrelia <i>burgdorferi</i>.) <br />
<br />
It is also known that relapsing fever spirochetes in soft-bodied ticks reside in tissues throughout the tick - whereas Lyme disease spirochetes are only found in the midgut.<br />
<br />
Thus a significant question arises: What role does a relapsing fever spirochete play in relation to its hard-bodied tick host, and how soon can a tick transmit infection with Borrelia <i>miyamotoi</i> after attachment? This appears to be unknown. <br />
<br />
Other questions based on how other relapsing fever strains also present themselves: How neurotropic is Borrelia <i>miyamotoi</i>? Can it become a latent infection, as was discovered in other relapsing fever strains? How rapidly does it differentiate into different serotypes found in different tissues? <br />
<br />
The answers to these questions - and more - are also unknowns until this bacteria is studied more carefully. Similar questions may also arise in research on Borrelia <i>lonestari</i> in Amblyomma <i>americanum</i> ticks - another relapsing fever type spirochete found in a hard-bodied tick.<br />
<br />
* Jan 19, 2013 Edited to add: Dr. Peter Krause offered a more recent estimate of 3-4,000 cases of B. miyamotoi occur in US annually.<br />
<br />
<hr height="1"><br />
<u>Image Credit:</u> Photography by Alan R. Walker, of Borrelia <i>theileri</i> infecting the blood plasma of a cow. Giemsa stained. Borrelia <i>theileri</i> is closely related to both B. <i>lonestari</i> and B. <i>miyamotoi</i>, and causes bovine Borreliosis in cattle. Source: http://commons.wikimedia.org/wiki/File:Borrelia-theileri-cow.jpg<br />
<br />
<b><u>References</u></b><br />
<br />
Human Borrelia miyamotoi Infection in the United States<br />
N Engl J Med 2013; 368:291-293 January 17, 2013 DOI: 10.1056/NEJMc1215469 <a href="http://www.nejm.org/doi/full/10.1056/NEJMc1215469">http://www.nejm.org/doi/full/10.1056/NEJMc1215469</a><br />
<br />
Carl-Johan Fraenkel, Ulf Garpmo,Johan Berglund. Determination of Novel Borrelia Genospecies in Swedish Ixodes ricinus Ticks. J. Clin. Microbiol. September 2002 ; 40:9 3308-3312 doi:10.1128/JCM.40.9.3308-3312.2002 <a href="http://jcm.asm.org/content/40/9/3308.full">http://jcm.asm.org/content/40/9/3308.full</a><br />
<br />
Rebaudet, Stanislas, and Philippe Parola. Epidemiology of relapsing fever borreliosis in Europe. FEMS Immunology & Medical Microbiology 48.1 (2006): 11-15. <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1574-695X.2006.00104.x/full">http://onlinelibrary.wiley.com/doi/10.1111/j.1574-695X.2006.00104.x/full</a><br />
<br />
Sarah A Hamer, Graham J Hickling, Rich Keith, Jennifer L Sidge, Edward D Walker, and Jean I Tsao. Associations of passerine birds, rabbits, and ticks with Borrelia miyamotoi and Borrelia andersonii in Michigan, U.S.A. Parasit Vectors. 2012; 5: 231.<br />
Published online 2012 October 11. doi: 10.1186/1756-3305-5-231 <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497883/"> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497883/</a><br />
<br />
Scott, M. C., et al. High-Prevalence Borrelia miyamotoi Infection Among Wild Turkeys (Meleagris gallopavo) in Tennessee. Journal of medical entomology 47.6 (2010): 1238-1242. <a href="http://www.bioone.org/doi/abs/10.1603/ME10075">http://www.bioone.org/doi/abs/10.1603/ME10075</a><br />
<br />
Mun J, Eisen RJ, Eisen L, Lane RS. Detection of a Borrelia miyamotoi sensu lato relapsing-fever group spirochete from Ixodes pacificus in California.<br />
<a href="http://www.ncbi.nlm.nih.gov/pubmed/16506458">http://www.ncbi.nlm.nih.gov/pubmed/16506458</a><br />
<br />
Ogden, Nick H., et al. Investigation of genotypes of Borrelia burgdorferi in Ixodes scapularis ticks collected during surveillance in Canada. Applied and environmental microbiology 77.10 (2011): 3244-3254. <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3126474/"> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3126474/</a><br />
<br />
Fukunaga M, Takahashi Y, Tsuruta Y, et al. Genetic and phenotypic analysis of Borrelia miyamotoi sp. nov., isolated from the ixodid tick Ixodes persulcatus, the vector for Lyme disease in Japan. Int J Syst Bacteriol 1995;45:804-810 <br />
<a href="http://ijs.sgmjournals.org/content/45/4/804.full.pdf"> http://ijs.sgmjournals.org/content/45/4/804.full.pdf</a><br />
<br />
Jonas Bunikis, Jean Tsao, Ulf Garpmo, Johan Berglund, Durland Fish, Alan G. Barbour.<br />
Typing of Borrelia Relapsing Fever Group Strains. Emerg Infect Dis. 2004 September; 10(9): 1661–1664. doi: 10.3201/eid1009.040236 <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320305/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320305/</a><br />
<br />
Scoles, Glen A., et al. A relapsing fever group spirochete transmitted by Ixodes scapularis ticks. Vector Borne and Zoonotic Diseases 1.1 (2001): 21-34. <a href="http://online.liebertpub.com/doi/abs/10.1089/153036601750137624">http://online.liebertpub.com/doi/abs/10.1089/153036601750137624</a><br />
<br />
Tamar Halperina, Nadav Orrb, Regev Cohena, Tal Hasina, Nadav Davidovitchc, Eyal Klementa, Raid Kayoufa, Gad Banethd, Dani Cohenb, Miri Yavzoria. Detection of relapsing fever in human blood samples from Israel using PCR targeting the glycerophosphodiester phosphodiesterase (GlpQ) gene. Acta Tropica. Volume 98, Issue 2, May 2006, Pages 189–195 <a href="http://www.sciencedirect.com/science/article/pii/S0001706X0600074X">http://www.sciencedirect.com/science/article/pii/S0001706X0600074X</a><br />
<br />
Schwan TG, Schrumpf ME, Hinnebusch BJ, Anderson DE Jr, Konkel ME. GlpQ: an antigen for serological discrimination between relapsing fever and Lyme borreliosis. J Clin Microbiol 1996;34:2483-2492 <a href="http://jcm.asm.org/content/34/10/2483.full.pdf">http://jcm.asm.org/content/34/10/2483.full.pdf</a><br />
<br />
Karan' LS, Koliasnikova NM, Toporkova MG, Makhneva MA, Nadezhdina MV, Esaulkova AIu, Romanenko VV, Arumova EA, Platonov AE, Maleev VV. [Usage of real time polymerase chain reaction for diagnostics of different tick-borne infections]. [Article in Russian] Zh Mikrobiol Epidemiol Immunobiol. 2010 May-Jun;(3):72-7. <a href="http://www.ncbi.nlm.nih.gov/pubmed/20734723">http://www.ncbi.nlm.nih.gov/pubmed/20734723</a><br />
<br />
Alan G. Barbour, Jonas Bunikis, Bridgit Travinsky, Anne Gatewood Hoen, Maria A. Diuk-Wasser, Durland Fish, and Jean I. Tsao. Niche Partitioning of Borrelia burgdorferi and Borrelia miyamotoi in the Same Tick Vector and Mammalian Reservoir Species. Am J Trop Med Hyg. 2009 December; 81(6): 1120–1131. doi:10.4269/ajtmh.2009.09-0208 <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841027/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841027/</a><br />
<br />
Relapsing Fever. Columbia University Lyme and Tickborne Diseases Research Center. <a href="http://www.columbia-lyme.org/patients/tbd_relapsing.html"> http://www.columbia-lyme.org/patients/tbd_relapsing.html</a><br />
<br />
Researchers discover new tickborne infection. WTNH News 8. January 18, 2013 <a href="http://www.wtnh.com/dpp/news/health/researchers-discover-new-tick-borne-infection">http://www.wtnh.com/dpp/news/health/researchers-discover-new-tick-borne-infection</a><br />
<br />
<div align="center"><!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com10tag:blogger.com,1999:blog-4073397588746430486.post-18338334244101271292012-12-13T22:53:00.001-10:002012-12-13T22:56:01.415-10:00Part Two: How A Skeptic Ended Up Seeing An ILADS Doctor<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhpTfZBk7w2-KklUDhkfmr1cmC25czuD5FIvn28L-GlEkk1Evbc70jcEJ2zqtbU_8852iGwFrqvwDTYtYWMDZOjD0dKAfMMSIVQ52d6ckPGGveqHOxnSdsMwxFpg1t4l6mBnLdTB3wpLJWm/s1600/Doxycycline.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="176" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhpTfZBk7w2-KklUDhkfmr1cmC25czuD5FIvn28L-GlEkk1Evbc70jcEJ2zqtbU_8852iGwFrqvwDTYtYWMDZOjD0dKAfMMSIVQ52d6ckPGGveqHOxnSdsMwxFpg1t4l6mBnLdTB3wpLJWm/s200/Doxycycline.jpg" width="200" /></a></div>In <a href="http://campother.blogspot.com/2012/12/part-one-how-skeptic-ended-up-seeing.html">the first installment</a> of this series, the circumstances which gave rise to my seeing an LLMD were outlined. Having issues getting proper diagnosis and treatment for an early acute case of Lyme disease, the inability to secure a referral to an infectious disease specialist, a referral to a doctor from local Lyme disease support groups, and being incredibly ill all led to my first visit with an LLMD.<br />
<br />
In today's installment, I'll talk about how I decided to take antibiotics long term, how the Lyme disease patient community became part of my life, and the inner conflicts which have arisen by being a patient with my condition.<br />
<br />
<b>On Being A Somewhat Different Chronic Lyme Disease Patient</b><br />
<br />
Unlike the majority of chronic Lyme disease patients who were surveyed, I did not have to see many doctors before my diagnosis. And unlike the majority of chronic Lyme disease patients, I still felt like modern medicine worked pretty well for me up to that point: If I got bronchitis - the doctor helped. If I got a sinus infection - the doctor helped. If I got an ingrown toenail... You get the idea.<br />
<br />
So for me, the health care system - at least up until my Lyme disease experience - worked well enough for me. I received as much care as I needed for the problems I faced and made few demands on the system because I was (for the most part) healthy.<br />
<br />
This perspective initially carried over to my LLMD: I thought we would have an appointment or two, I'd check in if I had a question or needed a prescription filled; I'd take antibiotics for a few weeks - and otherwise, our paths probably wouldn't cross again unless I got another EM rash someday. <br />
<br />
But as I reached the month mark and realized how lousy I felt, I wasn't so sure about stopping antibiotics. I was <i>severely</i> ill. And when I stopped antibiotics, I discovered that within a few days I was even less functional and in even more pain than I was while taking antibiotics. <br />
<br />
I told my LLMD, "I don't understand. I thought I'm supposed to feel better by now. I caught this early." My LLMD said, "This is Lyme. This is how it is."<br />
<br />
<i>What do you mean, "This is how it is?"</i><br />
<br />
At that point in the game, my brain was so cognitively impaired I had to take notes and try to reason through this explanation given over time - but to be frank, nothing made sense at that point because I was too ill and wasn't tracking conversations well. <br />
<br />
I found out that the choice to continue taking antibiotics rapidly became a pragmatic one: <br />
<br />
Every time I stopped taking antibiotics, the worst of my symptoms would return and I would drop out of being an active member of society. <br />
<br />
With the antibiotics, I was eventually able to walk up and downstairs at a slow to normal speed. I could drive short distances, I could run some errands, I could walk to the train station, and even begin working part time again. I'd still be in some pain and have some fatigue - but I could at least do <b>something</b>.<br />
<br />
Without the antibiotics, I would be overcome with pain and fatigue and begin losing cognitive ground again. I would have trouble leaving the bed - let alone leaving the house. The pain and fatigue were so overwhelming that any stoic attempts on my part to push past them failed. <br />
<br />
I didn't like this new reality - but I didn't want to lose my job. <br />
<br />
