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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