Saturday, December 31, 2011

0 Freedom Of Information Request On Vancouver Complex Chronic Disease Clinic

The Vancouver Sun recently reported on the results of a freedom of information request on the upcoming Complex Chronic Disease clinic in Vancouver, Canada. Gwen Barlee, Lyme disease advocate, was disappointed with the results of her request, saying that she thought "the government appears to be dropping the ball again on taking a proactive approach to managing, diagnosing and treating Lyme disease in British Columbia."

Both pros and cons of the clinic are examined in this article.

Read More Here:

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Saturday, December 24, 2011

0 Wishing You Peace This Holiday Season

Happy Solstice, Happy Chanukah, Merry Christmas, and Happy New Year to all observing.

Peace on earth for everyone from Camp Other Blog.

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Friday, December 16, 2011

0 Science Article: Oral Bacteria Opens Door To Allow Pathogens In

In today's Science Daily, there is an article on a study showing how one specific oral bacteria, Fusobacterium nucleatum, can provide a gateway for other bacteria to enter human blood vessels and make people sick.


Original Source:
Yann Fardini, Xiaowei Wang, Stéphanie Témoin, Stanley Nithianantham, David Lee, Menachem Shoham, Yiping W. Han. Fusobacterium nucleatum adhesin FadA binds vascular endothelial cadherin and alters endothelial integrity. Molecular Microbiology, 2011; 82 (6): 1468 DOI: 10.1111/j.1365-2958.2011.07905.x

Reading this reminded me of an earlier post and comments I made about a paper by Judith Miklossy: Alzheimer's disease - a neurospirochetosis.

In my comments there, I stated:

"I think it's possible that infection can be part of the precursor or a cascade effect that gets the ball rolling towards Alzheimer's Disease (AD) - but the question remains: Why do plenty of people have Bb or HSV-1 or any of a number of infections who do not develop AD?"

Maybe this is what makes the difference. Maybe Fusobacterium nucleatum has to cross the endothelium and open the gate for bacteria such as Bb or oral Treponema to cross the blood-brain barrier. If Fusobacterium nucleatum can travel to the brain first, then perhaps these other bacteria will follow on its heels and lead to neurological damage.

It seems further studies to seek Fusobacterium nucleatum in brain biopsies alongside other bacteria could provide some evidence that this is what has happened.

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Friday, December 9, 2011

0 New Ehrlichiosis Strain Causing Disease In Sweden

Researchers at the University of Gothenburg's Sahlgrenska Academy have discovered a brand new tick-borne infection. Since the discovery, eight cases have been described around the world, three of them in the Gothenburg area, Sweden.

The disease-causing agent is bacteria known as Neoehrlichia mikurensis. This bacterium was identified for the first time in Japan in 2004 in rats and ticks but had never before been seen in Sweden in ticks, rodents or humans.

One notable symptom of the disease - alongside typical tickborne infection symptoms such as fever and diarrhea - is the development of deep vein thrombosis.

Read more here:


It's always prudent to keep in mind that Borrelia burgdorferi (as well as other Borrelia) are not the only bacteria that can be transmitted by ticks. Many different diseases can be contracted - bacteria, viral, and protozoal. One can be bitten by a tick and infected by a coinfection and not be infected by Borrelia at all - though it is more likely in many parts of the world for the tick to be infected with Borrelia as well.

The rule of "if the tick was on me for less than 24 hours, I'm probably okay" is not a real rule. The twenty-hour hour minimum for Lyme disease transmission time was based on limited research, and research on transmission time for many coinfections has indicated far less attachment time is needed for an infection to develop.

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Wednesday, December 7, 2011

0 Comments On 2011 Lyme and TBD Conference Summaries

I have a few comments to make as they come up on October's 2011 conference.

I may add and repost to this entry a few times - stay tuned.

1) I looked at this part of the summary on Dr. Reinhard K. Straubinger's talk on “Canine and Equine Lyme Borreliosis” focused on Lyme borreliosis in animals, especially in dogs and horses:

"The highly variable surface protein VlsE is, according to current knowledge, exclusively expressed in the mammalian host. The invariable region IR6, and even a shorter peptide sequence of IR6 called C6 were found having a high potential as specific antigenic components in serologic test systems. This was shown by evaluating sera from infected humans, dogs, monkeys and mice. In experimentally infected dogs, C6-specific IgG antibodies appeared 3 weeks post infection; hence almost one week earlier than antibodies detected with ELISA based whole-cell preparations. Additionally, another benefit became clear when testing sera of people and dogs before and after antibiotic treatment. Contrary to antibodies against whole-cell components, research demonstrates that C6-antibodies declined substantially a few months after treatment. However, in animals with low C6-antibody levels prior to treatment, the decline obviously was minimal post treatment. Despite their high specificity for borrelial contact, C6-antibodies do not necessarily correlate with clinical signs in dogs and false-positive results may result from maternal antibodies in puppies born to infected bitches."