I reasoned to myself that I knew a few diseases were treated with longer courses of antibiotics so there was risk management for such situations - and considered treatment was probably low risk, provided I didn't stop antibiotics and restart them often as that would create antibiotic resistance. Or if I decided to stop and wanted to restart - I could restart with a different antibiotic which was effective in order to avoid resistance.<br />
<br />
I rationalized my decision at each step, and I did so directly in response to the improvements I experienced while on antibiotics - but also due to the projected loss if I stopped antibiotics entirely. <br />
<br />
I knew the risks to continue the drugs were there - and the risks to stop them were as well. I thought I was damned if I did...and damned if I didn't.<br />
<br />
<b>The Ups And Downs Of My New Condition</b><br />
<br />
When I first went off antibiotics and symptoms resurgence occurred, I joined a few online support mailing lists for Lyme disease patients and asked if people knew what was happening to me. I was also in so much pain, I wanted someone else to complain to who would understand and not have to dump on my friends about it. <br />
<br />
Outside of Lymeland, my healthy friends knew I contracted Lyme disease - but they could not relate to what I was going through. A few of them had Lyme disease in the past and got it treated - but none of them had developed the kind of problems I had. None of them had symptoms which were as severe as mine or had lasted as long. <br />
<br />
It was frustrating, because I didn't understand why my path wasn't the same as theirs. It made me wonder just what was in that tick that bit me that I ended up so much sicker than any of them had been. <br />
<br />
Not knowing what else to do, I read the posts and archives on my patient mailing lists and struggled to understand what had happened to me. It was challenging because reading and comprehension came very slowly; I had to take notes because I kept forgetting things. <br />
<br />
Before I could understand what was happening to me, a clear picture began to form of what life was like for many patients diagnosed with chronic Lyme disease: <br />
<br />
- Most people there had symptoms for a long time before they were given a diagnosis of chronic Lyme; <br />
- Most had already seen multiple doctors who had not been able to diagnosis them - or they were diagnosed with something else but were told their case was "atypical"; <br />
- Most felt disowned and dismissed by the medical community at large; <br />
- Most if not all had their lives destroyed in some way by the onset of these symptoms which continued plague them.<br />
<br />
Patients who were once married were divorced, due to having partners who were unwilling to be supportive or adapt to the reality of their illness. Patients who lost five and six-figure jobs had to sell their homes and downsize considerably - sometimes moving back in with their elderly parents. Patients who were once avid hunters and rock climbers had to stop doing what they loved and either sold their gear or enshrined it prominently in hopes of using it someday in the far off future. <br />
<br />
I didn't know what to make of myself and how I fit into all of this as time went on. It was overwhelming to hear how much physical suffering everyone had endured, how much personal loss everyone experienced, and how much humiliation everyone went through at the hands of various medical professionals.<br />
<br />
I swore to myself. <i>This wasn't going to be me.</i> After all, I just had early Lyme disease. <i>Not this chronic stuff.</i> Right?<br />
<br />
But as time went on, I realized that as early as my infection had been treated, something wasn't right because like the rest of the group - I was still quite sick. <br />
<br />
I was barely able to work part time even with extended treatment. I would get home, take off my shoes, and immediately lie down. I would wait two or three hours before getting up to attempt making myself dinner. And after a simple dinner, I would lie down and pass out for the night. <br />
<br />
There was no energy to go out and socialize. It hurt too much to return to clubbing, hiking, and biking. My plan to take surfing classes on Hawaii's beaches was scuttled...There was no money to do it, anyway. <br />
<br />
Periodically, I would stop all antibiotics and take painkillers and anti-inflammatory medication instead. But each time, the symptoms which made me totally dysfunctional would come back, and I would give in to taking the antibiotics again and double my consumption of yogurt and acidophilus capsules. Pain medication - over the counter and prescription, both - had little effect on the symptoms I had. <br />
<br />
Slowly, very slowly, I improved. Months later, I eventually managed to get a new, full time job - and by the time I did, I was about 80% of my pre-tickbite baseline for health. I was initially relieved and thrilled, because to me this meant <i>I'd finally made it</i>. I thought I'd gotten past the Lyme disease, and wrote off remaining 20% of symptoms as residual fatigue and odd random aches which would heal in time.<br />
<br />
This little victory was to be short-lived, however, as after many months of no antibiotics (I had decided to quit, having felt mostly better), I began to relive that sinking sense of decline I'd had the previous year. Cognitive abilities began to wane. Energy lacked. More new symptoms I never had before joined the chorus. I fell behind at work. I attempted to telecommute. But long story short: I had to leave this job, too.<br />
<br />
I went to my new family doctor and saw a few specialists and tried to figure out if anything else was going on. We tested for autoimmune disorders - nothing. CBC and metabolic panels - nothing. Vitamin deficiencies? Okay, I was slightly low on B-12, but that was easily correctible. <br />
<br />
Nothing else showed up, though. And yet I continued to decline and become increasingly useless. Despondent. <i>Exhausted.</i><br />
<br />
Concerned for my sanity, I decided on my own to consult with a therapist and see if depression or other psychiatric conditions could be causing any of my symptoms. The therapist's evaluation of my situation was that I was somewhat depressed, but the nature and magnitude of my symptoms indicated I had a medical problem that wasn't being properly addressed. <i>What problem?</i> The therapist had no idea.<br />
<br />
Not finding any answers from my family doctor, specialists, or therapist, I returned to my LLMD. There, the reason for some of the absolute worst of my symptoms had been revealed: My spiking fevers, sweats, chest compression, and shortness of breath which began attacking at night were pinned down to babesiosis, a tickborne disease caused by babesia - protozoa which cause symptoms similar to malaria. The grinding fatigue and cognitive slowing I'd been struggling with may also have been caused by this organism. <br />
<br />
It turned out babesia treatment was the best investment I ever made since the entire Lyme disease debacle began, as it began to alleviate my most serious symptoms. It enabled me to sleep more than three hours a night, restored a huge chunk of my cognitive ability, stopped sharp stabbing pains in my legs, and restored my breathing to normal.<br />
<br />
I improved, but to this day have still not returned to my former health before the tick bite.<br />
<br />
<b>Trying To Make Sense Of It All</b><br />
<br />
A couple years prior to this point, I went into my situation expecting to take a couple weeks' worth of antibiotics then go back to work. I didn't expect to experience not only a protracted improvement - but also an improvement followed by a more serious decline.<br />
<br />
After my cognitive abilities began to improve again, I tried to make sense of my situation: On one hand, clinical trials had shown that only a subset of the most symptomatic patients enrolled improved with additional antibiotic treatment. But on the other hand, I had my own experience with antibiotics over a longer trajectory than those in trials, and had seen greater improvement. On one hand, anecdote is not evidence. On the other hand, I had nothing else to go on because there was no officially sanctioned treatment from the Infectious Disease Society of America, who labeled my condition as being "Post Lyme Disease Syndrome" - hypothesized to be an autoimmune-like disorder. <br />
<br />
Tired of having either the contested and hotly debated chronic Lyme disease or the ill-defined Post Lyme Disease Syndrome, I wanted answers. <i>Where were they?</i> Where was the scientific research which would determine my diagnosis without any doubt? <br />
<br />
My patient support groups and research I'd read reinforced the idea that Borrelia <i>burgdorferi</i> could cause a persistent infection. But I'd also read that molecular mimicry was associated with Lyme arthritis - at least in some instances. I began to read through all the research I could find, and see if I could independently draw my own conclusions about my condition. <br />
<br />
I half jokingly wanted someone to conduct a clinical trial pitting antibiotics against non-antibiotic analogs which contained the anti-inflammatory component. I thought maybe this would answer some questions as to whether it was the anti-inflammatory component of antibiotics which alleviated patients' symptoms - or the antibacterial one. But it was quickly pointed out to me that if any patients were still infected, this would be considered an unethical trial if those patients were placed in the analog arm. I dropped that idea.<br />
<br />
I had looked to enroll in clinical treatment trials for either chronic Lyme disease or Post Lyme Disease Syndrome, willing to bet on either horse in this race - but neither was ever running on the NIH-NIAID track whenever I looked. And to this day, there has been no Post Lyme Disease Syndrome treatment trial, and no test of the hypothesis that PLDS - outside of Lyme arthritis - is autoimmune in nature. So my career as a lab rat was over before it could even start.<br />
<br />
I wanted to do everything right, and not rely on anecdote alone for my treatment - even if it showed some signs of success. I looked for how I could engage in the research needed to help myself and others - but there was no avenue open for this, either.<br />
<br />
So here I was, stuck doing something which I didn't think I'd be doing in the first place and which I wanted to understand: How could I have ended up taking antibiotics longer term when officially published trials indicated that more antibiotics were not better? I thought that as someone with a research background, that I would have used the outcome of those trials as a basis for my decision. I didn't.<br />
<br />
One could argue I did it out of desperation. That's probably true. I was so seriously sick, I didn't know what else to do. I was desperate for relief and at one point, nearly suicidal with pain. So desperation played a role - there is no denying that. It was the reality of the situation.<br />
<br />
But it really began with the need for a short course of antibiotics to begin with - and ending up continuing it because the alternative was much worse.<br />
<br />
And at the time, it was really the only option presented to me by any medical professional outside of pain medicine, and I needed to make sure my brain worked in order to hold down even a part time job - opiates and narcotic pain medicine would have stolen away what brains I had. <br />
