Friday, October 28, 2011

6 ILADS 2011 Conference

I was kinda expecting that at some point, this sign would show up on my feed:


No Burrascano. Missed part of Maloney. Horowitz was also MIA. Only got to see part of Jones, as I'd already taken a coffee break.

Maybe tomorrow will be better if I can haul myself out of bed early on a Saturday... If.

More on this event in the future - especially if there is more to see.


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Tuesday, October 25, 2011

0 Stony Brook Young Investigators Series On Lyme Disease

Ixodus ticks that carry B.burgdorferi.
Photo Credit: http://www.freewebs.com/
lymeandautism/GF-596-4ticks_cm.jpg
Stony Brook University has an online journal of science called The Young Investigators where students from the school write an in-depth article with citations on different topics.

Nadya Peresleni, Editor in Chief of the journal and undergraduate class of 2011, wrote a report on Lyme disease that I think is pretty good - it's detailed, touches upon the controversy over treatment in a matter-of-fact manner, describes the immunological and inflammatory aspects of the infection, and leaves some ideas about areas to target for future treatment options.

I found this paragraph to be of interest, and there is much more in the article that is good to read:
"Along with Dr. Benach's work, the laboratory of Professor Martha B. Furie has published on the role of interferon-gamma (IFN-γ), a cell-signaling molecule of the immune system, in the endothelial tissue of a genetically engineered mouse model that was infected with B. burgdorferi. 
"IFN-γ is like a molecular switch that turns on chronic inflammation," explained Dr. Furie. When the bacteria disseminate throughout the body after the tick bite, they activate the endothelium and begin the inflammatory process by attracting T lymphocytes that secrete IFN-γ [22]. The inflammation was found to be due, in large part, to a synergistic effect of B. burgdorferi and IFN-γ, which together activate the transcription of a series of genes in endothelial cells. These genes encode chemokines, or chemoattractants, specific for T lymphocytes. 
Interestingly, there seemed to be selection for those T lymphocytes that secreted more IFN-γ, and the result was a positive feedback loop that generated more and more IFN-γ, leading to a state of chronic inflammation in the tissue. The damage to human tissues is likely caused by the body's reaction to the bacteria, not the bacteria themselves [22]."

Yes, but the question remains as to whether the damage left behind is causing symptoms - or if the inflammation is caused by bacteria which are still viable is part of the problem... Or both.

This article mentions persistent infection and offers citations to examples - and it also mentions the above kind of mechanism for producing symptoms.

Check out the entire article here: http://www.younginvestigators.com/article-lyme-disease-overview.php


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0 News: New Molecular Test Could Detect Early Lyme Disease

The Guardian has written about a new molecular test using nanoparticles which was developed by Alessandra Luchini, of George Mason University, to initially detect cancers. The new test is being used in clinical trials to detect early Lyme disease - even if there is no rash present in the infected patient.

Excerpt that will be of interest to readers:
"Q: In years to come, is this something that could be available in hospitals? 
That's the hope we have. The first clinical trial is on the detection of Lyme disease. A fraction of patients get a skin rash but for those without the rash it is very difficult to diagnose. So with the particles we are able to capture the antigens that come from the spirochaete that is the causative agent of Lyme disease. If we see in the urine a piece of the bacteria of the spirochaete, we are sure that the patient has Lyme disease. We are gathering all the evidence and then we will need to go first for FDA approval before it is available in clinics. 
Q: How much earlier will you be able to detect Lyme disease? 
Lyme disease has a window of two to three weeks before seroconversion [production of antibodies in the host blood, indicating infection]. With our tests, we're able to detect it before seroconversion, because we're not looking for the antibodies, we just look for the spirochaete. I would say here, yes, by weeks, and earlier diagnosis would be beneficial for the prognosis."
Comment: One thing this does make me wonder about is how similar this test is to Temple Douglas' hydrogel nanoparticle test for early detection of Lyme disease. Maybe it's time to do a compare and contrast of patent application content?

MORE here at the link: http://www.guardian.co.uk/technology/2011/oct/23/bright-idea-nanoparticle-trap-cancer

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0 News: Antibiotic Shortages Affect Patients

This just in from the Internal Medicine website: Antimicrobial Shortages Affect Patient Quality.