It brought to mind the following paper and a passage within it:

Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation. Stefan S. Tunev, Christine J. Hastey, Emir Hodzic, Sunlian Feng, Stephen W. Barthold, Nicole Baumgarth.


"We did not include the VlsE protein in our studies, a surface-protein thought to subvert the immune response to B. burgdorferi through extensive genetic variation within the host. However, the N40 strain of B. burgdorferi, which we have used here, does not seem to express this protein, based on transcriptional analysis of the IR6 region of vlsE. Moreover, we found no evidence of seroconversion to the C6 antigen of vlsE from strain B31 (S. W. Barthold, unpublished). Recent sequence analysis of the N40 genome has confirmed that N40 vlsE and BBK01 are on different plasmids and that the vlsE locus is indeed significantly different compared to B31, the commonly used VlsE-expressing Borrelia-strain."

So what do we know about C6 tests, briefly?

C6 Lyme ELISAs are based on the synthetic peptide C6, which corresponds to the invariable region IR6 of the surface antigen VLsE.

IR6 is supposed to be highly preserved in all pathogenic strains of Borrelia, and is only expressed in vivo. It evokes a strong immune response.

As a diagnostic antigen, the C6 peptide shows only minor cross-reactivity to other pathogens (e.g. spirochetes for syphilis).

Knowing this, it's interesting to point out that using the C6 ELISA may not work as well for testing a host which is infected with a strain of N40 Borrelia. How can it, when this strain of N40 does not express the vlsE protein?

I have to wonder how many other strains may have vlsE on different plasmids - and not only that - a different locus?

2) Dr. John Aucott’s talk on “Early Lyme disease” reported from the SLICE prospective cohort and his Maryland studies. I want to point out this part of the summary:

"He emphasized that the classic description of a “bull’s eye rash” occurs only 20% of the time – it is not the most common manifestation of the Lyme rash. Rather, a uniformly red or reddish-blue rash, round or oval in shape, with sharply demarcated borders is most common. Most often the rash develops in places such as the knee, groin, or arm pit, occurring at prime tick season, such as the late spring and early summer."

It's important to know that these varied descriptions of so-called "bull's eye" or EM rashes found in Lyme disease are not the only variations found in Lyme disease culture positive lesions.

In an earlier entry about Dr. Vijay Sikand's testimony at an FDA Lymerix Vaccine Review, Dr. Vikand reported this about EM rashes:

"[...] However, erythema migrans is not a single beast. Certainly this is the one which we easily recognize and which I just referred to.Before I continue with further slides, let me point out that the erythema migrans lesions you are about to see are all biopsy lesions which were laboratory proven to be caused by Borrelia burgdorferi.

Sometimes erythema migrans can present as a pustular lesion as is this one in the popliteal fossa inviting the scalpel of a surgeon.

Sometimes the lesions are vesicular in nature, inviting a diagnosis perhaps of herpes simplex infection.

Sometimes our round lesion is actually triangular.

Sometimes it doesn't even look round or red at all and invites a diagnosis of an intertriginous fungal infection in the groin of this patient who was biopsied and proven to have Lyme disease.

Sometimes the lesion is more plaque-like, inviting diagnosis of nummular eczema, psoriasis, or other similar lesions.

Sometimes it is in unusual locations.

Sometimes it is large like this one. Sometimes it is small with satellite areas. Sometimes it is multiple, appearing almost like urticaria or erythema multiform.

Sometimes, as in this individual who was a placebo recipient in the Lyme 008 SmithKline Beecham trial, it presents with other manifestations of early dissemination. This individual came in mainly because he was concerned about his face and it felt kind of funny and it was weak on one side. When I asked him whether he had had any unusual rashes, he said oh do you mean this one, and he showed me his arm with that EM. This is simply to illustrate the infranuclar 7th nerve palsy with which he presented. This patient, by the way, had no history of a tick bite or any unusual antecedent illness which he could remember."

If Sikand's testimony is anything to go on, one has to wonder about the reliability of the "bull's eye rash" as a diagnostic marker.

(For what it's worth, my own EM rash was large, oval, dark red, slightly elevated, and expanding for several days after the bite.)

3) Dr. Karen Newell Rogers presented a talk about novel ways to target chronic inflammation and chronic immune activation among patients with chronic Lyme disease.