<br />
I did it because no other options were presented to me, no one else knew how to treat my condition, and the boundaries defining my condition were ill-defined. I definitely had Lyme disease - at least at one point. I definitely had babesia, and now I can never donate blood again. I don't know if any other pathogen was in that tick and will likely never know; perhaps some entirely different microorganism which was antibiotic responsive was killed off by my efforts. <br />
<br />
After some time has passed, I've noted that the most severe of my symptoms have not returned. I'm hesitant to say they're permanently gone, given how I was at 80% of my baseline before, only to decline again. And while I'm not well enough to work, I'm not so disabled I can't get out of bed and do a number of basic tasks - provided I pace myself.<br />
<br />
Arriving at this stage, I have had to reevaluate how I decide to treat my condition. Since I'm concerned about antibiotic resistance and allergies, I wanted to avoid taking more antibiotics. And since I'm concerned about the condition of my digestive system, I thought stopping antibiotics was in my best interest. So I have stopped again, and tried other methods of treating my symptoms - but none have been effective enough to worth noting. <br />
<br />
Today, life goes on - to some degree. I am not improving. I miss working. I miss doing all the things I love to do that I - like so many others on the mailing lists I inhabited - cannot do. <br />
<br />
And I debate about what to do next - especially if my symptoms deteriorate more. I am on a rollercoaster where I can't be sure how I'm going to be affected next, and most of the medical community seems ill equipped to know how to manage a patient with my condition. <br />
<br />
This is not a blame thing, by the way - this is a simple fact. And yet, if the projections are anything to go by, I am the medical face representing tomorrow's patients: More of us are going to be chronically ill, and have to cope with complex conditions. What can we do to set the groundwork in place to prevent others from becoming chronically ill as I have - and to effectively help those who have become as ill as I am?<br />
<br />
(Part three of this series next: The pseudoscience and science of chronic Lyme disease. Part one of this series <a href="http://campother.blogspot.com/2012/12/part-one-how-skeptic-ended-up-seeing.html">is here</a>.)<br />
<br />
<div align="center"><!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com5tag:blogger.com,1999:blog-4073397588746430486.post-67055895925165700152012-12-05T21:02:00.003-10:002012-12-13T23:32:04.791-10:00Part One: How A Skeptic Ended Up Seeing An ILADS Doctor<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjKSKM_pPrrX31BdgnbBBJklt6BJFrn4D9l0Qwg9o8Pp_ANOtIFwPKUPxW-8OOpK1IaMgw2gSyOrE6mfF1sTeDMQmWOdvk8zAPH1vJh5YIEOocycFh1e3AnyDdvlf9rNrwYPv9zBh4xQaHD/s1600/Tick_%2528PSF%2529.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="197" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjKSKM_pPrrX31BdgnbBBJklt6BJFrn4D9l0Qwg9o8Pp_ANOtIFwPKUPxW-8OOpK1IaMgw2gSyOrE6mfF1sTeDMQmWOdvk8zAPH1vJh5YIEOocycFh1e3AnyDdvlf9rNrwYPv9zBh4xQaHD/s200/Tick_%2528PSF%2529.png" width="200" /></a></div>Early November 2012, the International Lyme and Associated Diseases Society - also known as ILADS - held their annual conference in Boston, Massachussetts. Due to the incoming frankenstorm, Sandy - and other reasons - I did not attend the conference. Instead, I joined hundreds of viewers in watching a prerecorded version of different ILADS conference presentations on livestream last weekend.<br />
<br />
I was originally going to give my own bullet summary about each of the conference presentations I viewed - but I think that if you are interested in what each of the presenters had to say, it's best to view a replay of their presentations during the next two weekends and view their slides on the ILADS website. It is going to take me a long time to write on the presentations I intend to single out.<br />
<br />
(I did write a quick overview of my initial impressions of the streamed video feed on a thread on Lymenet Europe, and that - along with other conference watchers' opinions - can be found here: <a href="http://www.lymeneteurope.org/http://www.lymeneteurope.org/forum/viewtopic.php?f=7&t=4383">Thoughts re ILADS 2012 Streamed Conference, Dec. 1-2 </a>)<br />
<br />
But before I write more extensively on specific conference presentations (and also grade them based on how much they are evidence-based) what I want to do today is share part one of a series of posts on how it is I got involved with ILADS and LLMDs in the first place. Not only as a patient - but as a skeptic. <br />
<br />
This series will hopefully shed some light on how someone like me would fall into ILADS' orbit instead of accepting the Infectious Disease Society of America's guidelines for the treatment of Lyme disease, and explain how someone like me has come to view the issue of chronic Lyme disease after several years of living with persisting symptoms.<br />
<br />
<b>How I Ended Up Seeing An LLMD</b><br />
<br />
It's important to offer some backstory so you know how I came to know ILADS doctors, and how some patients with similar backgrounds such as my own may end up seeing an ILADS doctor - or even more generally, what is called a Lyme Literate Medical Doctor (LLMD). <br />
<br />
It should be noted that the term "Lyme literate doctor" is in and of itself almost meaningless to most people, and in various circles it can mean anything from an infectious disease specialist to a doctor who knows enough about Lyme disease to know it when he sees it and will treat it. For the sake of discussion here, a Lyme literate doctor is one who knows about multiple tickborne infections, is willing to treat patients using longer courses of antibiotics than the IDSA guidelines state, and does not put a hard limit on either treatment duration or dosage.<br />
<br />
But I digress... Here's my story:<br />
<br />
One day several years ago I went for the hike in the mountains, and that evening, found a tick embedded in my back. I was alone, there was no one else around to remove it, and I am certain I removed it improperly. <br />
<br />
Fast forward... I developed a rash around the bite site, and went to a local clinic to get it checked out. I was told I was having a localized allergic reaction to the bite, and that there wasn't any Lyme disease in the area I'd been bitten. In fact, I was told Lyme didn't exist in the area and was rare in the state. <br />
<br />
The doctor gave me a prophylactic dose of doxycycline, but little did I know at the time that it wouldn't be enough. In another week, my rash had expanded, I felt like I was getting a flu, and I returned to the clinic - only to be prescribed Zithromax and get diagnosed with a sinus infection. I got very sick after I finished my Z-pack (the full story in all its gory detail is <a href="http://campother.blogspot.com/p/about.html">on this page</a>), had to get dropped off at the door to the clinic rather than walk there, and during my appointment was told again that I couldn't have Lyme disease. Lyme disease wasn't endemic to the area in which I'd been bitten. But nonetheless, a blood draw for an ELISA was taken at my insistence. <br />
<br />
The test result came back negative, and I was told that I did not have Lyme disease. However, what I did not know at the time - and learned later - is that people don't always immediately produce antibodies to Borrelia burgdorferi, the bacteria which causes Lyme disease. It can take 4-6 weeks to produce a positive antibody response. <br />
<br />
I also learned later that taking antibiotics early in infection can abrogate the immune response to the degree that antibodies may not register on the test even if you are infected. (Fortunately, this was not the case with me, as some time later I did have a positive test.)<br />
<br />
<a href="http://www.cdc.gov/lyme/faq/index.html#accurate">Even the Centers For Disease Control (CDC) - viewed by many chronic Lyme disease patients as being too restrictive in its approach to diagnostic criteria, testing, and treatment of Lyme disease - has made it clear that these two factors can lead to a false negative in testing for early Lyme disease</a>.<br />
<br />
By now, you might be sitting there wondering where I'm going with all this. It's this simple: <br />
<br />
<i>My family doctor knew nothing about Lyme disease.</i><br />
<br />
My (now ex) family doctor did not think I had Lyme disease because of where I was bitten - and missed the <a href="http://en.wikipedia.org/wiki/Pathognomonic">pathognomonic</a> (which means a symptom which is the gold standard for diagnosis) sign of Lyme disease which should have led to my immediate treatment with a few weeks of doxycycline - if not a few weeks of IV Ceftriaxone.<br />
<br />
<i>The doctor did not even treat me based on the IDSA's own guidelines when they should have.</i><br />
<br />
I am considered in the minority among chronic Lyme disease patients - at least so far as I know. The <a href="http://www.healthpolicyjrnl.com/article/S0168-8510(11)00101-1/abstract">largest survey of chronic Lyme disease patients that I know of</a> was conducted by Lorraine Johnson of lymedisease.org, a patient advocacy organization. The results indicated that in their survey of over 4,500 patients with chronic Lyme, 73% were not diagnosed within a year. And many patients report not remembering receiving a tick bite, not seeing an EM rash, and having to see numerous doctors before receiving a diagnosis of Lyme disease. <br />
<br />
This was not me. I am the person who, in many ways, was already an outlier in life - and now I had become an outlier among outliers; the estranged among the estranged.<br />
<br />
Had my family doctor known what I had and referred me to an infectious disease specialist immediately - and had that specialist seen the severity of my symptoms - odds are good I would not be here writing all this here for you to read.<br />
<br />
But between having gone online to contact Lyme disease support groups for a referral, and my inability to get a referral to an infectious disease specialist, I ended up seeing a LLMD for diagnosis and treatment.<br />
<br />
My LLMD told me that I was in fact a textbook case of Lyme disease, and it was astonishing that I had not received treatment right away. I agreed, knowing exactly what happened to me and just how seriously ill I was, I did not understand why this happened to me. <br />
<br />
When I returned to the original clinic a couple times, enlarging EM rash and all, that should have been the signal to act. Instead, it was written off.<br />
<br />
My LLMD informed me that he and the state health department knew the region in which I'd been hiking was endemic for Lyme disease, and further follow up with the state health department confirmed this as true. My LLMD immediately gave me my first round of antibiotic treatment, and while I should have had IV antibiotics, I could not because insurance would not cover it. I also could not afford to pay for it out of pocket because I stopped working when I got too sick.<br />
<br />
I had a test for Lyme disease and at that point, my test was positive. And as I continued to get sicker while on treatment, my LLMD suspected I had a coinfection and tested me for a few - of which babesiosis also came back positive, and it made sense because my symptom presentation matched the diagnosis.<br />