For those who are treating tickborne illnesses, this excerpt may be particularly of importance to you:

"The drugs reported most frequently to be unavailable or in short supply include the intravenous formulation of trimethoprim/sulfamethoxazole (Bactrim), amikacin (Amikin), aztreonam (Azactam), foscarnet (Foscavir), and penicillin G."

Other drugs are listed as well, of which the shortage will affect many people this flu season as one of them is Tamiflu.

(Now would be a good time for more startups to invest in not only antibiotic drug development, but phage therapy as well.)

MORE on how patients have been affected and why this is happening can be found at the link: http://www.internalmedicinenews.com/newsletter/conference-coverage/singleview40841/id-docs-antimicrobial-shortages-threaten-patient-care-quality/802aeb528c.html

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Thursday, October 20, 2011

0 Where Have All The Sane Lyme Patients Gone?

Here is an exchange I've seen elsewhere on the internet, names removed to place more focus on the content:

Do you think that morgellons stuff is a joke? Or lida mattman saying that Lyme can be transmitted by doorknobs and pens? Or that every sample she's ever seen shows Lyme?

No, those who put forth these theories are not joking. And no, I do NOT believe these things. And YES, I think they are damaging.

there are minions ready to believe anything.

This is true --patients who remain ill and find themselves fighting mainstream treatment guidelines have become angry and confused, and almost anything sometimes seems possible to them. They lack the scientific/medical background to distinguish.

Sober? Maybe. Not when they insist that mcsweegan is poisioning their well water though. I've heard some crazy stuff.

This is an old story. Let's move on. The baton has passed.

More sober and savvy than most people who have ever posted here? Sure. But that is like saying that they see and hear better than Helen Keller.

Many times people work behind the scenes because of forums like sci.med, which have gotten issues so knotted and confused.

I know some people with Lyme who aren't extremists. But they're few and far between.

Define extremist: In some circles, simply believing the cure didn't take after 28 days doxy is considered extreme. I find that if I talk to people logically and rationally they can respond in kind. Most people I have met in Lyme are turned off by the outrageous antics of the most notorious protagonists here, and I will not name the names. I don't know who you have met --but those I speak to, while sometimes empathetic, are NOT marching in line with a RICO lawsuit.

I've seen more than one "llmd" and waited in their waiting rooms with other lyme patients and heard them start talking or started talking with them. They're "informed" but don't seem to distinguish between what is good information and what isn't.

They are very confused by the situation --but the confusion starts with what medicine has handed down to them, not with the patients. If you create an artifactual disease that people don't have, then the patients who don't fit your model might be accused of factitious illness. It's a very frustrating situation for patients. The psychopathology starts with medicine, and patients are caught up and then labelled pathological, themselves. It is one of those Freudian boxes --the patients find there is no way out.

I don't see a lot of rationality anywhere.

It's hard to be rational in the face of an irrational situation that predated your involvement.

I don't think that two wrongs make a right and that rigid academic experts views are "balanced" by the views here.

Of course I do not believe this --I am simply saying that extremism begets extremism. I hold to my view that the dysfunction in Lyme was kicked off by biomedicine and not by patients.

It is just as easy to conclude that both are wrong and that maybe the "truth" is somewhere in between. Or nowhere in between but somewhere else entirely.

You must resolve dysfunction before you attempt to learn the truth.

I think you're glossing over things. Let's say you reject what the  academics say. Why does that mean that you have to buy into what Lida Mattman says?

I don't buy into what Mattman says. And nor do I reject academic research --some of what the academics say is right-on. But some of them have misused their craft and trampled the scientific method (perhaps unwittingly) in the process creating an unduly restrictive disease definition, discarding or twisting data, and spawning an untenable, dysfunctional situation out in the field. Most patients who appear dysfunctional once they get to Lyme were perfectly functional before --it is the scene and the situation --the disturbing dissonance between patient experience and medical paradigm-- that is at fault.

Rejecting the false negatives on elisa or western blot doesn't mean accepting a specific Lyme speciality lab's test results does it?

we don't need to keep debating this --of course not.

Have Lyme patients made things better?

Sadly things have not gotten better, but worse, IMO.

So you didn't answer the question. Where have all the sane Lyme patients gone?  Where is the forum, in real life or on the internet where I can find them? Where do they dominate? Where is rationality revered over reactionary radicalism?

