Lyme disease, science, and society: Camp Other

Sunday, May 8, 2011

9 Abstract: Evaluation of in-vitro antibiotic susceptibility of Bb

I was recently asked about this study in comments, since there has been much discussion about this research in the Lyme disease patient community online:

Evaluation of in-vitro antibiotic susceptibility of different morphological forms of Borrelia burgdorferi

My opinion of it thus far is one of waiting and seeing - I'm not sure what to think yet and I'm waiting to hear more information... I'm guessing this is an initial publication of findings and a more detailed paper similar to Dr. Sapi's cancer research papers will be published in the near future.

Tinidazole
I have a number of questions and thoughts on it, and prior to this publication, I had the impression that tinidazole has helped a number of Lyme disease patients - but there has been limited research on it (See: Brorsons).

The Brorsons stated in their 2003 paper, An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole:

"Acridine orange staining, dark-field microscopy and transmission electron microscopy revealed that, when the concentration of TZ (Tinidazole) was ≥ MBC, the contents of the cysts were partly degraded, core structures did not develop inside the young cysts, and the amount of RNA in these cysts decreased significantly. When cysts were exposed to TZ, both the spirochetal structures and core structures inside the cysts dissolved, and the production of blebs was significantly reduced."

But I digress...

To take each question and thought about Dr. Sapi's latest paper by point:
"Three morphological forms of B. burgdorferi (spirochetes, round bodies, and biofilm-like colonies) were generated using novel culture methods."
Is there a description of these novel culture methods? Have they been through a process of verification and validation? How are they superior to other methods?

If different media is used other than BSK/BSK-H, it would be good to know if that affects the results in some fashion.
"Minimum inhibitory concentration and minimum bactericidal concentration of five antimicrobial agents (doxycycline, amoxicillin, tigecycline, metronidazole, and tinidazole) against spirochetal forms of B. burgdorferi were evaluated using the standard published microdilution technique."
What exactly were the concentrations?

It's important to know, and compare against other studies which have been done in vitro. Of all the literature I've read on this, standardization of these documented concentrations is lacking.

And to note: This was an in vitro test, not in vivo. Given everything that is known about Bb's behavior in vivo, in vitro tests will only give us part of the picture. More on that in a minute, below...
"The susceptibility of spirochetal and round body forms to the antibiotics was then tested using fluorescent microscopy (BacLight™ viability staining) and dark field microscopy (direct cell counting), and these results were compared with the microdilution technique. Qualitative and quantitative effects of the antibiotics against biofilm-like colonies were assessed using fluorescent microscopy and dark field microscopy, respectively."
How do these tests compare to one another relative to results found for each? How do the novel culture methods affect outcome relative to standard culture methods?

How is something biofilm-like, versus a biofilm?
"Doxycycline reduced spirochetal structures ~90% but increased the number of round body forms about twofold. Amoxicillin reduced spirochetal forms by ~85%–90% and round body forms by ~68%, while treatment with metronidazole led to reduction of spirochetal structures by ~90% and round body forms by ~80%. Tigecycline and tinidazole treatment reduced both spirochetal and round body forms by ~80%–90%."
This is interesting... Some of these results match earlier research findings on specific antibiotics used to treat Bb.

In 2008, Xiaohua Yang, Andrew Nguyen, Dan Qiu, and Ben Luft did some research on the effectiveness of tigecycline and doxycycline on Borrelia burgdorferi in vitro in In vitro activity of tigecycline against multiple strains of Borrelia burgdorferi: http://jac.oxfordjournals.org/content/63/4/709.short

In this abstract it was stated:

"Tigecycline inhibited the growth of and killed the organism more rapidly than doxycycline. Tigecycline was able to kill B. burgdorferi within 24 h at clinically achievable concentrations (> 1 mg/L). In contrast, doxycycline was bacteriostatic and required 48–72 h to achieve its maximal inhibitory effect. The anti-Borrelia activity of the antibiotics was tested against 20 different isolates from three species. Tigecycline was 16- to 1000-fold more active than doxycycline at immobilizing Borrelia for the 20 isolates tested."

The MIC versus the MBC is important to know, and it affects outcomes on a timeline.