<br />
What I experienced early on in this LLMD's office was not what I'd experienced in my local clinic. First, the LLMD knew about early Lyme disease and knew where endemic areas in the state were. I had no idea where they were - nor did the previous doctor I'd seen. The LLMD was well informed about different coinfections ticks can carry. At the time, I knew nothing about coinfections - and I barely knew anything about Lyme. The LLMD also ran additional tests to rule out other conditions at the time, and make sure nothing outside of tickborne infection was missed. I appreciated the thorough analysis.<br />
<br />
The appointment was thorough, and I got the impression my new LLMD was more competent than the doctors I had seen in my local clinic. And over the following months, this LLMD's treatment took me from being unable to think straight, hardly being able to walk, and being in so much pain I had been contemplating suicide to slowly thinking again and walking from the bedroom to the mailbox and back.<br />
<br />
So here are the factors which lead to my getting involved with the world of LLMDs and ILADS:<br />
<br />
- Repeated misdiagnosis of early infection by my family doctor when I had a glaringly obvious EM rash.<br />
- Being denied a diagnosis due to a negative ELISA when the doctor should have known it was given too early to result in a positive test.<br />
- The inability to get a referral to an infectious disease specialist.<br />
- The impression that the LLMD was knowledgable and competent, and more knowledgable and competent than doctors at my clinic.<br />
- Being believed that I was in fact as severely ill as I had stated.<br />
- Receiving an extensive exam and having a full medical history taken - more time was spent with me than any doctor had ever spent on me.<br />
- Being given tests to rule out any other conditions - both tickborne coinfections and non-tickborne related medical conditions.<br />
<br />
So to any family doctors who are out there who have a patient in front of them with an expanding dark red oval rash with no central clearing and a tick bite in the middle of it: Treat them. Don't wait for a positive blood test result. A little doxycycline goes a long way in early Lyme disease and helps patients avoid becoming a late stage case or take on this controversial diagnosis of chronic Lyme disease.<br />
<br />
But the number one factor which landed me in the LLMD's office cannot be emphasized enough: <br />
<br />
I was very, VERY sick. Sicker than I had ever been in my entire life. What I had did not feel like a mild or even moderate flu-like illness. I had so much pain in my body, it felt bone-breaking. I had a high fever and shortness of breath. I had so much inflammation and weakness in my arms that I could not wash my own back. I could not stand in the shower. This went on for weeks, and did not match in magnitude or form the experience that <a href="http://www.cdc.gov/lyme/diagnosistreatment/Stories/index.html">a patient, John, describes of his own brush with Lyme disease on the CDC's website</a>.<br />
<br />
I needed to see someone who would treat me, and I wasn't going to go to some alternative doctor who was going to give me herbs and supplements and send me on my way. The clinic had already blown me off. And my friends were concerned about me - some even thought with my symptoms that I should see a neurologist - but getting an appointment for one had its own slow timeline.<br />
<br />
When I ended up looking online and called a few local Lyme disease support groups and told them about what happened to me and asked which clinic I should go to, I was informed by multiple members of these groups that my experience was not that uncommon; that I was better off getting an appointment with an LLMD right away.<br />
<br />
Lyme disease patient advocacy played a role in my getting to see a LLMD. Before I had made any of my phone calls, I had never heard of an LLMD nor did I know what it meant. I did not know all about how LLMDs treated patients. All I knew was that I had contracted Lyme disease recently and needed help. And who else do you call about specific diseases outside of doctors who treat them other than other patients who have them?<br />
<br />
At that stage, I did not know there was a controversy surrounding Lyme disease. That would come later. All I knew at this stage was that I had early Lyme disease and it needed treating. The pain needed to stop - and stop soon.<br />
<br />
(Part Two next: <a href="http://campother.blogspot.com/2012/12/part-two-how-skeptic-ended-up-seeing.html">How I decided to take antibiotics long term, how the Lyme disease patient community became part of my life, and the inner conflicts which have arisen by being a patient with my condition</a>. Followed up by Part Three: Lyme disease pseudoscience and science.)<br />
<br />
<div align="center"><!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com7tag:blogger.com,1999:blog-4073397588746430486.post-83715712476505272192012-11-30T21:36:00.003-10:002012-11-30T21:36:36.714-10:00Placeholder: ILADS 2012 Conference Remarks<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTKE3C1lJIVX_Ooi8W2DAXIMkf04yTbEJTZUp0m7oqpM5XTkUfFjbwT_0K5aJYopJRlQ7ixb2c6Xr7P1uCo0qpZhhfm9W0oEaxQgTtOR_TpqrmjLu_2c6auERLTiBozuGFmxcTWpT2rkbj/s1600/supportlymeresearch.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="153" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTKE3C1lJIVX_Ooi8W2DAXIMkf04yTbEJTZUp0m7oqpM5XTkUfFjbwT_0K5aJYopJRlQ7ixb2c6Xr7P1uCo0qpZhhfm9W0oEaxQgTtOR_TpqrmjLu_2c6auERLTiBozuGFmxcTWpT2rkbj/s200/supportlymeresearch.png" width="200" /></a></div>
<br />
<br />
<br />
<br />
<br />
<div style="text-align: center;">
Coming soon... ILADS 2012 Conference Remarks - watch this space.</div>
<div style="text-align: center;">
<br /></div>
<div style="text-align: center;">
<br /></div>
<div style="text-align: center;">
<br /></div>
<div style="text-align: center;">
<br /></div>
<div style="text-align: center;">
<br /></div>
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com0tag:blogger.com,1999:blog-4073397588746430486.post-18812362652033000852012-11-30T15:40:00.000-10:002012-11-30T21:49:11.176-10:00Late November Newsletter From Camp Other<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZ1pn7qgjYaXS4QBbrPiITk2XbHullGdUeR5XNthMLiy5_7Z_T3sLslaxg_BEBBjFOaUJLUKOx0WR-OGUpTM0T-r-RdOYK3l9jP96zgGMbySVds4BQDR4yUTw6XXaXONn7gNuohYY1Oi0G/s1600/neurons.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="166" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjZ1pn7qgjYaXS4QBbrPiITk2XbHullGdUeR5XNthMLiy5_7Z_T3sLslaxg_BEBBjFOaUJLUKOx0WR-OGUpTM0T-r-RdOYK3l9jP96zgGMbySVds4BQDR4yUTw6XXaXONn7gNuohYY1Oi0G/s200/neurons.jpg" width="200" /></a></div>
There are a few announcements I'd like to make today... <br />
<br />
For those of you who are here for the first time, via Twitter: Welcome to Camp Other blog. I'm glad to see you here, and I look forward to having interesting discussions with you both here and on Twitter. <br />
<br />
Whether you are new to this blog or a returning visitor, the following announcements may help you make sense of what's been happening here at Camp Other blog:<br />
<br />
<b>An Effort to Change Writing Style and Reporting</b><br />
<br />
Joining Twitter is a recent move I made in the past couple of weeks in order to pick up more great writing on science and links to posts from science bloggers. <br />
<br />
In some ways, this is great because I'm learning more, and I recommend following those I follow because there are a lot of interesting articles out there. But in other ways, this is a humbling experience because there are so many good writers out there - and once I've read them, I can't help but notice there is room for improvement here.<br />
<br />
I'm not a professional blogger and do what I do for my own education and share it with others. I never attempted to make this blog a profitable enterprise because I felt that the information was something everyone should have and I wanted to remain neutral by not being funded by anyone who could be perceived as having editorial influence over my posts. This is how it has been - and this is how I want this site to continue - even if someday I manage to become a professional writer in the future.<br />
<br />
Open source or not, after reading more science blogs and articles, I can only see that learning from those already in the trenches longer than I have been will teach me how to be a better blogger for everyone. <br />
<br />
One thing I am already noticing, unfortunately, is that blogs which are more accessible than mine in some way - those which reach a wider audience, or those which are high volume and have short, focused posts - are blogs which are going to be difficult for me to emulate.<br />
<br />
Reason being: I am suffering from a medical condition which affects my cognitive abilities and energy. My ability to either stay focused on one topic or publish a brief post is challenged due to having chronic fatigue and trouble focusing. <br />
<br />
Ironically, having more fatigue doesn't translate into shorter posts - it comes coupled with altered executive function in my brain - so I can ramble on and write a long post yet have trouble getting to the point.<br />
<br />
I'd like to make an effort to change this, but where to begin? I could use some advice as to how to overcome these stumbling blocks and make my blog not only more easily readable for a wider audience but also optimize and work with the cognitive abilities I do have.<br />
<br />
<b>REMOVED: The Poll On What Causes Persisting Symptoms of Lyme Disease</b><br />
<br />
For almost a year, a blogspot poll widget was on the upper lefthand corner of this blog. It asked readers to select among a number of choices as to the cause for persisting symptoms in patients after initial treatment of Lyme disease. <br />
<br />
In recent weeks I have been monitoring the output of this widget and decided in all fairness it needed to be removed because votes were not being recorded and displayed accurately: One week I would see a score of over 110 votes, and the following week it would dip down to 93 - only to waver between 97 and 92 in the following weeks.<br />
<br />
Any poll should be gaining and not losing the total number of votes. So it got voted off the Camp Other island, and I won't be using that widget again. Other online sources reported similar issues with this widget as well, and had I known in advance it was a problem, I would have used a different poll widget.<br />
<br />
Despite this setback, know that each choice and the most recent results will be discussed in a future post. <br />
<br />
<b><u>A sneak preview:</u></b> A little over 90% of readers who responded to the poll thought that Lyme disease can be a chronic and persisting infection after initial treatment - while a little over 30% thought persisting symptoms that occur after initial treatment are caused by an autoimmune condition.<br />
<br />
<b>The Challenge Of Being Both A Patient And Researcher: Bias</b><br />
<br />
I placed a request on Twitter earlier today asking followers for any information on scientists who study the disease they themselves have - and in particular, blog about it. <br />
<br />
I'm hoping to ask them a few questions about how they handle the issue of bias, and how they sort out other research they read about their own condition in order to know which leads to follow, which leads are cold, and which leads are questionable.<br />
<br />
