2 Viral Genetics Update On Chronic Lyme Drug, VGV-L

Today Viral Genetics posted a letter to shareholders with the following information which relates to their experimental chronic Lyme disease candidate, VGV-L.

The letter stated:

"We are still finalizing scheduling a meeting with the FDA and our team to discuss our Lyme disease pre-IND submission from earlier this spring. Scheduling has been difficult with the number of people involved and the looming summer season. Following this meeting we expect to have a clear road map to follow towards clinical trials"

I am looking forward to hearing more about this meeting. It seems there have been a number of delays on the pre-IND road for VGV-L so far, though, and I can't predict when one is going to see progress on getting this treatment to trial stage.

Now might be the time to contact Viral Genetics and begin asking them questions about what sort of ideas they are coming up with in terms of clinical trial design. As a chronic Lyme disease patient reading along, your input may be informative and useful for researchers.

Stay tuned for more updates on VGV-L as I get them.

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0 Commentary: 20/20 And Needing A New Focus For Lyme Disease

This past Friday, the ABC program, 20/20, aired a show on medical mysteries. Included in this show were segments on people who fly into a rage at certain sounds (misophonia), eat rocks or other unusual non-food items (pica), and one on a girl with Lyme disease who is speculated by doctors to have developed a condition known as foreign accent syndrome (FAS) due to being coinfected with Bartonella.

While I have sympathy for everyone dealing with such conditions and hope everyone who was interviewed for the show gets better, what I'm about to write isn't about their personal interest stories.

Instead, I want to discuss how the media portrays the strange and unusual case to get higher ratings while other stories and information about tickborne infections are either downplayed or avoided.

On Dr. Phil's show several weeks ago, a young model was interviewed - a photogenic young woman who was having partial seizures and self-medicating to treat her pain. While there is evidence that people with Lyme disease can experience seizures, these cases are considered to be in the minority. In Friday night's 20/20 show, a teenager in high school who contracted Lyme disease and Bartonella was speculated to have developed a condition known as foreign accent syndrome (FAS). This is a documented condition, and while I think more evidence is needed to provide a link between Bartonella as its cause in this instance - FAS is even rarer than seizures are.

These stories are getting aired because the media tends to want to focus on the strange and unusual in order to grab viewers' interest and get ratings. The delivery must generate buzz and be sensational in approach in order to get traffic and fixed stares. And this is exactly what the promos for Dr. Phil's show on the young model, Stephanie, tried to achieve - as well as promos by 20/20's on Elaina, the teenager with FAS.

Most viewers at home seeing these shows are watching it because of the weird factor. They see the promo and want to know more, perhaps with their own internal dialogue of, "Wow, that's weird, I wonder how that happens - and does this really happen or is it just made up?" or, "Gee, that's messed up - glad it's not me. But I'm curious, so I'll watch." Some people just have a thing for watching other people's problems in general, and segments like these appeal to their nature.

For those of us who suffer from a disease that is portrayed on television, the first thing that happens is praise. The initial comments from the Lyme disease patient community are congratulatory. They contain the good cheer of finally getting more recognition for what ails us, those of us who have been suffering with chronic Lyme disease and/or coinfections.

And then, the next round of responses trickle in from other patients - a second wave which is not as cheery as the first and criticizes the shows for picking out one narrow and possibly rare symptom and putting it in the spotlight while the rest remain in the darkness.

Then the real, serious criticism gets rolling in the third wave, which is about how these shows will question the afflicted about the true nature of their condition and whether or not they are "faking it". From the perspective of a number of Lyme disease patients, this criticism could be heard regarding the exchanges about Dr. Phil asking the model if she was faking her condition, and in his not arguing against Dr. Auerwater's position that chronic Lyme disease is not a verifiable condition.

Indignant responses fly. Suddenly, what began as a great show for spreading awareness has become a show where a number of people see the value of airing it - yet admit it fell short of their hopes for letting people know what Lyme disease and coinfections are really like and what impact persisting symptoms have had on people's lives.

People just like them. People just like the guy next door, who was mowing the lawn one week and playing soccer afterwards - and now can't make the walk to his mailbox, let alone get to work.

As I see it, there has to be more of an effort in the media to offer education about what Lyme disease and coinfections are from a scientific perspective, and educate people on the most common symptoms which people will experience. From a personal interest perspective, more people need to see how these conditions affect middle class working adults with children of their own.