Comparing Tigecycline to doxycycline sounds like comparing an axe to a thousand papercuts - the former is just going to be more immediately effective than the latter... And if Bb happens to disseminate rather quickly in an individual patient, there's a chance the doxycycline prescribed may not be enough to adequately treat the patient if you're going by this MIC - especially if one of Bb's strategies is to evade the immune system. (Let's not even get into how ineffective doxycycline is for prophylaxis for now...)

More recently, in 2010, Louis Ates, Christa Hanssen-Hübner, Douglas E. Norris, Dania Richter, Peter Kraiczy and Klaus-Peter Hunfeld conducted the study, Comparison of in vitro activities of tigecycline, doxycycline, and tetracycline against the spirochete Borrelia burgdorferi.

In their abstract they stated:

"The overall rank order of MIC90s was tigecycline (≤0.016 mg/L) > ceftriaxone (0.03 mg/L) > cefotaxime (≤0.125 mg/L) > doxycycline (0.25 mg/L) > tetracycline (0.25 mg/L). The rank order of MBC90s was tigecycline (0.5 mg/L) > ceftriaxone (2 mg/L) > tetracycline (16 mg/L) > doxycycline (16 mg/L) > cefotaxime (>16 mg/L).

High in vitro activity of the new glycylcycline against Borrelia was further substantiated by time-kill experiments performed with B. afzelii isolate EB1. Parallel testing of tigecycline and ceftriaxone demonstrated a bacteriostatic effect for 0.016 mg/L of tigecycline and for 0.03 mg/L for ceftriaxone after 72 h of incubation. Moreover, tigecycline was bactericidal at a concentration of 0.25 mg/L showing a > 3 log10 unit reduction of the initial inoculum, whereas for ceftriaxone a concentration of 2 mg/L was needed."

So as you can see in this earlier research, tigecycline is highly effective in vitro, and doxycycline is ranked much further down the list of effectiveness.

Stepping into our time machine again, and going back to 2004 to Klaus-Peter Hunfeld, Thomas A. Wichelhaus, Rebecca Rödel, Georg Acker, Volker Brade, and Peter Kraiczy's study, Comparison of In Vitro Activities of Ketolides, Macrolides, and an Azalide against the Spirochete Borrelia burgdorferi: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC310164/

Now this was measuring an entirely different group of antibiotics, with the following results:

"The ketolides were the most potent against borrelial isolates on a micrograms-per-milliliter basis. For all agents except cethromycin and telithromycin, the MIC at which 90% of isolates were inhibited (MIC90) and the MBC at which 90% of the isolates were killed were ≥0.01 μg/ml and > 0.25 μg/ml, respectively."

and

"In our study, the rank order of activity by classical macrolides and azalides against borreliae clearly corresponds to the effectiveness of these agents as revealed by in vitro susceptibility studies and clinical treatment trials to date (2, 4, 5, 7, 8, 9, 11, 23, 24), demonstrating higher in vitro effectiveness for azithromycin (MIC90, 0.0156 μg/ml) than for erythromycin (MIC90, 0.0625 μg/ml), roxitromycin (MIC90, 0.0625 μg/ml), and clarithromycin (MIC90, 0.0312 μg/ml). Median MICs of the different substances, however, tended to vary over a 10-fold range between individual strains, with the B. garinii isolate PSth and the B. afzelii isolate EB1 showing the highest MICs for both the classical macrolides and the ketolides."

So in this study, of the antibiotics looked at, ketolides were more effective than macrolides, and azithromycin was more effective than other macrolides.

We also see that MIC's are different for different European Bb isolates. More on that below, in another cited study.

And then they said this about treatment failure:

"Classical macrolides and azalides frequently fail in the therapy of early LD (7, 14, 17, 26), and clinical relapse has been observed following conclusion of treatment (14, 17, 26). Moreover, it has been speculated that resistance may develop in borreliae preexposed to erythromycin owing to resistant subpopulations (25). Based upon our findings, however, the ketolides were superior in vitro on a micrograms-per-milliliter basis when tested alongside classical macrolides under identical test conditions in BSK."