One of the walls I find myself banging against as I continue to write this blog is my concern over the issue of bias: <i>Can a patient research their own disease and its causes and treatment without bias, or is there always going to be a certain amount of bias in what one reads and writes about because one is a patient?</i><br />
<br />
Not sure I can sort out all the issues around this, but I wanted to bring up the question because I think it is an important one. I'd like to explore this more.<br />
<br />
<b>Sick, Symptomatic, And Struggling</b><br />
<br />
I mention it only in passing because I am still not posting as frequently as I hoped: <br />
<br />
I'm not doing so well lately. I suspect the symptoms I'm having are due to a new condition and I am in the middle of getting referrals to specialists to help sort it all out. In the meantime, hopefully I can find a way to continue to do research and blog more regularly.<br />
<br />
And there is a certain level of frustration I'm experiencing here which is difficult to put into words, but it basically boils down to, "I'm sick and tired of being sick and tired, and sick of being poked, prodded, biopsied, scanned, bled, x-rayed, ultra-sounded, and analyzed in general."<br />
<br />
I am not a number... but I have felt like one. (I'd rather say, "I am not a number, I'm a free man" - but I'm not sure how many of you reading along would catch that ref.)<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com0tag:blogger.com,1999:blog-4073397588746430486.post-51687437578373597952012-11-30T13:18:00.003-10:002012-11-30T21:52:35.795-10:00A Pocket Review of Dr. Steere's NEJM Reinfection Editorial<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi7VUkURZuda2UH_0vEJ8DYvuu0iULC4d9HqNC7Ypw_8TxmsiKs7tYqLBEvt6s_sHf7l52o1krAq0nw6PVl7WBb9T9OgrhesuwrOUl7NL-nML1SpPvl8W60VJIZNRcELlWdcu3KhfdR3HIT/s1600/borreliaglom.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi7VUkURZuda2UH_0vEJ8DYvuu0iULC4d9HqNC7Ypw_8TxmsiKs7tYqLBEvt6s_sHf7l52o1krAq0nw6PVl7WBb9T9OgrhesuwrOUl7NL-nML1SpPvl8W60VJIZNRcELlWdcu3KhfdR3HIT/s1600/borreliaglom.jpg" /></a></div>I finally had the opportunity to sit down and read Dr. Steere's editorial which accompanied Nadelman et al's study, "<a href="http://www.nejm.org/doi/full/10.1056/NEJMoa1114362">Differentiation of Reinfection from Relapse in Recurrent Lyme Disease</a>". <br />
<br />
Before I comment on the editorial, I want to acknowledge the research which was accomplished in the study as it deserves more attention.<br />
<br />
I think it was an interesting study on two counts: <br />
<br />
One, it showed that in a group of 17 patients, it was highly unlikely that a patient would get reinfected with the same genotype of Borrelia burgdorferi compared to one with which they'd previously been infected. Does this suggest that patients have some form of immunity to specific genotypes - or is this a reflection of random chance of infection with specific genotypes? <br />
<br />
Two, it provided evidence in two patients that a person can be infected with one genotype of Borrelia burgdorferi in skin - while an entirely different genotype can be found in the blood. The significance of this has yet to be determined, but it does raise some interesting questions about the nature of Borrelia burgdorferi infection. How often are patients coinfected with different types of Borrelia burgdorferi? Are these genotypes competitive in any way? Can one genotype affect a patient more profoundly than the other? If there is a delay in treatment, can one genotype be more effectively treated than another?<br />
<br />
The findings from this study inspire curiosity and more questions about the nature of Lyme disease.<br />
<br />
<b>Thoughts on the editorial, "Reinfection versus Relaspe in Lyme Disease"</b><br />
<br />
Now that I have acknowledged two interesting findings from the Nadelman reinfection study, I have to say that unlike the connections made by Dr. Steere, I do not see the relationship between data presented in this study and patients who have been infected with Lyme disease and continue to have persisting symptoms after initial treatment.<br />
<br />
Any good study and its findings stand on their own and an editorial on them by the authors themselves is usually unnecessary. The work should speak for itself, and I think this study does well to demonstrate a relationship between the presence of new genotypes and reinfection in a small group of patients who were bitten by ticks in the same geographic location. <br />
<br />
If there is an editorial accompanying research, it should in some way enhance or broaden our understanding and appreciation of the findings - and by extension, lead our curiosity to new horizons. <br />
<br />
Unfortunately, Dr. Steere's editorial is not additive in nature. It does not add nuance to or a greater appreciation of the reinfection study - nor does it address the kind of questions raised above which directly apply to his study. Instead, his editorial seems to stretch the findings' significance in order to provoke discussion on chronic Lyme disease based on claims that a small percentage of patients' erythema migrans rashes have been thought to indicate a relapsing infection.<br />
<br />
<b><u>References</u></b><br />
Robert B. Nadelman, M.D., Klára Hanincová, Ph.D., Priyanka Mukherjee, B.S., Dionysios Liveris, Ph.D., John Nowakowski, M.D., Donna McKenna, A.N.P., Dustin Brisson, Ph.D., Denise Cooper, B.S., Susan Bittker, M.S., Gul Madison, M.D., Diane Holmgren, R.N., Ira Schwartz, Ph.D., and Gary P. Wormser, M.D. Differentiation of Reinfection from Relapse in Recurrent Lyme Disease. N Engl J Med 2012; 367:1883-1890November 15, 2012DOI: 10.1056/NEJMoa1114362<br />
Allen C. Steere, M.D. Reinfection versus Relapse in Lyme Disease. N Engl J Med 2012; 367:1950-1951November 15, 2012DOI: 10.1056/NEJMe1211361<br />
<br />
ALSO, to read my detailed report on the Nadelman reinfection study, see:<br />
<a href="http://campother.blogspot.com/2012/11/what-does-reinfection-study-have-to-do.html">http://campother.blogspot.com/2012/11/what-does-reinfection-study-have-to-do.html</a><br />
<br />
<div align="center"><!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com2tag:blogger.com,1999:blog-4073397588746430486.post-89908835895908458432012-11-23T13:26:00.002-10:002012-11-27T19:55:37.837-10:00Lyme Research Alliance Response To Reporting On Reinfection Study<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhO3qXLw4xQCsS8OaRdOboYzXG0VsaA-T7FdFGNVxC47FKt8MvmcQ1NMhcoo7aPitbtmGmiaqfcEMUmbyuObTGuMliKH8Gzy2eS4KHK6P1Oe0jFLOR5ydZlzSaKMbG_wxjzjjuSNOXidC_0/s1600/newspaperncoffee.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="149" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhO3qXLw4xQCsS8OaRdOboYzXG0VsaA-T7FdFGNVxC47FKt8MvmcQ1NMhcoo7aPitbtmGmiaqfcEMUmbyuObTGuMliKH8Gzy2eS4KHK6P1Oe0jFLOR5ydZlzSaKMbG_wxjzjjuSNOXidC_0/s200/newspaperncoffee.jpg" width="200" /></a></div>
The executive director of the Lyme Research Alliance responded to the New York Times' article, “<a href="http://www.nytimes.com/2012/11/15/health/new-infection-not-relapse-brings-back-symptoms-of-lyme-disease-study-finds.html">New Infection, Not Relapse, Brings Back Lyme Symptoms, Study Says</a>” which refers to the Lyme disease reinfection study recently published in the NEJM:<br />
<br />
<a href="http://www.nytimes.com/2012/11/23/opinion/lyme-disease-study.html">http://www.nytimes.com/2012/11/23/opinion/lyme-disease-study.html</a><br />
<br />
(original text removed in observance of NYT copyright policy.)<br />
<br />
Current Active Research Projects which are listed on LRA's site:<br />
<a href="http://www.lymeresearchalliance.org/research_projects.html">http://www.lymerese</a><a href="http://www.lymeresearchalliance.org/research_projects.html">archalliance.org/research_projects.html</a><br />
<br />
<hr height="1" />
<br />
For the most part, I agree with Mr. Wild's statement. I only have some questions about this sentence: "This limited study supports the theory that Lyme is effectively treated by one short course of antibiotics, yet numerous scientists vehemently disagree."<br />
<br />
I would have phrased it differently and stated it as "This limited study supports the theory that Lyme disease is <i>always</i> effectively treated by one short course of antibiotics, yet numerous scientists vehemently disagree."<br />
<br />
There is a body of research which provides evidence that Lyme disease is not always effectively treated with one short course of antibiotics - even the IDSA's 2006 Guidelines state up to 10% of <i>early acute</i> cases of Lyme disease result in treatment failures. Those same guidelines cite studies on late stage Lyme disease cases which are treated according to the guidelines, yet patients are recorded as having relapses and not returning to their former health pre-infection.<br />
<br />
In addition to the guidelines, there are case studies, research studies, and individual patient reports of relapsing symptoms after initial treatment.<br />
<br />
At the same time, not everyone who contracts Lyme disease goes on to have persisting symptoms after initial treatment. The reason why some patients develop chronic Lyme disease and some do not is not clear. A delay in receiving initial antibiotic treatment appears to play a role - and the genotype of bacteria infecting a given patient and the patient's immune profile may also play a role in development of persisting symptoms. More research is required to understand the cause of chronic Lyme disease.<br />
<br />
<br />
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com0tag:blogger.com,1999:blog-4073397588746430486.post-23865698309221747282012-11-21T16:11:00.003-10:002012-11-22T22:16:04.976-10:00What Does The Reinfection Study Have To Do With Chronic Lyme or Post Lyme Disease?<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgofZ0IPL70nZUPMYFJLwmKN0nPwljdUTm5w1RlWu3qWkjBEIV2fDZ7k5pbWJng-Hbl4S0bFbVUNkL4m80FuwCXXi5incEh9jpFaUH39ujK5VOmuVXnM9PGpF9nn4uP7vRQn4TRy73YbdXs/s1600/320px-Gehirn_lobi_seitlich.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="120" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgofZ0IPL70nZUPMYFJLwmKN0nPwljdUTm5w1RlWu3qWkjBEIV2fDZ7k5pbWJng-Hbl4S0bFbVUNkL4m80FuwCXXi5incEh9jpFaUH39ujK5VOmuVXnM9PGpF9nn4uP7vRQn4TRy73YbdXs/s200/320px-Gehirn_lobi_seitlich.png" width="200" /></a></div>
Last week, a number of media outlets wrote articles referring to a study published in the New England Journal of Medicine (NEJM), "Differentiation of Reinfection from Relapse in Recurrent Lyme Disease". <br />
<br />
Since I wanted to see what was actually stated in the study, I acquired a copy of the full text of this publication to see for myself why the authors might have given some journalists the impression that chronic Lyme disease - or even post Lyme disease syndrome - does not exist.<br />
<br />
Side note: One important thing to know is that at the time I wrote this entry, I had <i>not</i> read the accompanying editorial by Dr. Steere which was published in NEJM. Given that the current entry was written based only on the study itself and has gotten quite lengthy, I will be writing separately about the editorial in the future.<br />
<br />
<b>Summing it up</b><br />
<br />
After reading through the paper, if I had to give a one sentence summary of what this study accomplished, this sentence at the end of it summed it up fairly well:<br />
<blockquote>
"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."</blockquote>
<br />