I have met many MANY sane Lyme disease patients. I am sorry you have not. They are everywhere.

Lyme patients are fully to blame for how they've responded to the medical establishment.

Lyme patients are between a rock and a hard place --they have been dismantled, dismissed, and made fun of; they have been misdiagnosed for so long they develop chronic illness when they could have been totally cured. Lyme patients are angry. But they have not often strategized well in the past, I'll grant you that.

It's been a very bad confluence of situations and personalities all around, I'm afraid. It is, in short, a disaster: But if you don't look to what has transpired in medicine and science to stanch out the dysfunction, you will be spinning your wheels to the end of time. Should Lyme patients do a better job of achieving this? Yes of course.



And another comment from a Chronic Lyme Disease patient seen elsewhere, from someone who reminds me of LymeEngima (but was not identified as such):

"I have Chronic Lyme and I hated the movie “Under Our Skin”.  All it did was try and instill panic in people who are already sick and vulnerable to making desperate choices.  [...]
The IDSA Guidelines scare me. The doctors who treat Lyme scare me. The treatments scare me and the fear and anger around the whole subject scares me. Nothing about Lyme resembles even handed scientific principles and more closely resemble hysteria."

Comments such as this are rare to come by online. Few Lyme disease patients have said anything negative about UOS or admitted that everything about Lyme disease scares them.



These comments are a prelude to my own post about why and how dealing with Lyme disease drives me crazy, so I put them here for review and discussion.

Any thoughts from those of you reading along?

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Tuesday, October 18, 2011

0 Abstract: European neuroborreliosis: neuropsychological findings 30 months post-treatment.

European neuroborreliosis: neuropsychological findings 30 months post-treatment.
Eikeland, R., Ljøstad, U, Mygland, Å., Herlofson, K., Løhaugen, G. C.
European Journal of Neurology.1468-1331.
http://dx.doi.org/10.1111/j.1468-1331.2011.03563.x

Background:  The aim of this study was to compare neuropsychological (NP) functioning in patients with Lyme neuroborreliosis (LNB) 30 months after treatment to matched controls.

Methods:  We tested 50 patients with LNB and 50 controls with the trail-making test (TMT), Stroop test, digit symbol test, and California Verbal Learning test (CVLT). A global NP sumscore was calculated to express the number of low scores on 23 NP subtasks.

Results:  Mean scores were lower amongst LNB-treated patients than amongst controls on tasks assessing attention/executive functions: (Stroop test 4: 77.6 vs. 67.0, P = 0.015), response/processing speed (TMT 5: 23.4 vs. 19.2, P = 0.004), visual memory (digit symbol recall: 6.6 vs. 7.2, P = 0.038), and verbal memory (CVLT list B: 4.68 vs. 5.50, P = 0.003). The proportion of patients and controls with NP sumscores within one SD from the mean in the control group (defined as normal) and between one and two SD (defined as deficit) were similar, but more LNB-treated patients than controls had a sumscore more than two SD from the mean (defined as impairment) (8 vs. 1, P = 0.014). Conclusions: As a group, LNB-treated patients scored lower on four NP subtasks assessing processing speed, visual and verbal memory, and executive/attention functions, as compared to matched controls. The distribution of NP dysfunctions indicates that most LNB-treated patients perform comparable to controls, whilst a small subgroup have a debilitating long-term course with cognitive problems.



Questions to consider:


1) If one did a protein study of the CSF between those in the small subgroup having a debilitating long-term course with cognitive problems and the rest of the neuroborreliosis group, would differences be found between samples?

2) What was the difference in scoring in this most affected subgroup compared to the other patients who had neuroborreliosis?

3) Is there research which uses the same methods and compares pre- and post-treatment neuroborreliosis patients?


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1 Chalcolithic Iceman Had Lyme Disease Over 5,000 Years Ago

Ötzi, The Iceman, Cometh...

Thanks goes out to Joanne, from the Looking At Lyme Disease blog for posting about an article from National Geographic on the Iceman, a mummified man who had died over 5,000 years ago and has been a treasure trove of information for scientists ever since.

The original article is found here:

Iceman Autopsy - Unfrozen: There was only one way scientists could unlock the mystery of the famous Iceman. Take away his ice.