There are a number of studies out there showing that Borrelia burgdorferi can be antibiotic resistant, with some being erythromycin resistant. Because of this, it is critical for doctors to weigh the use of erythromycin in patients - especially pregnant women with Lyme disease - against the risks of another antibiotic which is more effective.

The surprising thing about Dr. Sapi's study, to me, is the part about amoxicillin being that effective at reducing both spirochetal and round body forms. I say this, because I thought earlier research points towards amoxicillin being a less effective treatment than doxycycline.

Did I miss something, though? I thought earlier research did not look at antibiotic impact on round body forms in general, though - other than the Brorsons' metronidazole and tinidazole research.

Image taken from Brosons' research, An in vitro study of the
susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole

But earlier research is out there which confirms the effectiveness of amoxicillin on Borrelia burgdorferi, and found in a 2003 publication, In Vitro Susceptibility Testing of Four Antibiotics against Borrelia burgdorferi: a Comparison of Results for the Three Genospecies Borrelia afzelii, Borrelia garinii, and Borrelia burgdorferi Sensu Stricto.

What's fascinating to note here, again, is that different isolates of Bb respond very differently to different antibiotics!

"In 7 out of 12 comparative evaluations (P  > 0.05), MBCs were significantly different among the three genospecies. B. garinii seemed to be especially susceptible to azithromycin, while amoxicillin had a significantly greater effect on B. burgdorferi sensu stricto compared to the other genospecies. Ceftriaxone had the lowest MBC with B. afzelii and increasingly higher MBCs with B. garinii and B. burgdorferi sensu stricto. Doxycycline did not show any remarkable differences in its effects on the three genospecies."

So amoxicillin apparently doesn't suck when it comes to treating Borrelia burgdorferi, but it's not as effective on the other genospecies. (C'mon, Dr. Luft, please get that test working so we know which Bb we have to treat it the most effectively right off the bat.)

If it is found in vivo that doxycycline creates round bodies that contribute to the spirochete's survival, then doxycycline - what is typically given to patients diagnosed early with Lyme disease - would be contraindicated.

Whether the round bodies are as relevant as a potential "stasis" of metabolism in Borrelia burgdorferi remains to be seen. Either way, in vivo findings are different from in vitro findings.

In vitro, tigecycline was said to be many times more powerful than other antibiotics in killing Borrelia burgdorferi...Yet as we can see from Barthold's experiments on mice, viable spirochetes are found after tigecycline treatment in vivo, and viable enough that they can be picked up by ticks and transmitted to a new host.

Is there any treatment which can be used that would ensure the destruction of these remaining spirochetes, and would their demise lead to the end of persisting symptoms in patients who have them - or would there be an ongoing immune dysregulation which was triggered by their existence which continues after they are all dead?

This is something I'd really like to see studied.

Getting back to the last bit of Dr. Sapi's paper...
"When quantitative effects on biofilm-like colonies were evaluated, the five antibiotics reduced formation of these colonies by only 30%–55%. In terms of qualitative effects, only tinidazole reduced viable organisms by ~90%. Following treatment with the other antibiotics, viable organisms were detected in 70%–85% of the biofilm-like colonies."
I'd like to see analysis of how each of the five antibiotics fared relative to one another within biofilm-like colonies, rather than a range. It'd be good to do a direct comparison of each antibiotic against each form in vitro including biofilm-like colonies.

So... On the whole, I'd say take note of the study, with the message that independent confirmation and reproducibility of the methods chosen and these findings are important - and it's good to make note of these findings in relationship to other research already completed.

If anyone heads to the University of New Haven on the 21st to see the presentation on this, I'd love to get a report from you in comments about what was said.

In the end, I'll leave you with this closing thought from a paper from 2005, In Vitro Susceptibility Testing of Borrelia burgdorferi Sensu Lato Isolates Cultured from Patients with Erythema Migrans before and after Antimicrobial Chemotherapy :

"... similar to failures of chemotherapy for Treponema pallidum in syphilis (24), clinical treatment failures have been reported to occur in early LB cases for almost every suitable antimicrobial agent (10, 12, 28, 38, 42). Furthermore, the currently available diagnostic techniques do not reliably discriminate among possible reinfection, true endogenous relapse, and coinfection with other tick-borne pathogens (12). These drawbacks together with the phenomenon of resistance to therapy in individual patients undoubtedly contribute to the inconsistencies surrounding the optimal treatment regimens for LB and are often misinterpreted and misused to support prolonged antibiotic treatment regimens. However, relatively few cases of culture-proven treatment failure have been published (19, 22, 28, 29, 37, 38, 39), and the underlying mechanisms of antimicrobial resistance in B. burgdorferi sensu lato remain unresolved."