If I'm to take it at face value, what this study does is provide evidence that when patients were properly treated early for previous erythema migrans (EM) rashes in the past and they presented with new EM rashes with obvious tick bites - they almost always contained a different kind of Lyme disease than one with which the patients had previously been infected. And with early treatment of patients found with new EM, most of those patients will go on to be fine until they are reinfected again.<br />
<br />
<i>Seems to make sense to me.</i><br />
<br />
This is what the study appears to have discovered, so at first glance I had yet to see what the findings in this paper have to do with evidence that chronic Lyme disease does not exist. Nor did I see where this study provides evidence that post Lyme disease syndrome does not exist, either.<br />
<br />
However, after digging a little deeper, I found one statement which suggested that data found in this study implied that chronic Lyme disease does not occur:<br />
<blockquote>
"[...] 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."</blockquote>
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.<br />
<br />
But one thing which I have stated before was that when it comes to Lyme disease, <i>the rash is not the disease</i>. The rash is a symptom of early infection. Untreated, it will eventually disappear. It may never recur during the same episode of infection. And in the meantime, depending on the strain one has, host factors, and without proper treatment, the infection will disseminate and spread to areas of the body far removed from where the rash first appeared. <br />
<br />
Because the patients in this study were treated either during the first sign of cutaneous infection or very early disseminated infection, they were far more likely to have been successfully treated than patients for which there was a delay in treatment or patients who were improperly treated (say with a shorter duration, or possibly a less effective or an incorrect antibiotic) earlier.<br />
<br />
Anyway, I have a few remarks on the paper:<br />
<br />
<b>On the significance of EM rashes under other conditions</b><br />
<br />
One of the concerns <a href="http://campother.blogspot.com/2012/11/co-comments-on-pseudoscience-of-chronic.html">I mentioned elsewhere</a> after reading online article after article was that journalists had not mentioned how EM rashes were relevant not only as a symptom of early infection but at other points.<br />
<br />
To some degree - and to my satisfaction - one paragraph of the study covered other reasons EM rashes would appear <i>outside</i> of the first sign of infection, and mentioned that an EM rash can show up and disappear only to reappear in untreated patients and also inappropriately treated patients. <br />
<br />
This is important to note, and I would hope that family and urgent care doctors can use the presence and timing of an EM rash relative to other symptoms to determine when more treatment is required. Dr. Jorge Benach has stated that satellite EM rashes which erupt within weeks to months after the initial EM are a sign of disseminated infection.[1] Dr. Brian Fallon of the Columbia University Lyme and Tickborne Disease Research Center has also made the same observation.[2] Combined with other clinical evidence and symptom presentation, patients with these rashes may require additional oral or intravenous antibiotic treatment.<br />
<br />
<b>Patients with new EM rashes have been reinfected.</b><br />
<br />
In addition to the summary statment cited earlier, one should take note of this particular passage in the study:<br />
<blockquote>
"Patients were treated with standard courses of antibiotics <i>at each episode of erythema migrans</i>, with subsequent resolution of the skin lesion or lesions."</blockquote>
The key words to keep in mind here are: "erythema migrans" and "appropriately treated patients". <br />
<br />
This study is about early acute Lyme disease including early disseminated infection. The patients who were followed during the course of the study were all treated for signs of early acute Lyme disease - not late stage, persisting disease. <br />
<br />
Based on this, I suspect the authors want readers to take away from their study is that these 17 patients who have an EM rash and are treated early in their infection have successful resolution of their Lyme disease - and any new EM rashes they have are a sign of a new infection which requires more antibiotics.<br />
<br />
In other words: <i>Early treatment is the key to greater success in treating Lyme disease effectively.</i><br />
<br />
<b>The value of finding different OspC RST types in different EMs.</b><br />
<br />
The keystone of the study is the evidence that different OspC RST types are found in each episode of EM when patients are followed over time.<br />
<br />
What does OspC RST strain mean? Citing a definition from an earlier paper:<br />
<blockquote>
"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.<br />
<br />
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. <br />
<br />
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. <br />
<br />
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.<br />
<br />
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."[3]</blockquote>
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". <br />
<br />
What is known not only from this paper but from many other papers is that different genotypes of Borrelia burgdorferi exist and may affect the clinical presentation of Lyme disease over time.[4-11] <br />
<br />
And as time goes on, new genotypes are also found to spread hematogenously. However, it is important to keep in mind that just because a genotype can disseminate easily <i>does not mean it is going to cause as much inflammation or have a particular tissue tropism</i>.<br />
<br />
For example:<br />
<blockquote>
"[...] 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 ]</blockquote>
According to research to date, the B. burgdorferi RST1 (OspC type A) genotype - followed by the RST3 (OspC type I) genotype - cause <i>greater inflammation and more severe disease</i> than other genotypes, establishing a link between spirochetal virulence and host inflammation.[ 3]<br />
<br />
It gets more complicated from here. Researchers are still learning how these different genotypes and subtypes interact with their hosts and host immunity.<br />
<br />
According to research (as is stated above) OspC type A RST1 and OspC type K RST2 account for approximately 60% of Lyme disease cases in the northeastern United States. <br />
<br />
Judging from other publications, northeastern US OspC genotypes more or less break down into this list:<br />
<br />
- Osp type K RST2 accounts for about 40% of that 60%.<br />
- OspC type A RST1 accounts for 20% of that 60%. <br />
- 20% of northeastern United States genotypes are mostly other RST1 and RST2 types.<br />
- The remaining 20% are a mix of RST3 which is dominated by OspC I RST3.<br />
<br />
That these different genotypes exist and have different pathogenicity is a fairly recent discovery and it is only just beginning to be understood. <br />
<br />
More is understood about more common OspC types than less common RST3 strains which are highly variable and found less frequently in animal and human hosts. Additional research on these genotypes is needed.<br />
<br />
So what kind of OspC RST types did patients have in this study on reinfection? It's a good question to ask, because if patients have genotypes of Borrelia burgdorferi which are more likely to lead to dissemination, then they (potentially) have a greater chance of invading more immune-privileged spots, such as joints, tissues, organs, and the central nervous system.<br />
<br />
Based on a review of the overall breakdown of different OspC RST types in this study, they did align somewhat with previous research on northeastern United States genotypes. <br />
<br />
OspC K RST2 was the dominant genotype found in skin, followed by a mix of OspC RST3 types then OspC RST1. That OspC RST3 types were more common than OspC RST1 differed from earlier research. Blood samples were somewhat different than those found in skin, with a combination of RST1 and RST3 types collectively outnumbering OspC RST2.<br />
<br />
There are some data sets which were not collected during this study which I would have wanted to see. For one thing, Borrelia burgdorferi samples were not taken from synovial fluid or cerebrospinal fluid (CSF) for OspC RST typing. We would also be missing any data from tissue biopsies as these are not routinely done, and are rather invasive for the patient. On the immunological side, the genetic backgrounds of patients with specific HLA-DRs were not revealed.<br />
<br />
<b>How this study does (or doesn't) relate to Chronic Lyme disease or post Lyme disease syndrome</b><br />
<br />
Patients with early disseminated infection were said to have had fever, arthralgias, headache, or fatigue which were present during the first episode of EM. The authors expanded on this point over time, demonstrating that in these 17 patients, early disseminated infection and more invasive genotypes (such as ospC A RST1 or ospC I RST3) were handily cured with a prompt course of antibiotics and that any future symptoms would be related to a new infection and not a relapse. <br />
<br />
Based on the OspC type data, the only way I can see that this study might be trying to disprove the existence of chronic Lyme disease is the authors' position that the evidence demonstrates that the same virulent strains found during the first episode EM rash that were treated were not present during the second episode in any patient. Therefore, by their deduction, the Borrelia bacteria did not persist in the time between EM rash episodes.<br />
<br />
In their opinion, evidence of a relapse would have been shown if the patient's samples demonstrated that the <i>same</i> Borrelia burgdorferi genotype would be present during <i>both</i> episodes of EM.<br />
<br />
However, is this the only conclusion one can draw from such a study? I have unanswered questions about it.<br />
<br />
Can the genetic background and varying immune system responses affect the course of Lyme disease in host mammals? (I already know the answer is yes here, but what I know is mostly about animal models. Is enough known about this as it relates to people?)<br />
<br />
How likely it is that an existing genotype of Borrelia burgdorferi found in tissues and CNS will migrate to the blood and EM rashes during ticks feeding on humans?<br />
<br />
In the study, given that in two patients the genotype of Borrelia burgdorferi from one skin sample did not match the genotype of that found in blood during the same episode, is there a possibility that in a handful of cases, antibiotics could successfully treat the EM rash produced by one genotype while not successfully treating a more virulent and invasive genotype if the infection had advanced for some time without treatment - say to more remote tissues such as organs or the CNS? <br />
<br />
Could a previous infection with a Borrelia burgdorferi genotype with specific tissue tropism coexist with the onset of an EM rash containing a new genotype? <br />
<br />
What happens if a patient has previous infection in which no EM rash was present or seen and it goes untreated - then that patient acquires a new infection with an EM rash on top of the first infection?<br />
<br />
I don't know the answer to these questions or how likely these scenarios are, but I suspect the last one I mention above is not entirely uncommon.<br />