Now this part below - especially in bold - really caught my eye:

"[...]Some researchers would argue that chronic inflammation requires the continuous presence of bacteria, whereas others would suggest that continuous presence of bacteria does not always result in inflammation and that exacerbations of chronic symptoms could result from infection with a different organism--or that chronic symptoms could re-cur from unrelated pro-inflammatory events. Potentially reconciling these seemingly conflicting perspectives on the mechanism of Lyme disease may be the effect of Borrelia burgdoreri’s bacterial by-products on Toll Like Receptors, (TLR)-mediated immune activation. TLR appear to be the “gate-keepers” of an inflammatory response. Bacteria, including Borrelia, produce products that, by binding to TLRs on the cell surface, promote leukocyte activation, cytokine production, and acute inflammation. In some genetic backgrounds of mice, acute inflammation is sufficient to fight off infection and resolve disease. In other mouse strains, the pathogens, or in this case the bacteria, get past TLR-induced inflammation and remain symptomatically undetectable in cells and tissues (Barthold, etc); Barthold et al. have found that no matter how severe or mild the disease in any of the genetically inbred strains of mice, there was no more inflammatory disease when the bacteria were eliminated."

Reading this, I reflect back on an earlier entry I made about the combination of genetics effect on individual immune systems AND persistent infection as both leading to ongoing symptoms in hosts:

Immune + Infection = HLA-DR alleles determine responsiveness to Borrelia burgdoferi:

Perhaps part of the answer to what is happening with ongoing symptoms lies both in Dr. Newell Rogers' work and Bettina Panagiota Iliopoulou, Mireia Guerau-de-Arellano, and Brigitte T. Huber's research?

It's certainly thought-provoking.

And Barthold's statement implies that ongoing inflammation is intimately tied to persisting infection.

How does one provide evidence this is the case?

Could the answer lie in longer term in vivo GFP and/or iRFP studies on mice and other mammals? Could it lie in maltodextrin enhanced imaging studies? Or something else?

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0 Review Of The 2011 Lyme and Tick-Borne Diseases National Conference

In October 2011, a national conference on Lyme and tick-borne diseases was held in Philadelphia by Columbia University and the Lyme Disease Association.

Here is a brief overview of the topics presented:

  • Dr. J. William Costerton’s riveting talk on “The Role of Biofilms in Chronic Bacterial Infections” reviewed the history of the discovery of biofilms, demonstrating that these biofilms enable micro-organisms to resist host defenses and antibiotics, enabling infections to become chronic.
  • Dr. Eva Sapi’s talk on “Killing Borrelia – an impossible job?” addressed various mechanisms associated with Borrelia burgdorferi that may help it to survive despite antibiotic treatment.
  • Dr. Jason A. Carlyon’s talk focused on Anaplasma phagocytophilum, the agent of human granulocytic anaplasmosis (HGA). This emerging tick-borne pathogen demonstrates stealth trickery, enabling it to avoid and even subvert immune cells.
  • Dr. Richard Marconi’s talk on “C-Di-GMP” described research demonstrating that the cyclic nucleotide, c-di-GMP, plays a critical role in regulating several important cellular processes.
  • Dr. Chris Earnhart’s talk described work developing a novel next-generation Lyme disease vaccine based on outer surface protein C. Osp C is expressed by all Bb species and strains and is expressed in the human host for several weeks before being down-regulated.
  • Dr. Robert S. Lane gave a brief overview of his research team's long-term studies of the ecology and epidemiology of Lyme disease in California, and then summarized some exciting recent findings regarding the genospecies and genotypes of Borrelia burgdorferi s. l. that infect the western black-legged tick and humans in this region.
  • Dr. Karen Newell Rogers presented a talk about novel ways to target chronic inflammation and chronic immune activation among patients with chronic Lyme disease. The primary controversy with Lyme disease has been whether the disease is the result of long-lasting bacterial infection or whether long-term symptoms result from a post-infectious, uncontrolled autoimmune response.
  • Dr. Robert Yolken’s talk on “Infections and Human Neuropsychiatric Diseases” focused on the Stanley Center’s work at Hopkins which has examined infectious triggers of psychosis.
  • Dr. Josep Dalmau’s talk on “The Clinical Spectrum and Cellular Mechanisms of Autoimmunity in NMDA and other synaptic receptors”. His pioneering work studying anti-NMDA receptor encephalitis shows how an immune response triggered by a tumor (e.g., ovarian teratoma) or perhaps an infectious process, results in antibodies that can attack critical receptors and synaptic proteins in the Central Nervous System involved in memory, behavior, cognition, and psychosis.
  • Dr. John Aucott’s talk on “Early Lyme disease” reported from the SLICE prospective cohort and his Maryland studies.
  • Dr. Reinhard K. Straubinger's talk on “Canine and Equine Lyme Borreliosis” focused on Lyme borreliosis in animals, especially in dogs and horses.
  • Dr. James Moeller presented a talk on “Immunologic aspects of neuropsychiatric illness: Lyme disease as model”.
  • Dr. Brian Fallon presented a talk on “Models of Chronic Lyme Disease”. The talk started with a review of the terms that refer to chronic symptoms and recommendations on how the the IDSA’s definition of Post-treatment Lyme Syndrome could be improved. This talk reviewed the evidence regarding models of persistent infection and/or persistent immune activation.
  • Dr. Andrew Walter reported on Ehrlichiosis and Hemophagocytic Lymphohistiocytosis (HLH) in cases of children diagnosed in Delaware.
  • Dr. Andrea Gaito provided an update on the clinical evaluation and treatment of Lyme Arthritis from an autoimmune perspective. Lyme arthritis occurs in sixty percent of patients with untreated Lyme disease.
  • Dr. Ingeborg Dziedzic presented an interesting (and at times entertaining) overview of how Lyme disease impacts the eye, emphasizing that the eye is in part like the skin and in part like the brain.
  • Dr. Vijay Thadani presented an overview of seizures and non-epileptic seizures, showing videos of both. Brain infections such as Lyme disease can lead to the development of epilepsy.
  • Dr. Steve Bock addressed complementary and integrative medicine approaches to the treatment of chronic Lyme disease.
  • Dr. Elizabeth Maloney addressed studies of antibiotic treatment of Lyme disease, providing a thoughtful and critical review of the literature to identify lessons, gaps, and future research needs.