And there you have it. This pretty much characterizes the scientific reasons contributing to the ongoing controversy, five years later: Yes, there are treatment failures; yes, they are hard to diagnose and distinguish from coinfection and reinfection; yes, there is antimicrobial resistance; yes, scientists state these issues contribute to what is viewed as a misuse of prolonged antibiotic treatment.

But if treatment is necessary - whether it is a relapse or a new infection - then treatment is necessary.

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Friday, May 6, 2011

6 Repost: Researchers on Persistence in Lyme Disease

The following is a repost from the Daily Kos.  Go to this link to see over 100 comments and counting on this post there: http://www.dailykos.com/story/2011/05/05/973226/-Researchers-on-Persistence-in-Lyme-Disease

Over the years I've had to hear the criticism from well-meaning strangers and some friends that Lyme Literate Doctors or LLMDs are treating a disease that does not exist, and that doctors who treat Lyme disease with long-term antibiotics are taking unfair advantage of patients.

Sometimes the discussion can get a little heated with their concern for me, as they think I may be making a mistake. I take a deep breath, and then I say to them, "I hear that you're concerned, and I can see you have issues with these doctors, but what if there is evidence that Lyme disease can infect individual patients for more than 3-4 weeks? Is it not reasonable to treat them with longer term antibiotics when there is evidence they have an existing infection?"

Usually they nod at this point, wondering where I'm going to go with the discussion next. So I ask, pointedly, "Other than looking at case studies, what about researchers who think Lyme disease may be able to persist, or at least have enough doubt that they know more research is needed to find out why a significant portion of the population who contracts Lyme disease has persisting symptoms? What's in it for them?"

I usually get a thoughtful look, and a lot of silence. So I continue.

"I'll tell you what's in it for them: The pursuit of scientific knowledge. Some people just want to know what really is going on with Borrelia burgdorferi, and they are working on figuring it out. Not without putting themselves in a position of controversy, either - but most continue to do the benchwork they need to do and publish."

Indeed, many people who are new to the controversy over Lyme disease being a chronic, persistent infection have heard about the doctors, heard about the IDSA; may have heard about various bills before their state senates and heard about the film, Under Our Skin.

But not everyone has heard about the research that can leave one questioning the common idea that Lyme disease is easy to treat and cure. Not everyone has read Cure Unknown, even though it is practically considered the Lyme patient community's go-to guide.

"Here, read this," a patient at a support group leans over a table, handing Cure Unknown to a newcomer, "Borrow it for as long as you want - we have more than one copy in the group, and it will help you understand the controversy."

I've seen this act take place a number of times, and for many patients it is their first exposure to the story of Lyme disease, how Dr. Willy Burgdorfer discovered the spirochete that caused Polly Murray and her family grief, the creation of Lyme disease support groups, the story of Dr. Joe Burrascano's Senate testimony in the early 1990's, and the ongoing controversy over Lyme disease.

It is also often their first exposure to researchers who are working to understand Lyme disease, and find out how the organism operates, and why some patients continue to have persistent symptoms after 21-28 days of oral antibiotics.

Some of this research is what I will cover here.

Beagles With Borrelia

Dr. Reinhard Straubinger, a researcher at Cornell University, New York, placed infected ticks on 19 beagles and allowed them to feed. Two months later, he tested the dogs and found 18 were infected with Borrelia burgdorferi, one was uninfected.

He then gave 12 of the infected dogs doxycycline or amoxicillin, and left 6 dogs untreated. Eleven of the twelve infected dogs had developed lameness and recovered on antibiotics, and their antibody response declined. Four of six untreated dogs went on to develop arthritis.