Source Link:
http://ngm.nationalgeographic.com/2011/11/iceman-autopsy/hall-text

The entire article outlines the process of extracting and examining tissues and food from within the mummy - an interesting read in itself. But the part that will stand out for Lyme disease patients is this bit:
"Perhaps most surprising, researchers found the genetic footprint of bacteria known as Borrelia burgdorferi in his DNA—making the Iceman the earliest known human infected by the bug that causes Lyme disease."
It would be interesting to know exactly which Borrelia burgdorferi strain was found and in which tissue sample(s) it was found.

And reflecting on this, this indicates that Borrelia burgdorferi has been around for a long time and in Europe for a long time.

More Information On The Iceman:
http://en.wikipedia.org/wiki/%C3%96tzi_the_Iceman

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Friday, October 14, 2011

1 Reader Mail Bag: What Lyme Disease Research Is Needed?

A reader, Misty, recently commented on my request for topics for discussion this week:

"I like all your ideas for topics - and hope you'll be able to continue posting. I love your "blog - it is one of the most sane Lyme sites on the web, if not the most sane and balanced.

What I wonder is - do we have enough information and diagnostic tools to be able to design useful studies on Lyme?

- we can't tell reliably who has it or doesn't
- the manifestations of Lyme in each person can be different and based on complications of co-infections and the genetic predisposition of the person to exaggerated inflammatory response
- then there is the pesky post-Lyme-Syndrome/Chronic Lyme issue of whether there is infection or post-infection inflammation

So, you may have covered it already, but I am interested in hearing about ideas for scientific studies - where is the research most needed?"

thanks,
misty

Well, Misty, addressing your questions and points:

I think we can design useful studies on Lyme disease even without being capable of accurately testing every patient who has Lyme disease. Improving serological testing and being able to accurately assess whether one has or does not have Lyme disease at present are only two pieces of the bigger picture, and there are more angles from which to approach the Lyme disease problem.

Research that can be useful in gaining a better understanding of what Borrelia burgdorferi and other Borrelia do is important to understanding how to effectively diagnose and treat infection and perhaps distinguish between patients who are affected by Lyme disease and those who are affected by a different condition.

Here's a few ideas I have on what to consider for further study:

1) Do a comparative study which looks at the proteins in the CSF of patients with chronic Lyme disease versus patients with late stage untreated and patients with acute Lyme disease.

Earlier this year, we've seen the study where hundreds of proteins were found in the CSF of patients with post-treatment Lyme disease symptoms and compared against patients with Chronic Fatigue Syndrome. The protein profile for each group was different, and each group's profile differed from healthy controls.

Let's take this study one step further, and see if there is a protein profile that distinguishes between patients who were designated as suffering from post-treatment Lyme disease symptoms and those who are  late stage and newly infected.

The outcome of this study may shed some light on what markers are present for different stages of the disease. Having different markers for different stages of the disease may help guide better test research and development.

References:
Steven E. Schutzer, Thomas E. Angel, Tao Liu, Athena A. Schepmoes, Therese R. Clauss, Joshua N. Adkins, David G. Camp II, Bart K. Holland, Jonas Bergquist, Patricia K. Coyle, Richard D. Smith, Brian A. Fallon, Benjamin H. Natelson. Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome. PLoS ONE 6(2): e17287. doi:10.1371/journal.pone.0017287 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017287

2) Conduct longer term in vivo GFP and/or iRFP studies on mice and other mammals.

In this GFP protein study on mice, spirochetes' motion was monitored in vivo rather than in vitro (go to link to watch video of spirochetes attaching to endothelial walls). Rather than study it for as short a period of time as was done, a longer time frame for study as well as multiple studies over time in the same hosts would be educational.

With longer term imaging, one can see if spirochetes become intracellular and for how long. One can see which parts of the body they travel to and see them hide in immunological niches. One can see how likely different strains are to enter the CNS and how quickly they enter the CNS post-inoculation. (We already know specific strains are more neurotropic than others, but how serious a problem is this for the host? Does it depend on the host animal?)

Perhaps a GFP or iRFP study on mice could also be combined with an antibiotic treatment study. If we can trace the activity and polymorphic state of spirochetes in vivo, then we can see if antibiotics of specific types can affect "cyst"-like forms of spirochetes in vivo, too.

3) Repeat Klempner intracellular studies with a longer observation time and longer ceftriaxone infusion.