READ MORE - Full Presentation Information Here:
2011 Lyme and Tick Borne-Diseases National Conference Summary Report

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Sunday, November 27, 2011

2 News: Substantial Increase In Tick Activity Concerns Canadian Officials

Good news from Canada about increasing Lyme disease awareness: The Kingston Whig Standard newspaper has written about the record number of ticks residents sent into the health unit for Lyme disease testing and the number of ticks found positive so far.


"Following a substantial increase in the number of ticks submitted for testing this year, officials with the local health unit hope to draw a bullseye around the issue of Lyme disease in order to prevent a rash of new cases in 2012.

Joan Mays, manager of health protection for the Leeds, Grenville and Lanark District Health Unit, said there have been 568 tick submissions to the health unit so far this year. Of these, she said, 40 have tested positive for the bacteria that causes the disease, with the health unit still awaiting the results of 271 tests."

Health unit officials noted that an extension of warmer temperatures through the season has led to longer tick activity during the year, and more Canadians are becoming aware of Lyme disease and sending their ticks in to be tested so they may find out if they may have the disease.

I find it encouraging that more people are sending in their ticks and health unit officials are taking notice. Lyme disease is in Canada and there is no sign it is going away. This is just one sign of greater awareness - but more early testing for Lyme disease in people would be even better.

Read more here:

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Tuesday, November 22, 2011

0 News: Judy Mikovits To Be Released On Bail

The latest report on the Mikovits case comes from the AAAS Science Insider:

Regarding the outcome of today's proceedings, the judge granted a request for a continuance on the extradition demand and asked Mikovits to return on the 19th of December.

Mikovits, who has denied wrongdoing through lawyers handling her civil suit, posted bail shortly after the hearing and has been expected to be released this evening.

More details on the case and discussion of a settlement can be found here, on the Ventura County Star site:

And here, Nature blog discloses that one of Mikovits' fellow researchers, Max Pfost, claims to have stolen her notebooks and to have given them to Mikovits', but Mikovits' denies this.

Nature blog also states:

The affidavits add a new wrinkle, alledging that Mikovits, a chronic fatigue syndrome researcher, was scheming with Pfost to “move the grants from WPI”. This includes about half of a US$1.5 million research grant (an R01) from the National Institute for Allergy and Infectious Diseases. In a meeting at a bar the night Mikovits was fired, Pfost claims: “She stated she was going to try to move the RO 1 grant and the Department of Defense (DOD) grants and stop the Lipkin study.”

More here:

The plot thickens... What really happened has yet to be seen.
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0 Article: The Mouse Trap: How One Rodent Rules The Lab

Slate recently posted a three part series on the use of mice in biomedical research and how that use has helped as well as hindered drug development and scientific understanding of human illness.