<br />
Either way, based on the patient background which is supplied in this study we cannot know because patients are reported as being treated successfully during the early stages of infection.<br />
<br />
I also don't know how often it occurs that a patient has persisting symptoms after initial treatment for Lyme disease and a new erthyema migrans is never seen during the course of their persisting symptoms. <br />
<br />
Given my experience as a patient, I can only make the observation that other patients in my situation seldom report seeing new rashes during the course of their condition. I think researchers should take a close look at the subset of those patients who are most severely ill and are housebound - they are an important subgroup to study because their odds of reinfection are very low.<br />
<br />
Related to this, there is one immediate key difference I also see between the patient group studied and chronic Lyme disease patients:<br />
<br />
The patient population in this group received a course of antibiotics each time an EM rash presented itself. Because they were treated early, presumably they had a good chance at recovering completely from their infection.<br />
<br />
Chronic Lyme disease patients and their doctors alike report that many chronic Lyme disease patients' conditions are discovered late, and symptoms and serology often reflect those of late stage Lyme disease patients - not early acute or early disseminated patients. <br />
<br />
It is this difference which makes me wonder about the applicability of such a study to a condition such as chronic Lyme disease or post Lyme disease syndrome. <br />
<br />
Patients with late stage Lyme disease are less effectively treated with antibiotics and can be refractory to treatment; studies cited in the 2006 IDSA Lyme disease treatment guidelines indicate that a fair percentage of late stage Lyme disease patients do not fully recover after antibiotic treatment - though the reason why is not entirely clear.[13] <br />
<br />
Development of an autoimmune-like condition has been hypothesized by the IDSA and various researchers as being the cause for persisting symptoms after initial infection, while other researchers suspect persisting infection might occur in some patients.<br />
<br />
<b>In the end...</b><br />
<br />
The study provides evidence that in 17 patients who are properly treated with antibiotics shortly after EM rashes appear, their infections resolve and they get new infections.<br />
<br />
If one supports a model of chronic Lyme disease and thinks that Borrelia burgdorferi can persist in the human host past initial treatment, then this study won't provide evidence either way as to whether or not this is the case:<br />
<br />
Part of the definition of chronic Lyme disease hinges on patients having been treated late in infection and/or treated improperly early in infection only to go on to develop later stage Lyme disease in the future.<br />
<br />
If one applies this definition, it is important to note that none of the patients in this study had a delay in treatment and proceeded to late stage symptoms before receiving antibiotic treatment. None of the patients were reported as showing signs or symptoms of Lyme disease between episodes of EM rashes; patients experienced only acute Lyme disease which was promptly treated. None of the patients were remarked as being part of the 10% of patients with acute Lyme disease who experience early antibiotic failure, either.[13]<br />
<br />
The study participants fit the characterization of the majority of Lyme disease patients who successfully recover from Lyme disease with early treatment - but it does not characterize those patients who do not.<br />
<br />
Conversely, if one supports a model of post Lyme disease syndrome, this study won't provide evidence either way as to whether or not this is the case: <br />
<br />
None of the patients in this study were reported on followup after a six month interval after any EM rash and subsequent treatment as having developed symptoms indicative of post Lyme disease syndrome. None of the patients were remarked upon as having any particular HLA-DR associated with the development of antibiotic refractory Lyme arthritis - or any potential marker for post Lyme disease syndrome.<br />
<br />
If patients have been symptom-free between episodes, this suggests that early treatment aborted the possibility of more serious infection, that patients had a genetic background which made it less likely they would develop antibiotic refractory Lyme arthritis, and/or perhaps early treatment in this small group led to avoidance of post Lyme disease syndrome as well.<br />
<br />
<b><u>Things I Ponder:</u></b><br />
<br />
<ul>
<li>The good news: If the results of this study can be extrapolated to a larger patient base, early treatment of Lyme disease as soon as one sees a new EM rash is more likely to lead to a positive outcome for the patient. </li>
<li>The bad news: This study says nothing about patients who either neither see a tick bite nor get a rash yet begin show other clinical signs of Lyme disease. Doctors have no easy way of diagnosing these patients and current IDSA guidelines do not cover management of such patients.</li>
<li>Patients were treated during early to early disseminated infection, when they were most likely to have a positive outcome from antibiotic treatment regardless of the genotype found in their samples.</li>
<li>There is no information provided about the health and quality of life of enrolled patients. Do they have any preexisting conditions? Have they ever been diagnosed with any condition with symptoms which overlap with those of Lyme disease? How does one make the distinction between these conditions and any symptoms associated with any stage of Lyme disease outside of an EM rash?</li>
<li>The timing, method, and duration of antibiotic treatment for each patient for each episode was not disclosed. Did all patients receive a course of oral doxycycline, or did some with more disseminated infections receive IV Ceftriaxone? This could have an impact on having a positive post-treatment outcome.</li>
<li>Regardless of which treatment patients received, how can family and urgent care doctors apply the data from this study to their practice? Hopefully they will see an EM rash and treat patients immediately, but unfortunately this does not always happen in clinical practice as not all EM rashes are properly diagnosed. (e.g. ringworm, eczema, etc.)</li>
<li>If infections had advanced past the early stage, I wonder which genotypes would have been found in other sample types had they been taken (synovial, CSF, other tissues). Would they have matched earlier research in previous papers or would they have been different?</li>
<li>Over time, is there a change in the kind of genotypes which infect human hosts? Do these genotypes have a "competitive" nature? How much lateral gene transfer occurs? </li>
<li>This study applies to the northeastern United States and to infections from Ixodes <i>scapularis</i> ticks. It does not apply to tick bites from Lone Star ticks, which are beginning to outnumber Ixodes <i>scapularis</i> ticks in some areas of the northeast and may carry different infections.</li>
<li>The public needs to be reminded that different ticks can carry different infections and look for other symptoms of those which may not be EM rashes.</li>
<li> Babesiosis and Rocky Mountain Spotted Fever are two other infection which come to mind where prompt treatment is necessary.</li>
</ul>
Well, this is what came to mind after reading this study. <br />
<br />
Any questions? Comments?<br />
<br />
Next up: Reviewing Dr. Steere's accompanying editorial...<br />
<br />
<b><u>Citations:</u></b><br />
1) Dr. Jorge Benach. Presenting at SB Southampton Dean's Lecture Series. Video posted Apr. 20, 2010. <a href="http://www.youtube.com/watch?v=TR-aY_S8q2E">http://www.youtube.com/watch?v=TR-aY_S8q2E</a> Approximate Timestamp: 40:20. "Multiple EM rash is sign of disseminated Lyme disease and requires IV or parenteral antibiotics." <br />
2) Columbia University Lyme and Tick-borne Diseases Research Center, <a href="http://columbia-lyme.org/patients/ld_lyme_symptoms.html">http://columbia-lyme.org/patients/ld_lyme_symptoms.html</a> Downloaded November 21, 2012.<br />
3) Strle K, Jones KL, Drouin EE, Li X, Steere AC. Borrelia burgdorferi RST1 (OspC Type A) Genotype Is Associated with Greater Inflammation and More Severe Lyme Disease. Am J Pathol. 2011 Jun;178(6):2726-39.<br />
4)Wormser GP, Brisson D, Liveris D, et al. Borrelia burgdorferi genotype predicts the capacity for hematogenous dissemination during early Lyme disease. J Infect Dis 2008;198:1358-1364<br />
5) Wormser GP, Liveris D, Nowakowski J, et al. Association of specific subtypes of Borrelia burgdorferi with hematogenous dissemination in early Lyme disease. J Infect Dis 1999;180:720-725<br />
6) Seinost G, Golde WT, Berger BW, et al. Infection with multiple strains of Borrelia burgdorferi sensu stricto in patients with Lyme disease. Arch Dermatol 1999;135:1329-1333<br />
7) Liveris D, Varde S, Iyer R, et al. Genetic diversity of Borrelia burgdorferi in Lyme disease patients as determined by culture versus direct PCR with clinical specimens. J Clin Microbiol 1999;37:565-569<br />
8) Jones KL, Glickstein LJ, Damle N, Sikand VK, McHugh G, Steere AC. Borrelia burgdorferi genetic markers and disseminated disease in patients with early Lyme disease. J Clin Microbiol 2006;44:4407-4413<br />
9) Wang IN, Dykhuizen DE, Qiu W, Dunn JJ, Bosler EM, Luft BJ. Genetic diversity of ospC in a local population of Borrelia burgdorferi sensu stricto. Genetics 1999;151:15-30<br />
10) Dykhuizen DE, Brisson D, Sandigursky S, et al. The propensity of different Borrelia burgdorferi sensu stricto genotypes to cause disseminated infections in humans. Am J Trop Med Hyg 2008;78:806-810<br />
11) Wei-Gang Qiu, John F. Bruno, William D. McCaig, Yun Xu, Ian Livey, Martin E. Schriefer, and Benjamin J. Luft. Wide Distribution of a High-Virulence Borrelia burgdorferi Clone in Europe and North America. Emerg Infect Dis. 2008 July; 14(7): 1097–1104.<br />
12) Strle K, Jones KL, Drouin EE, Li X, Steere AC. Analysis of Borrelia burgdorferi Genotypes in Patients with Lyme Arthritis: High Frequency of RST 1 Strains in Antibiotic-Refractory Arthritis. Am J Pathol. 2011 Jun;178(6):2726-39.<br />
13) Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2006;43:1089-1134<br />
<br />
<b><u>Additional Resources:</u></b><br />
<ul>
<li> An update on the diagnosis and treatment of early Lyme disease: "focusing on the bull's eye, you may miss the mark".<a href="http://www.ncbi.nlm.nih.gov/pubmed/17945460"></a></li>
<li>Detection of established virulence genes and plasmids to differentiate Borrelia burgdorferi strains. <a href="http://iai.asm.org/content/early/2012/01/23/IAI.06326-11.short">http://iai.asm.org/content/early/2012/01/23/IAI.06326-11.short</a></li>
<li>Crowder CD, Matthews HE, Schutzer S, et al. Genotypic variation and mixtures of Lyme Borrelia in Ixodes ticks from North America and Europe. PLoS One 2010;5:e10650-e10650. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0010650">http://www.plosone.org/article/info:doi/10.1371/journal.pone.0010650</a></li>
<li>Whole-genome sequences of thirteen isolates of Borrelia burgdorferi.<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3028687/"> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3028687/</a></li>