Also - give two weeks' ceftriaxone then provide no treatment for a few months. Try a different duration of ceftriaxone. Recheck the host animal for signs of infection at 3 months, 6 months, a year, then two years.

How can an in vivo study of this issue be completed?

References:
Kostis Georgilis, Monica Peacocke, and Mark S. Klempner. Fibroblasts Protect the Lyme Disease Spirochete, Borrelia burgdorferi, from Ceftriaxone In Vitro. Journal of Infectious Diseases. Vol. 166, pp. 440-444. 1992.
Mark S. Klempner, Richard Noring and Rick A. Rogers. Invasion of Human Skin Fibroblasts by the Lyme Disease Spirochete, Borrelia burgdorferi. The Journal of Infectious Diseases. Vol. 167, No. 5 pp. 1074-1081. May 1993. http://www.jstor.org/pss/30112679

4) Use new maltodextrin enhanced imaging study in animal subjects (and later people) to see where bacteria is.

This is a very new imaging method, but the advantages are clear: Maltodextrin is viewed by pathogenic bacteria as food, whereas regular mammalian cells (human, mouse, other) and even commensal or friendly bacteria in the gut do not view maltodextrin as food and they work to eliminate it.

With the addition of a maltodextrin contrast agent, one should be able to see where pathogenic bacteria are present in the body in vivo and do so safely.

And there's more:
"In experiments using a rat model, the researchers found that the contrast agent accumulated in bacteria-infected tissues, but was efficiently cleared from uninfected tissues. They saw a 42-fold increase in fluorescence intensity between bacterial infected and uninfected tissues. However, the contrast agent did not accumulate in the healthy bacterial microflora located in the intestines. Because systemically administered glucose molecules cannot access the interior of the intestines, the bacteria located there never came into contact with the probe. 
They also found that the probes could detect as few as one million viable bacteria cells. Current contrast agents for imaging bacteria require at least 100 million bacteria, according to the researchers. 
In another experiment, the researchers found that the maltodextrin-based probes could distinguish between bacterial infections and inflammation with high specificity. Tissues infected with E. coli bacteria exhibited a 17-fold increase in fluorescence intensity when compared with inflamed tissues that were not infected."
All of these items in bold are of particular interest to those wishing to see where Borrelia burgdorferi is present during infection. If - as a number of researchers have stated - Borrelia burgdorferi are actually low in number and produce high amounts of inflammation in tissues, maltodextrin contrast should be able to confirm this finding. We'd also have a better idea of where the bacteria is in vivo without having to do a tissue biopsy, and be able to detect biofilms if any have formed.

Initial studies should be conducted on animal models, and if proven safe and effective, I see no reason why human studies wouldn't follow.

References:
Xinghai Ning, Seungjun Lee, Zhirui Wang, Dongin Kim, Bryan Stubblefield, Eric Gilbert, Niren Murthy.Maltodextrin-based imaging probes detect bacteria in vivo with high sensitivity and specificity. Nature Materials, 2011; DOI: 10.1038/nmat3074
Scientific American: http://blogs.scientificamerican.com/lab-rat/2011/07/25/making-bacteria-visible/
Science Daily: http://www.sciencedaily.com/releases/2011/07/110718121605.htm
Nature: http://www.nature.com/nmat/journal/v10/n8/full/nmat3074.html

5) Complete more treatment studies on patients with documented late stage Lyme disease and coinfections such as Ehrlichiosis and Babesiosis.

If it's problematic to differentiate between those who suffer from a chronic, persisting infection and those who suffer from an autoimmune disorder, then circumvent the issue by finding people who are truly late stage, untreated Lyme disease patients who have coinfections and study how long it takes for them to get well on combination treatments.

Many Lyme patient activists promote more studies for those of us suffering from persistent post-treatment symptoms when perhaps it is more advantageous to first push for the study of patients who have never been treated and have evidence of late stage symptoms. There are far more studies on acutely infected patients than there are on late stage patients, and this needs to be addressed, I think, in order to bridge the gap between acute cases and post-treatment cases (chronic Lyme; PLDS) and work past any controversy.

6) Run comparative studies on all labs which conduct Lyme disease tests - C6/ELISA and Western Blot IgM and IgG.