This three part series kicks off with "The Mouse Trap: the dangers of using one lab animal to study every disease", which examines the rise in the use of the murine (mouse) model  to test new pharmaceuticals and get a better understanding of human processes in illness. We also learn that this model - useful as it has been - has its drawbacks.

 Mark Mattson, neuroscientist, finds that murine studies may not accurately represent what happens between the study and control group when the control group is often overfed, sedentary, and develops cancer, renal problems, and diabetes - unlike a wild mouse living in its normal habitat. It was later discovered that medication which worked in chubby rodents did not go on to work in rodents with a normal weight and activity level.

Furthermore, in clinical trials on humans later on, the difference between plump mice and a diverse group of humans was too great. A drug which worked in the rodents did not work in humans at all.

Cheap, efficient, and mass produced, these mice are raised in germ-free barrier rooms and sometimes pumped with antibiotics. The ease in which they can be raised, bred, and genetically modified to single out specific processes similar to those in the human body to study has made mice very popular for researchers. While they can closely model many processes in the human body, are they a close enough match for modeling and testing everything?

Mattson argues they are not, and that science needs to wake up and take a closer look at how heavily mice have been used to make decisions that affect human medicine. He's not the only one, either - Clif Barry, the nation's leading expert on tuberculosis, thinks the murine model has shortcomings too. This is no clearer than in work in his own field: The latent form of TB that humans get is not one which can be found in mice. Mice do not experience a latent stage of TB - they only get progressively weaker, age, and die.

This particular passage from the article gave me a moment to pause and reflect:
"[...] for some patients a latent case of tuberculosis can suddenly become active. The granulomas rupture and propagate, spilling thousands of organisms into the lungs, where they can be aerosolized, coughed up, and passed on to a new host. Left untreated, the infection migrates into the bloodstream and other organs; widespread inflammation leads to burst arteries or a ruptured esophagus; and in about half of all cases, the patient dies.

The layered granuloma is the defining feature of human tuberculosis: The place where the host fights the infection (successfully or not), and the necessary site of action for any drug. To cure the disease, a treatment must be able to penetrate each ball of cells, whatever its type or composition; every last bacterium must be destroyed. "It's the structure of those granulomas that makes it so difficult to treat TB," says Barry. And they simply don't exist in mice.

If you infect a mouse with TB—if you spritz a puff of infected air into its nostrils through a trumpet, as so many labs do around the world—the animal's lungs quickly fill up with bacteria and immune cells, like a nasty case of pneumonia. There are no discrete balls of tissue, no well-defined granulomas sheathed in fibrin, no array of structures that harbor the bugs at various stages of development. The mice have no special, latent form of TB, either, and no way to pass on the disease. They simply die, after a year or two, of a slow and progressive decline.

That's why we've made so little progress using mice to generate new drugs and treatments, Barry tells me."
The article continues to outline the history behind why mice have become the dominant research model to use to determine whether or not a drug or treatment plan will be tried in clinical trials on people, and also discusses the setbacks generated by this decision. In the end, the verdict is that using mice has distinct limitations and a number of studies may be invalidated and useless because of it.

It does get me to wondering, of course, as to how useful the murine model is for studying Borrelia burgdorferi. Perhaps in some ways it is useful, but in others it is less so: Dr. Stephen Barthold has said mice are a poor model for neuroborreliosis.

And this does raise the question of which details are important in a study that the layperson will miss when reading it. The average person will read about the study design, and perhaps some discussion and the conclusion - but will one question the decision to use one research animal model over another? What about primers? What about media? What about any number of small details that once changed could result in a different outcome?

Read the full Slate article, and continue with the next two articles in the series. It is a fascinating look into the world of biomedical research, tradition, and profit.


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Saturday, November 19, 2011

0 News: Judy Mikovits, CFS Researcher, Has Been Arrested

While not directly about Lyme disease, any news about Chronic Fatigue Syndrome (CFS) can be notable to the Lyme disease community as some patients have been diagnosed with CFS and any research on persisting fatigue and its cause has been of interest.

This is big news. While all the specifics behind the charges are unknown at this time, Retraction Watch just published that Judy Mikovits, a researcher involved in the XMRV controversy, has had a warrant out for her arrest for felony charges and was arrested in Ventura County, California, yesterday.

More information can be found here:

And here:

Mikovits' court appearance is scheduled for Nov 22, 2011 at 1:30PM in the Ventura County Superior Court.

More details on this as the story unfolds.

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Friday, November 11, 2011

5 News: Infected Ticks Found In New Brunswick

Dear Canadian doctors: Yes, Virginia, there IS Lyme disease in Canada. Please step up to the plate and diagnose and treat the growing number of Canadians with Lyme disease. Thank you...