With this education, more people would be able to relate to the people on the screen and be willing to look into the possibility that they might have a tickborne infection and seek medical advice and testing. They would at least be alerted to the possibility.

With the edutainment of the strange and unusual offered, there isn't enough there for the viewer to grasp the possibility that they, too, may be suffering from this disease - or to know what signs to look for in the future if they do come down ill with tickborne infections.

If someone sees the story of a patient with partial seizures or FAS, they may shrug off the story and not apply it to their own experience of having joint aches, muscle pain, headaches, and blurred vision, and say to themselves, "Thank god I have fibromyalgia and eye problems and not Lyme disease or Bartonella - this stuff is weird". And maybe their current diagnosis is correct. However, there's a chance it's not. In which case, they are better off having the knowledge so they can decide to investigate another diagnosis.

The strange and unusual won't help viewers relate what they see on the screen to their own situation. Truly spreading awareness means educating people on the symptoms for conditions one is most likely to see. It doesn't mean that there aren't exceptions or that unusual symptoms can't occur. It just means that what most people with a given condition experience what one expects to see and to get based on the majority of cases which have occurred.

One more point about the media's focus and where I think it should be - then I'll go:

Why is it that we can easily find these sensationalized stories about unusual symptoms about Lyme disease - but there's seemingly little television coverage of what seems to be the most costly case of Lyme disease in the country - the Lyme disease contracted by senior banker Ina Drew, who worked at JP Morgan Chase, whose absence from work due to Lyme disease led to those remaining in the office making decisions leading to a $3 billion trading loss?

Yes, you did not misread that. $3 BILLION.

You would think this story would be pretty sensational and the media would put this on 20/20 and other shows right away.

There is the personal cost of Lyme disease to the individual. This the media does well to portray to a certain degree. But then there is the cost to their family, their job, and society as a whole. This has not been portrayed that well. It needs to be.

 Image Credit: Peter Wolber

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1 Three Notable NIAID 2012 Research Projects On Lyme Disease

The National Institute of Allergy and Infectious Disease (NIAID) is conducting some Lyme disease related research which I think readers should know about. There are a number of projects to be found on the Project Reporter web site which may be fascinating, but I took the time to select and highlight a few projects which would be of greater interest to patients suffering with Lyme disease and/or its coinfections.

Project: AN INTRACELLULAR NICHE FOR BORRELIA BURGDORFERI
Institution: TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR
PI: Skare, Jonathan

Description (by applicant):

Lyme disease, caused by the spirochetal bacterium Borrelia burgdorferi, is the leading arthropodborne infection in the United States and causes significant morbidity in endemic areas. If untreated B. burgdorferi can persistently infect individuals even though the host mounts a potent adaptive immune response such that antibodies obtained from infected patients or experimentally infected animals effectively kills in vitro cultivated B. burgdorferi. In addition, a robust cell-mediated proinflammatory response is observed that induces IL-6, IL-12 and IFN- and inhibits IL-10. Furthermore, the spirochete can resist complement killing demonstrating that this important component of the innate immune response is not sufficient to eliminate B. burgdorferi infection.

The observation that B. burgdorferi persists in such a hostile environment indicates that the spirochete is adept at evading the host immune response via mechanisms that have not been completely elucidated. One possibility is that B. burgdorferi invades host cells and survives at low levels. Recently we have determined that B. burgdorferi invade both immortalized and, more importantly, primary cells (both fibroblasts and endothelial cells) and persist as viable cells in o-culture. In addition we have preliminary data suggesting that the ability to invade host cells involves both integrin binding and Src kinase activity.

In this application we propose to further characterize the internalization of B. burgdorferi and track the fate of B. burgdorferi within thes infected cells to determine how they affect the localized host response following infection. To accomplish this we will use both in vitro correlates of invasion and intracellular survival as well as in vivo imaging of experimentally infected mice as readouts for our studies.

Specifically, we propose to:

(1) Characterize the invasion of Borrelia burgdorferi into primary fibroblasts. The working hypothesis here is that B. burgdorferi exploits invasion as an additional mechanism to avoid host clearance. Our preliminary studies demonstrate that B. burgdorferi invasion is not dependent on host fibronectin, but does involve B1 integrins other than a5B1. In this Aim we will identify the subunit that pairs with B1 to promote invasion and will also evaluate how B. burgdorferi traffics within these cells; and

(2) Determine if invasion is required for B. burgdorferi persistence in vivo. Our working hypothesis is that invasion contributes to persistence by providing an immunoprotected niche for B. burgdorferi. Since Src kinases are required for borrelial internalization in vitro, we will determine whether Src kinase inhibitors alter the infectivity potential of B. burgdorferi in vivo. In addition to standard cultivation and molecuar approaches, novel in vivo imaging will be employed to assess how the inhibitor affects colonization.