Test all existing labs for sensitivity and specificity for various strains including Borrelia lonestari and miyamotoi - include the relapsing fever Borrelias. It would be informative to know how all the labs perform and why they receive the results they do.

These are just some of the ideas I have on studies which could be conducted that give us more answers.

Regardless of these suggestions, one has to be aware of the limitations of using animal studies to model what happens in human infection. For one thing,  even non-human primate studies may not show evidence of a Borrelia burgdorferi brain infection, even with an N40 strain of Bb which is neurotropic. For another, mice do not get brain infections and are thus a poor model for studying neuroborreliosis.

References:
Ramesh, G., Borda, J., Dufour, J., Kaushal, D., Ramamoorthy, R., Lackner, A., & Philipp, M. (2008). Interaction of the Lyme Disease Spirochete Borrelia burgdorferi with Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosis. American Journal Of Pathology, 173 (5), 1415-1427 DOI: 10.2353/ajpath.2008.080483
Diego Cadavid, Tim O'Neill, Henry Schaefer, and Andrew R. Pachner (2000). Localization of Borrelia burgdorferi in the Nervous System and Other Organs in a Nonhuman Primate Model of Lyme Disease.Laboratory Investigation, 80 (7), 1043-1054

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Sunday, October 9, 2011

0 Article: Equine Borreliosis


Came across this article on equine Borreliosis, "The State of Lyme Disease".

If you are a horse owner, it's important to know the common symptoms of equine Lyme disease: shifting leg lameness, myalgia (muscle pain), dermal hypersensitivity, behavior changes, weight loss, uveitis, and neurological signs.

Sounds similar to the symptoms that people get with Lyme disease.

An interesting point to be made in this article is about the value of retesting in horses:
"It is also difficult to determine response to treatment with serological testing, because B. burgdorferi antibody levels are known to persist for years in humans and are also apparently long-lived in horses. Retesting is suggested four to six months after treatment to see if there is a decrease in serological values. This retesting can be questionable in determining response to treatment because horses are likely to be exposed and possibly reinfected post-treatment if living in areas of high tick density."
So, is the implication here that a decrease in values on a blood test is sign of progress against the disease?

It's true that if the horse is exposed and reinfected post-treatment in an endemic area that having shown a long-lived antibody response from a previous infection makes a new test result less useful. At the same time, a horse could have been reinfected, so then one has to look at a clinical diagnosis based on symptoms for a diagnosis. This is another thing which is similar for people with Lyme disease.

Having a more solid direct detection test which could distinguish between an active infection and past infection would be excellent. What does it take to create a test like this for Lyme disease?

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Friday, October 7, 2011

4 Admin Update: Scavenger Hunt Extension, Vote On Topics, Busyness

To my readers:

Hope you have been having a decent week and that this weekend is a good one, too.

As for me... I have been either busy or markedly unwell during the past week and a half, thus the slow down in posting frequency here.

I think there's a correlation there, too: Any time I do not get enough rest and push a little more than I should, I end up paying for it.  This has been what has happened recently, and today I had a really hard time getting out of bed.

Hopefully this weekend will be better.

Lyme Disease Research Scavenger Hunt Announcement

Regarding the Lyme Disease Research Scavenger Hunt, I am giving participants an additional week. Please submit your entries for Round Three no later than next Friday, October 14th, 12 am Hawaiian Time.

After the 14th, if no entries have been submitted for Round Four, I will post the answers for both Round Three and Round Four.

I expect the game will have a few more rounds through November, at which point the winner will get to pick the topic of their choice related to Lyme disease and coinfections which I will hand illustrate.

Request For Feedback: Vote For One Of Next Week's Post Topics

I'm outlining some upcoming topics for new posts and would like to hear from feedback from you.

Which of the following are of the most interest to you? How would you rank them in order of importance?

  1. Why is (or isn't) neuroborreliosis a big problem?
  2. Commentary: Scientific rigor and providing evidence for chronic Lyme disease
  3. Commentary: Why (and how) contracting Lyme disease has driven me crazy
  4. Lyme disease animal studies
  5. Part 2:The Value of Anecdotal Evidence (Here's a link to Part 1.)
  6. Other: _________________ (topic YOU think is important to read about)

Keeping it simple for now, narrowing it down to these few choices.

Okay, I'm going to call it a night. I'm tired.

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The Camp Other Song Of The Month


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