Deer ticks found on Grand Manan

The provincial Health Department recently identified a breeding population of blacklegged ticks, properly Ixodes scapularis, sometimes called deer ticks, infected with Lyme disease at North Head, Grand Manan.

"We only confirmed that in the last week or so," New Brunswick's Chief Medical Officer of Health Dr. Eilish Cleary said in an interview from Fredericton Thursday.

Last year scientists confirmed a similar breeding population in the Millidgeville area of Saint John.

Scientists believe these creatures are moving north as the climate changes, bringing Lyme disease with it, Cleary said.


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2 Article: Anaplasmosis Plus Lyme Disease In Dogs = Sick As Dogs

The West Salem Veterinary Clinic reposted part of an August 2011 article on its site in the La Crosse Tribune in Wisconsin recently.

The original article is found here:

Here are two paragraphs I want share with all dog lovers out there:
Anaplasmosis phagocytophilum, previously known as Ehrlichia equi, is very prevalent in this area. It is spread by the same ticks as Lyme Disease and it can be a co-infection (both infections occurring at the same time) with Lyme Disease. Experts at IDEXX Laboratories, the manufacturers of the IDEXX SNAP® 4DX™ test, maintain that when a dog contracts Lyme disease or anaplasmosis alone, its immune system is more likely to suppress disease. However, a dog with both infections at once is more likely to become sick. IDEXX created the 4DX test to test for Heartworm, Lyme, Anaplasmosis, and Ehrlichia canis (another tick-borne disease that is not as prevalent in this area.)

If your dog shows any of the previously listed symptoms, he or she should be examined and tested. If your dog is positive for anaplasmosis, he or she should have a complete blood cell count performed to further evaluate for active disease. If your dog lives in this area, he or she should be on tick control year-round, screened with the 4DX test annually and vaccinated for Lyme Disease. Visiting dogs from other areas need tick control and screening as well. You cannot catch these diseases directly from your dog, but you are exposed to the same ticks in the environment as your dog, so be sure to use tick repellent on yourself and check for ticks on yourself as well as on your dog on a daily basis.

Now, my question is, how much more severe is the course of infection in humans who are infected by both Borrelia burgdorferi and Anaplasmosis phagocytophilum?

How do humans differ from dogs in this infectious disease model?

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0 News: Massachusetts Proposal For Lyme Research Institute Trust Fund

News from The Cambridge Chronicle, where the Beacon Hill Roll Call records the votes of local representatives on seven roll calls and local senators on two roll calls from the week of October 31-November 4. One of this week's proposals is for establishing a special trust fund for Lyme disease research at the Universty of Massachusetts Medical School at Worcester:

LYME DISEASE RESEARCH (H 349) - The Higher Education Committee is considering a proposal that would establish a Lyme disease Research Institute Trust Fund to provide grants to the University of Massachusetts Medical School at Worcester for Lyme disease research.

The committee recently held a hearing on the bill. Supporters said current private funding is not sufficient to stop the proliferation of this serious tick-borne illness that if left untreated, can lead to serious heart, neurological, eye and joint problems.

James Gilbert, 32, of Dorchester lost his mother a few years after her diagnosis of late-stage Lyme disease. Gilbert himself was diagnosed with Lyme disease when he was 14. He was treated with antibiotics and though he noticed a marked decline in his overall health even after the antibiotic treatment concluded, he was able to function without debilitating hindrance until he turned 22. He was a tri-lingual "A" student who was attending Georgetown University when he began to suffer severely disabling health complications.

Gilbert submitted written testimony to the committee because his disease prevented him from traveling to the hearing. He noted that today he cannot work and has been forced to apply for Social Security disability benefits.

He said, "It is obvious that Lyme disease is still a mystery to the medical community, worthy of deeper scientific attention. The disease is also improperly viewed by the Infectious Disease Society of America. This has resulted in inadequate treatment methods and unnecessary, continuous suffering by the afflicted."

Gilbert urged creation of an Institute that is "sensitive to the needs of patients, and one whose research and treatment programs push the boundaries of traditional methodologies to improve patient care."

Source link:

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Tuesday, November 8, 2011

0 Two Notable Antibiotic Articles - Long-term Effects & Alternatives

H. pylori: Friend or foe?
Answer: It depends...
I know some of you reading along may have already seen this, but I think it bears mentioning again and also bears mentioning for those who may not have seen it: The New York Times recently published an article on the long-term effects of antibiotic usage, "In Some Cases, Even Bad Bacteria May Be Good".