Six months later, all the dogs were necropsied. All the treated dogs still had spirochetes in their tissues, albeit at a reduced load - but had a persisting infection, as if they had not been treated.[1]

Straubinger observed that in untreated dogs, their antibodies had consistently risen throughout the study - but treated dogs had a "dip" in their antibodies. Their antibodies initially decreased during treatment, but as time went on, they were on the rise six months after initial infection - probably due to the surviving spirochetes, according to Straubinger.

Straubinger went on to do a similar study as a controlled study with 16 beagles who were treated with different kinds of antibiotics after four months of disseminated infection. He then went on to treat 12 of the dogs with antibiotics for one month. After a little over a year, he performed a necropsy on them and found that spirochetes were detected in low levels in multiple tissues regardless of antibiotic choice.[2]

Of Mice and Men

Dr. Stephen Barthold and Dr. Emir Hodzig, of the University of California at Davis, have done a number of well-known studies on mice.

In 2008, he treated one group of mice with ceftriaxone three weeks after infection with Borrelia burgdorferi (Bb) and treated another group of mice with ceftriaxone much later on - four months after initial infection.[3]

Each of these two groups had their own control group of mice which were not treated with antibiotics.

All the mice were tested. The results: One month after treatment, none of the mice had clinical signs of Lyme disease, nor could cultures detect Bb.

But two of five mice had positive Bb cultures. Three months later, one mouse transmitted living spirochetes to 9 uninfected ticks. Five mice were examined one month after treatment and their tissues were positive for Bb DNA.

To add to the story, three months after treatment, tissue of two of these mice still had positive tissue samples, two could transmit living spirochetes to uninfected ticks, and one mouse could transmit an infection to another via a skin graft.

After the mice were necropsied three months after treatment, small numbers of spirochetes were still found in collagen-rich areas of the mice's tissues in their hearts, tendons, and ligaments.  It didn't matter how soon they'd been treated, either: all of them had spirochetes.

In his abstract, Dr. Barthold states:

"...when some of the antibiotic-treated mice were fed on by Ixodes scapularis ticks (xenodiagnosis), spirochetes were acquired by the ticks, as determined based upon PCR results, and ticks from those cohorts transmitted spirochetes to naïve SCID mice, which became PCR positive but culture negative. Results indicated that following antibiotic treatment, mice remained infected with nondividing but infectious spirochetes, particularly when antibiotic treatment was commenced during the chronic stage of infection."

These live spirochetes could be transmitted, but oddly, Dr. Barthold could not get them to grow in culture.

Are these spirochetes pathogenic, though? Do they cause disease, can they replicate? Barthold states in his abstract that they are nondividing but infectious.

Trial of Tigecycline

After these experiments, in 2010 Barthold and Hodzic went on to test the effectiveness Tigecycline on persisting Borrelia burgdorferi in mice.[4]

In his paper, Barthold states:

"Clinical assumptions are complicated by the ephemeral, variably recurrent, and diverse nature of both objective clinical signs and subjective symptoms of Lyme borreliosis. What is not known is whether or not antibiotic treatment completely eradicates the infection, and this has generated debate among the medical and lay communities."

He admits to the controversy over the persistence of Lyme disease after antibiotic treatment, and also states it is not known if it completely eradicates infection.

He continues:

"Antibiotics are likely to kill most B. burgdorferi organisms, but the immune system is needed to fully eliminate the remaining spirochetes. However, therein lies the challenge, since Borrelia burgdorferi has evolved to persistently infect fully immunocompetent hosts. Persistent infection has been shown to be the rule, rather than the norm, in a variety of laboratory animal species, including mice, rats, Peromyscus leucopus, hamsters, gerbils, guinea pigs, rabbits, dogs, and nonhuman primates. Based upon culture and/or PCR, persistent infections have also been documented in humans from both Europe and the United States Therefore, the “mop up” phase, which is dependent upon the immune system, is likely to be ineffective against an agent such as B. burgdorferi, which is highly effective at evading host clearance."

In the study itself, a new first-in-class antibiotic, tigecycline (glycylcycline), was evaluated during the early dissemination (1 week), early immune (3 weeks), or late persistent (4 months) phases of Borrelia burgdorferi infection in C3H mice (mice bred to emphasize joint inflammation).