The overall goal of these studies is to determine the extent in which an intracellular locale contributes to borrelial persistence.

PUBLIC HEALTH RELEVANCE: Borrelia burgdorferi, the etiologic agent of Lyme disease, is the most common arthropod-borne infectious agent in the United States, and, as such, represents an important Public Health issue. The studies described in this application are designed to address how B. burgdorferi is able to persist effectively in infected mammals despite effective innate immune killing mechanisms and a potent adaptive immune response directed against this pathogen. The hypothesis being tested herein is that B. burgdorferi is capable of low-level intracellular survival in non-immune cells as an additional strategy to prevent borrelial host clearance.

Link: http://projectreporter.nih.gov/project_info_description.cfm?aid=8300386&icde=12284856

Comment: This really begins fulfilling my wishlist, and I look forward to the imaging study videos that I hope will be made and posted online. If there is some sort of confirmation of intracellular Bb in vivo this may explain why some patients need additional antibiotics and why existing treatments may be inadequate as a matter of timing.

This next project is bound to generate discussion, as it involves the potential role of toxins in Borrelia burgdorferi. In this case, the researcher is looking for gene clusters in Borrelia burgdorferi which may create cytolysins similar to the toxins which are found in Staphylococcus aureus, Listeria monocytogenes, and Clostridium botulinum.

Project: A COMMON DENOMINATOR OF PATHOGENESIS; A RARE OPPORTUNITY FOR NOVEL THERAPEUTIC DE(VELOPMENT)
Institution: UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN
PI: Mitchell, Douglas

Description (by applicant):

Abstract: The 20th century witnessed several major advances in medicine. Perhaps most important were the discovery of antibiotics for bacterial infections and effective vaccines for several major viruses. Unfortunately, the creation of effective vaccines for bacteria has lagged behind analogous anti-viral strategies. Compounded with the rise in antibiotic resistance and a lack of interest from the pharmaceutical industry in pursuing novel antibiotics, we risk losing the fight against bacterial pathogens.

Described herein is an unconventional strategy to exploit bacterial toxins as both novel targets for antibacterial agents and antigens for vaccine development. To intelligently address the increasing threat posed by bacterial pathogens, more effort is needed to uncover the molecular underpinnings of virulence. Our group specializes in the use of bioinformatics, in vitro reconstitution, and genetic manipulation to identify and characterize gene clusters that are responsible for the biosynthesis of virulence-promoting cytolysins. The best-known toxin in this family is the highly modified peptide, streptolysin S (SLS, produced by Streptococcus pyogenes).

SLS production is required for the infective process, but not essential life processes. Our work has uncovered SLS-like toxins are synthesized by at least three other notorious human pathogens, including Staphylococcus aureus, Listeria monocytogenes, and Clostridium botulinum. We aim to study the potential role of the SLS-like toxin in an additional organism, Borrelia burgdorferi (Bb), which causes Lyme disease.

Although widely known, the Bb molecular mechanism of pathogenesis is inadequately defined. If the SLS-like toxin was indeed employed during Bb infections, this would represent the first demonstration of toxin utilization in this family of organisms and would prompt a major revision of borrelioses.

Because bacteria typically employ disparate pathogenic mechanisms, the conserved, SLS-like pathway provides a rare opportunity to develop more broadly applicable, yet targeted countermeasures. From our perspective, new antimicrobial strategies should directly target the pathogenic mechanism, rather than DNA replication, protein synthesis, or the cell wall. This approach holds enormous potential, as these drugs will theoretically be resistant to resistance.

This project will identify inhibitors of SLS toxin biosynthesis for the specific purpose of developing novel antibacterials. Moreover, SLS is non-immunogenic, rendering it an unfeasible candidate for vaccine development.

We have succeeded in generating attenuated variants with the anticipation that these can be used for raising toxin-neutralizing antibodies. The notion of immunizing against a bacterial toxin represents a potentially general strategy for future vaccine development.

With this proposal, we aim to not only fundamentally shift the accepted view of Bb pathogenesis, but also to challenge the paradigm that antibiotics must kill bacteria and non-immunogenic toxins are intractable vaccine candidates. These seemingly unrelated goals are actually quite intertwined. Our approach rests on the philosophy that a more complete understanding of toxin biosynthetic pathways and chemical structure can be rationally exploited to design novel therapeutics.