After reading the above link, I found it fascinating and disturbing that antibiotics not only could contribute to obesity - the hypothesis originally being test driven by the writer - but that antibiotic use could also lead to allergies, inflammatory bowel disease, asthma, and gastroesophageal reflux. These are conditions which are not only common in Lyme disease patients, but in the general population as well.

Among the astonishing findings in this article:
  • Eradicating H. pylori infections entirely leads to the inability of ghrelin (a hunger hormone secreted in the stomach) to decrease in the stomach, thus leaving the brain to think it's always time to eat more. Therefore, lack of infection = eating more = weight gain.
  • Researchers found that the ratios of various bacteria in the guts of obese mice and obese humans were significantly different from those of lean controls, suggesting that altering the stomach’s microbial balance with antibiotics might put patients at risk for gaining weight. H. pylori is not the only culprit for change.
  • Less H. pylori in someone's system is associated with a greater risk of not only asthma but gastric reflux disease as well.
  • The human body contains a very complex bacterial ecosystem which we don't know anywhere near as much about as we should. Knowing about it is important in understanding the cause for disease and how to prevent it.
  • It's not just antibiotics that are changing the human microbiota - many aspects of modern life, including diet, smaller families, more hygienic practices and improved public sanitation, are affecting our bacterial communities.
The research cited contains sobering news and adds to the realization that as much as antibiotics have brought deadly infections under control and saved lives, they can have negative side effects and possibly more longer term consequences than at first realized.

All this said, I have been an advocate of antibiotic usage to treat Lyme disease - especially in its early stage and with a clear case of neuroborreliosis - because antibiotics have been tested and used in clinical trials for many years for their effectiveness. It's  important in the case of neuroborreliosis to ensure that treatment can pass the blood-brain barrier, and so far antibiotics have been tested which are demonstrated to have this property.

So I still stand by the use of antibiotics for their effectiveness and documented record for helping patients everywhere. However,  I am aware that in the future, antibiotics may not work as well as they once did due to antibiotic resistance, and this knowledge of longer term effects concerns me as well. Alternatives will need to be found that are safe and effective.

What sort of treatment could be available other than antimicrobial herbs?

The answer may be as close as your local wallaby.

Okay, well, for most people reading this, wallabies are hardly local to them - unless you are one of my Australian readers or you have a decent zoo nearby.

Last month, Byte Size Biology blog published an entry on the innate immune system and research on cathelicidins, specifically those peptides found within marsupials - including wallabies - which can fight off infection.

A baby kangaroo (joey) or wallaby is born in its fetal stage and must travel across its mother's abdomen and into a pouch to complete development. This can expose the fragile fetus to all sorts of germs, so what protects it? While the joey has adaptive immunity which is quite undeveloped, it can produce some killer all-purpose peptides he can use against microbes.

The same class of peptides are produced in Kanga’s milk. (Think of the idea as being similar to colostrum in cows, perhaps?) Collectively they are known as cathelicidins. Only about 30 amino acids long, these highly charged molecules kill both gram-positive and gram-negative bacteria.

Preliminary studies were conducted on the use of cathelicidins as antibiotics. The author of Byte Size Biology wrote:
"They used cathelicidins from wallaby and platypus to kill human pathogens: P. aeruginosa, K. pneumoniae and A. baumanii, including antibiotic resistant strains. Cathelicidins were much more effective than, well, antibiotics against those bacteria. Also, cathelicidins did not kill human red blood cells, which makes them a potential drug. Of course, immune reaction against cathelicidins as a foreign still needs to be checked, among many, many other things, but the whole idea of looking at marsupials is that, as mammals, they may be able to supply us with clues on how to synthesize a cathelicidin to be used as a drug in humans."
More research is needed, obviously, but this may be one option to antibiotics sitting in your medicine cabinet of the future.

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Sunday, November 6, 2011

2 Admin Update: Lyme Disease Awareness and Outreach

There are a lot of ways to spread support for Lyme disease awareness. Some people make web sites, some people make Lyme disease related clothing, some people make bracelets and other jewelry, and then others make the popular Lyme disease support ribbons. Some people hold fundraisers like Lyme walks or benefits at local bars.

Here in the virtual world, we can't really give each other tangible items to wear and hold, but we can make representations of them.

I've been searching far and wide to find something that would represent my strong desire for support for more Lyme disease research, and perhaps my search-fu is broken, but I couldn't find anything suitable after googling "Lyme disease support ribbon" and "research".

So I initially found a commercial support ribbon generator and played with it... Netting this result:

And I realized that wasn't really working for me.