Mice were treated with high or low doses of tigecycline, saline, or ceftriaxone. After 3 months of treatment, infection was assessed using cultures, quantitative ospA real-time PCR, and subcutaneous transplantation of joint and heart tissue into SCID mice (severely compromised immune deficient mice).

The result was that tissues from all saline-treated mice were culture and ospA PCR positive, tissues from all antibiotic-treated mice were culture negative, and some of the tissues from most of the mice treated with antibiotics were ospA PCR positive, although the DNA marker load was markedly decreased compared to that in saline-treated mice.

Antibiotic treatment during the early stage of infection appeared to be more effective than treatment that began during later stages of infection.

The viability of noncultivable spirochetes in antibiotic-treated mice (demonstrable by PCR) was confirmed by transplantation of tissue grafts from treated mice into SCID mice, with dissemination of spirochetal DNA to multiple recipient tissues, and by xenodiagnosis, including acquisition by ticks, transmission by ticks to SCID mice, and survival through molting into nymphs and then into adults.

Furthermore, PCR-positive heart base tissue from antibiotic-treated mice revealed RNA transcription of several B. burgdorferi genes. These results extended previous studies with ceftriaxone, indicating that antibiotic treatment is unable to clear persisting spirochetes, which remain viable and infectious, but are nondividing or slowly dividing.

Dr. Staubinger, Dr. Barthold, Dr. Hodzic, and their teams are not considered researchers on the fringe, but mainstream researchers who have approached the issue of persistence with an open mind.

One person everyone might want to listen to regarding the possibility of Borrelia burgdorferi's ability to persist in its host is its very own discoverer, who stated the following during an interview:

"I am a believer in persistent infections because people suffering with Lyme disease, ten or fifteen or twenty years later, get sick [again]. Because it appears that this organism has the ability to be sequestered in tissues and [it] is possible that it could reappear, bringing back the clinical manifestations it caused in the first place. These are controversial issues for microbiologists, as well as the physicians who are asked to treat patients."

~ Dr. William Burgdorfer, discoverer of the Borrelia burgdorferi spirochete, 2009



So we know the spirochetes persist. Researchers know they do. The evidence we need to consistently provide is of their infectious nature after antibiotics have been used. Why this issue of persistence is considered controversial remains a question, given that syphilis can enter a latent, dormant state in its host.

In 2009, Gary Wormser, who denies the existence of Chronic Lyme disease, wrote his own critique of some of these studies:

"What are causes of the attenuation of the spirochetes that persist posttreatment? Are they in the process of dying? Are they producing mRNA, and if so, which mRNA? Are they motile? Can they replicate? Are they genetically altered? Can they regain pathogenicity? "

In his own conclusion, he states, "The biological nature of these spirochetes is unclear," along with some caveats about the likelihood of their being pathogenic.[5]

He thinks they are not infectious. Other researchers - like Barthold - think they are infectious. Patients who have experienced relapsing-remitting symptoms definitely think they are, and would like to put this issue to rest and find treatment that is 100% effective. In the meantime, antibiotics are the treatment of choice.

This is why I push for more research. The research that has already been done is noteworthy and requires further investigation, and only by determining the truth can the controversy be put to rest.

My future directions suggested for researchers:
1) Use non-murine models for study - higher order mammals with more collagenous tissue around their brains
2) After animals have been treated with antibiotics and spirochetes found in tissue, instead of killing them, study them for a few years and repeatedly expose infected host animals to stress (in accordance with study design for ethical treatment of animals).
3) Periodically retest animals for antibodies, PCR, and culture, including CSF and ultimately, brain tissue. Use advanced testing methods in development.

Who knows, maybe it will happen - at the end of Barthold's Tigecycline study he stated, "Further studies are under way in the mouse model to determine if the postantibiotic-persistent organisms return to a cultivable and pathogenic state or if they eventually die out."