<li>Blog entry: <a href="http://campother.blogspot.com/2012/05/lets-not-be-rash-about-erythema-migrans.html">Let's Not Be Rash About Erythema Migrans<br />
<br />
<br />
</a> </li>
<div align="center">
<!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a> <small>
This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons Attribution-</a></small>
<small>NonCommercial-ShareAlike 3.0 Unported License.</small></div>
</ul>
Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com1tag:blogger.com,1999:blog-4073397588746430486.post-62681747736613493802012-11-19T09:54:00.000-10:002012-11-19T10:10:55.797-10:00CO Comments on "The Pseudoscience of Chronic Lyme"<div align="clear:both" class="separator" text-align:="text-align:"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgEvAw1ijA4bPkmx7_NwYTdns9dniNfWFLpYokBpkj2suvah08K6u5ZKBnshogzRQHbsPDN1Rff2QdMGShxcZZuaPwJiu_MT17WjXh3h4tcNbFMZSuahQsx3w0KLyVnkO7E1v-ePC577UZr/s1600/Lymebite.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgEvAw1ijA4bPkmx7_NwYTdns9dniNfWFLpYokBpkj2suvah08K6u5ZKBnshogzRQHbsPDN1Rff2QdMGShxcZZuaPwJiu_MT17WjXh3h4tcNbFMZSuahQsx3w0KLyVnkO7E1v-ePC577UZr/s1600/Lymebite.png" /></a></div>During the weekend, Ed Yong, who writes for <i>Discover</i> magazine's <a href="http://blogs.discovermagazine.com/notrocketscience/">Not Exactly Rocket Science</a> blog, of alerted me on Twitter to Cassandra Willyard's blog post on The Last Word on Nothing blog - <a href="http://www.lastwordonnothing.com/2012/11/16/the-pseudoscience-of-chronic-lyme/">"The Pseudoscience of Chronic Lyme"</a>. Not wanting to pass up the opportunity to comment on some journalists' bungling of how to interpret the significance of the <i>New England Journal of Medicine</i> (NEJM) published study, <i>Differentiation of Reinfection from Relapse in Recurrent Lyme Disease</i>, I decided to stop by and read what Cassandra and others had to say and leave a few comments.<br />
<br />
So far, commenters are asking good questions and pointing out some logical oversights in what we have read, which is constructive. <br />
<br />
I don't know that I recommend it for casual reading for a number of chronic Lyme disease patients, though - particularly if you are in a headspace where you are currently very angry about your condition being treated dismissively and can't hold up to reading anything which is skeptical about the existence of chronic Lyme disease. But I will say that if you can handle it, it might be worth it to stop by and periodically read the comments.<br />
<br />
So far, I've left two comments on Cassandra's blog in response to her original post and another commenter:<br />
<br />
<blockquote>"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.<br />
<br />
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.”<br />
<br />
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.<br />
<br />
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.<br />
<br />
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.)<br />
<br />
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.<br />
<br />
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: <a href="http://spirochetesunwound.blogspot.com/2012/11/inflammatory-spirochete-debris-left.html">http://spirochetesunwound.blogspot.com/2012/11/inflammatory-spirochete-debris-left.html</a><br />
<br />
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.<br />
<br />
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.<br />
<br />
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."</blockquote><br />
And the second comment:<br />
<br />
<blockquote>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.<br />
<br />
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.<br />
<br />
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.<br />
<br />
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.<br />
<br />
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)<br />
<br />
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.<br />
(Serology might help – but you have to suspect Lyme disease first.)<br />
<br />
(As an aside, you might want to check out this discussion on Lymenet Europe: <a href="http://www.lymeneteurope.org/forum/viewtopic.php?f=6&t=3856">http://www.lymeneteurope.org/forum/viewtopic.php?f=6&t=3856</a> – if only because of the references offered.)<br />
<br />
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?</blockquote><br />
* That should have been "joint" tissue, not "tendon".<br />
<br />
When I wrote these comments for their intended audience, my goal was to focus on what by their standards would currently count as evidence they relied on in order to focus on the relevance of erythema rashes in infection. I avoided discussion of other issues I could have gotten into - such as the accuracy of early serological testing and differences in antibody response during infection - because my focused comment was already long and thought these topics were not as closely related.<br />
<br />
One thing that has changed between the time I posted these comments and now: I now have a copy of the full text of the NEJM reinfection paper. So I am in the process of reading it, examining the data, and seeing how the authors correlate their findings with chronic Lyme disease. More later...<br />
<br />
<u>Edited to Add</u>: When I talk about being skeptical about there being "sides" to the debate, what I am really meaning to say is that while two sides have developed over time, the only side that really matters is the truth.<br />
<br />
<div align="center"><!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com0tag:blogger.com,1999:blog-4073397588746430486.post-2050727297367948122012-11-15T18:42:00.002-10:002012-11-16T15:54:48.847-10:00Do Not Conflate Reinfection With Absence Of A Chronic Condition<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhEOotLQkK0TmW8YDUlOwjyT2M2jcvdnyxPDi0zjxLJop-v9R34LEQZjz23kDHK0ghQq2y49PRC60a_IXhSizSFbQZO1SnUjaHACxB2XwtS-cuSySgXJRc3eMVras0Tq2CNhT2-nQBTsq-v/s1600/xkcd_duty_calls.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhEOotLQkK0TmW8YDUlOwjyT2M2jcvdnyxPDi0zjxLJop-v9R34LEQZjz23kDHK0ghQq2y49PRC60a_IXhSizSFbQZO1SnUjaHACxB2XwtS-cuSySgXJRc3eMVras0Tq2CNhT2-nQBTsq-v/s320/xkcd_duty_calls.png" width="290" /></a></div><br />
It's been a busy day for Lyme disease in the media today. And for me, too, as I have been trying to do some education (translation: damage control) regarding the inaccuracies which were reported concerning the findings from small study on Lyme disease that was recently published in the <i><a href="http://www.nejm.org/doi/full/10.1056/NEJMoa1114362?query=featured_home">New England Journal of Medicine</a></i> (summary only; full text behind pay wall). <br />
<br />
With a sample size of 17 participants, the study advanced the idea that most patients who have new erythema migrans (also called "bull's eye") rashes have been reinfected and do not have a previous relapsing infection. Bacteria sampled from the new rashes and run through PCR do not match bacteria from old rashes from a previous infection - therefore, patients have been reinfected. <br />
<br />
In and of itself, these findings are not problematic. And they make sense, knowing what is known about EM rashes and immune responses to Borrelia <i>burgdorferi</i>. It is only one small study, and I don't see it as earth shattering nor does it tell anyone everything there is to know about Lyme disease. <br />
<br />
But what follows <i>is</i> problematic: A number of online news articles stated that this outcome provides evidence that Chronic Lyme Disease and (unwittingly, in some cases either implied or by extension) Post Lyme Disease Syndrome <i>do not exist</i>.<br />
<br />
Now, while most Lyme disease patients with persisting symptoms support a chronic infection model, there may be some people who develop an autoimmune condition such as Post Lyme Disease Syndrome due to having had Lyme disease. I simply don't know, and think more research is required on this subject. But either way, the conflation of this small study's findings with the nonexistence of a chronic condition is erroneous. <br />
<br />
Even by the IDSA's standards, some interpretations of Dr. Allen Steere's editorial which accompanied the study (<a href="http://blogs.nejm.org/now/index.php/supervillain-or-drama-queen-differentiation-of-reinfection-from-relapse-in-recurrent-lyme-disease/2012/11/14/">briefly blogged about here on the NEJM</a>) seemed to get it wrong. On one hand, Dr. Steere acknowledges persisting symptoms and he states that "infection-induced autoimmunity, retained spirochetal antigens, or both may play a role in this outcome." And on another, a number of journalists seemed to gloss over this statement and not mention it - alongside stating or implying that a new, acute infection is the <i>only</i> reason patients get ongoing or new symptoms.(<i>Um, late stage untreated neuroborreliosis, anyone? Coinfections? These things can happen on occasion...</i>)<br />
<br />
This is incorrect, and so I've tried to correct this inaccuracy in reporting by responding to media outlets online. I've spent a good part of today looking online for articles which I could respond to about this issue, and noted that several news outlets and online magazines either do not allow comments on posts related to this topic or require one to post comments using Facebook and other services which not everyone uses. But I posted to as many places as I could, and wrote more or less the following comment in most locations:<br />
<br />
<blockquote>"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.<br />
<br />
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.<br />
<br />
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.<br />
<br />
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.<br />
<br />
One study like this is not enough to set the course for Lyme disease, which is an emerging infectious disease which requires more research."</blockquote><br />
In other words, as it bears repeating: <i>The rash is not the disease.</i><br />
<br />
I really don't know what else I can say in response to these articles. I've made my point where I can, short of writing letters to the editor. <br />
<br />
Other than this, of course, I recommend responding in your own way to these articles online and cite research that has been published or is currently in progress on Chronic Lyme Disease, Post Lyme Disease Syndrome, or both. And if you're a patient, inform people about the science that is out there and let them know you are in the 10-20% of patients who has persisting symptoms after initial infection with Lyme disease. <i>You exist. Your condition is real.</i><br />
<br />
<div align="center"><!-- Creative Commons License for Camp Other at http://campother.blogspot.com/ --> <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license"><img alt="Creative Commons License" src="http://i.creativecommons.org/l/by-nc-sa/3.0/88x31.png" style="border-width: 0;" /></a><br />
<small>This <span href="http://purl.org/dc/dcmitype/Text" rel="dct:type" xmlns:dct="http://purl.org/dc/terms/">work</span> by <a href="http://campother.blogspot.com/" property="cc:attributionName" rel="cc:attributionURL" xmlns:cc="http://creativecommons.org/ns#">Camp Other</a> is licensed under a <a href="http://creativecommons.org/licenses/by-nc-sa/3.0/" rel="license">Creative Commons<br />
Attribution-NonCommercial-ShareAlike 3.0 Unported License</a>.</small></div>Camp Otherhttp://www.blogger.com/profile/10224408965529778101noreply@blogger.com4