So I've been working on creating my own awareness and support badge, and here is my rough draft:

What do you think?

It's only a rough draft, mind you, and will need to be rescaled.

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Saturday, November 5, 2011

0 News: Tickborne Disease Outbreak Hits Australia

Brushtail possum
While there has been some controversy over the existence of Lyme disease in Australia, there is no debate over the existence of another tickborne illness, Tularemia - also known as rabbit fever caused by the bacteria, Francisella tularensis.

There are now two reported cases of Tularemia in residents from Tasmania, though the disease is more common in Asia and the US.

Reading about this news originally reminded me of a film I watched a few years ago, Rabbit Proof Fence - and it made me think that more surveillance than ever is needed for rabbits downunder... However, in this case, it was handling possums which gave the unlucky pair the infection. And even though ticks carrying Tularemia are often found on rabbits, the bacteria can affect 250 different species of mammals and birds.

The bacteria which causes the disease can live in wet environments for months and can be transmitted by contact, eating infected animals and through biting insects such as mosquitos, flies, and ticks.

Symptoms include fever, headaches, joint stiffness and shortness of breath. Complications include bone infection, infection of the sac around the heart(pericarditis), meningitis and pneumonia.

It is treatable with antibiotics but can be fatal if left untreated.

Read more:

Video Announcement:

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Wednesday, November 2, 2011

0 Science Articles: Probiotics As Anti-inflammatories, Bacterial Gene Transfer

Probiotics Effective in Combating Antibiotic-Associated Diarrhea, Studies Find; 'Good Bugs' Look Promising as Anti-Inflammatory Agents

In four different studies presented at the American College of Gastroenterology's (ACG) 76th Annual Scientific meeting in Washington, DC, researchers explored the effectiveness of probiotics for antibiotic-associated diarrhea; as an anti-inflammatory agent for patients with ulcerative colitis, psoriasis and chronic fatigue syndrome; and for people with abdominal discomfort and bloating who have not been diagnosed with a functional bowel disorder, such as irritable bowel syndrome (IBS).

American College of Gastroenterology

READ MORE at source:

Bacteria May Readily Swap Beneficial Genes: Microbes Trade Genetic Coding for Antibiotic Resistance and More

Much as people can exchange information instantaneously in the digital age, bacteria associated with humans and their livestock appear to freely and rapidly exchange genetic material related to human disease and antibiotic resistance through a mechanism called horizontal gene transfer (HGT).

Chris S. Smillie, Mark B. Smith, Jonathan Friedman, Otto X. Cordero, Lawrence A. David, Eric J. Alm. Ecology drives a global network of gene exchange connecting the human microbiome. Nature, 2011; DOI: 10.1038/nature10571

READ MORE at source:

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Tuesday, November 1, 2011

0 Institute of Medicine Final Report on October 2010 Tickborne Disease Workshop

Back in October 2010, the Institute of Medicine (IOM) held a workshop which was broadcast online live (and remains available at TV worldwide), Critical Needs and Gaps in Understanding: Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases: The Short-Term and Long-Term Outcomes.

The workshop participants were members of the Institute of Medicine, various researchers, doctors, and members of the Lyme disease patient advocacy community.

A preliminary summary report on the workshop was published by the IOM in April 2011. Now, an official final report has been published and is available on PubMed:

For a more detailed table of contents, try:

Editors: Committee on Lyme Disease and Other Tick-Borne Diseases: The State of the Science.

Source: Washington (DC): National Academies Press (US); 2011.
The National Academies Collection: Reports funded by National Institutes of Health.


It was obvious to participants at the workshop that a significant impasse has developed in the world of Lyme disease. There are conflicts within and among the science; policy; politics; medicine; and professional, public, and patient views pertaining to the subject, which have created significant misunderstandings, strong emotions, mistrust, and a game of blaming others who are not aligned with one’s views. Lines in the sand have been drawn, sides have been taken, and frustration prevails. The “walk in the woods” process of conflict resolution or a similar process seems necessary for creating a new environment of trust and a better environment for more constructive dialogue to help focus research needs and achieve better outcomes. Such a process does not imply a compromise of the science but rather is needed to shift to a more positive and productive environment to optimize critical research and promote new collaborations.

I'd have to say this is a good report for those who are new Lyme disease and other tickborne illnesses to read in order to get an idea of what issues concern researchers and patients.

In terms of an action item plan and treatment to help patients, though, this report is lacking in either and what is sorely needed at this point in time.

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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:
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:

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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:

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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:

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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, 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.

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:

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:

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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?"


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.

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

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?

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.

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.

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:
Science Daily:

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.

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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