References:
1. Straubinger RK, Summers BA, Chang YF, Appel MJ. Persistence of Borrelia burgdorferi in experimentally infected dogs after antibiotic treatment. J Clin Microbiol. 1997 Jan;35(1):111-6.
2. Straubinger RK. PCR-Based quantification of Borrelia burgdorferi organisms in canine tissues over a 500-Day postinfection period. J Clin Microbiol. 2000 Jun;38(6):2191-9.
3. Hodzic E, Feng S, Holden K, Freet KJ, Barthold SW.Persistence of Borrelia burgdorferi following antibiotic treatment in mice. Antimicrob Agents Chemother. 2008 May;52(5):1728-36. Epub 2008 Mar 3.
4. Stephen W. Barthold, Emir Hodzic, Denise M. Imai, Sunlian Feng, Xiaohua Yang,
and Benjamin J. Luft Ineffectiveness of Tigecycline against Persistent Borrelia burgdorferi. Antimicrobial Agents and Chemotherapy, Feb. 2010, p. 643–651.
5. Gary P. Wormser, Ira Schwartz. Antibiotic Treatment of Animals Infected with Borrelia burgdorferi. Clin Microbiol Rev. 2009 Jul;22(3):387-95.

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4 Video: What The Internet Is Hiding From You

I just watched this video with Eli Pariser, where he talks about what the internet doesn't let you see because it is tailored with you in mind.

This is almost ten minutes of video you don't want to miss, because it talks about how completely different results are shown for two people who are looking up the same keyword.

This means that one person who is interested in Lyme disease and conspiracy theories will get more results that include those two concepts - whereas a person who is interested in Lyme disease and scientific research will get more results that include those two concepts when they type the keywords, "Lyme disease" into their browsers.

It's important to be aware that what you don't see can be as important as - if not more important than - what you are actually seeing online. Anything that makes you uncomfortable, challenges your point of view, or is different may be hidden from you by design.

Watch this video. I think everyone should see it, the message is important whether you are looking up information on Lyme disease, US politics, health care plans, and anything you can think of entering into that little search box at the top of your browser...



How do you fix this?

Google needs to set it up so we have the option to turn filters on and off that involve personalization.

Until then, the wider a variety of different terms you use frequently in searches - including ones that you disagree with - the wider the number of results you are bound to get in return. They'll just get included in your filter by default if you use them often enough - even if you don't read all the results.

If you're liberal and searching for something on politics, put "GOP", "Republican", and "conservative values" into your searches every once in a while. Use "liberal Democrats" "social Democrats", "progressive values" into searches if you're conservative every once in a while. And for good measure, throw in "libertarians", "green politics", and "economy" in with any of those randomly and see what crops up.

You can do the same thing with just about anything to throw off Google's existing filter system, and use different search engines with different data sets just to see how their own internal algorithms work. Consider it your own science experiment in data manipulation - it's better you manipulate your own data than to let someone else do it.

Additional note: The spinning disk in the middle of the screen is a TED issue, if you see it - nothing to do with Camp Other. Keep watching despite it - it's worth the effort and you can see what you need to even with it there.
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Thursday, May 5, 2011

0 Daily Kos Posting Today At 6PM EST

There will be a post on Lyme disease and spirochetes which persist after antibiotic treatment today at 6PM EST, 3PM PST, 12PM HAST.

Please read the Lyme Disease Awareness stream at this link:

http://www.dailykos.com/blog/Lyme%20Disease%20Awareness

A repost of the above entry will we posted to this blog later.

Apologies for the somewhat slow week - have been dealing with serious fatigue.
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Sunday, May 1, 2011

0 Administrivia: Camp Other on Daily Kos For Lyme Disease Awareness

And now the announcement I've been meaning to make this weekend (and part of the reason for my continued delay in adding comments to the most recent Friday Four post and decision to put the Friday Four on hiatus for at least one month):

I am going to be writing and posting to the Daily Kos during May for Lyme Disease Awareness month.

My first post permalink is here: http://www.dailykos.com/story/2011/05/02/972070/-Camp-OtherLyme-diseasescience?detail=hide

I will be posting some posts specifically for the Daily Kos audience, so they will only be available if you go to the Daily Kos site. The remainder of my posts I intend to cross-post to both this blog and the Daily Kos diary

I have not yet determined how long I will have a presence on Daily Kos - I will see how this goes and what level of discussion posting there provokes. I look forward to seeing what happens.
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9 Administrivia: FAQ updated

The Camp Other FAQ was updated recently with a few questions and answers.

More administrivia is scheduled to be reported later today if all goes to plan.

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The Camp Other Song Of The Month


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