Public Health Relevance: Bacterial pathogens employ numerous mechanisms to evade the human immune system. We have discovered a novel strategy within the organism that causes Lyme Disease, who's pathogenesis remains largely enigmatic. A greater understanding of these processes will lay the foundation for developing the next generation of antimicrobial drugs.

Link: http://projectreporter.nih.gov/project_info_description.cfm?aid=8145943&icde=12284856

Comment:

Wait... I thought Radolf & co. said Borrelia burgdorferi does not produce a toxin? I know Donta patented some genes in Bb he saw as being analogous to a toxin.

Is there now evidence of newly researched genes which create a toxin in Bb? Or is this an old hypothesis which is being revisited?

Project: ASSESSMENT OF PATIENTS WITH BORRELIA INFECTION
Institution: NIAID
PI: Marques, Adriana

Description (by applicant):

Lyme disease is a multisystem illness caused by infection with the spirochete Borrelia burgdorferi and it is the leading vector-borne disease in the United States. Our current work addresses the following areas in Lyme disease: development of new tests and biomarkers for infection, investigation of persistence of infection with B. burgdorferi in humans, search for the cause of Southern Tick-associated Rash Illness (STARI), and investigation of the role of immune response in Lyme disease and PLDS.

One of the main problems in Lyme diagnosis has been the lack of highly specific and sensitive assays for B. burgdorferi and the lack of a test that could be used to assess response to therapy. Such assays should greatly facilitate the accurate diagnosis of Lyme disease and assessment of response to therapy in individual patients. Currently, no such test is available.

We have developed a new test using the luciferase immunoprecipitation systems (LIPSs) for profiling of the antibody responses to a panel of B. burgdorferi proteins for the diagnosis of Lyme disease. A synthetic protein consisting of a repeated antigenic peptide sequence, named VOVO, had the best diagnostic performance, similar to the C6 test (a diagnostic test using a peptide ELISA that we have helped develop and is highly sensitive and specific). The VOVO LIPS test displays a wide dynamic range of antibody detection spanning over 10,000-fold without the need for serum dilution; and offers an efficient quantitative approach for evaluation of the antibody responses in patients with Lyme disease.

Recent studies have shown that B. burgdorferi may persist in animals after antibiotic therapy and can be detected by using the natural tick vector (Ixodes scapularis) to acquire the organism through feeding. Whether this occurs in humans is unknown.

We have implemented a new clinical protocol to investigate the utility of this approach for identifying persistence of B. burgdorferi in treated human Lyme disease.

STARI is a rash similar to the rash of Lyme disease that occurs in persons residing in southeastern and south-central states and is associated with the bite of the lone star tick, Amblyomma americanum. The cause of the rash is unknown, as it is the natural course of the disease.

We have a clinical protocol to investigate the cause of STARI, and we are applying new genomic tools that identify bacteria based on species-specific sequences in the 16S rRNA ribosomal genes to the skin biopsies from patients with STARI.

Inflammatory innate immune responses are critical in the control of early disseminated infection, while adaptive immune responses are vitally important, particularly the humoral immune response, in controlling spirochete levels in tissues and resolution of Lyme arthritis in animal models. We are examining the antibody response to immunogenically dominant antigens of B. burgdorferi in PLDS patients and controls.

Further investigation of the anti-borrelia immune response may help in elucidating the pathogenic mechanism of PLDS and yield important information for future approaches to diagnosis and treatment. We have a clinical protocol in which we use DNA microarrays to characterize gene expression patterns in skin biopsies from individuals with EM, with the aim of capturing the human host response to pathogen exposure.

We are also investigating the differences in immunological response between predominantly lymphocytic meningitis and predominantly neutrophilic meningitis. Results from these studies will serve as a window into the fundamental biology of the infection.

Link: http://projectreporter.nih.gov/project_info_description.cfm?aid=8336099&icde=12284856

Comment:

The existence of the VOVO LIPS test is nothing new - reports on the development of this test have been around since 2010. Also, there is already information about a chronic Lyme disease xenodiagnosis study out there.

It seems like this project has a large scope - or consists of more than one project under the same umbrella. So far, no project end date has been posted for this entry.

What would be of most interest to me would be finding differences in immunological response between patients with acute Lyme disease and those with assumed PLDS - something Alaedini has already been studying.

(Side note: I thought that it was already determined that Borrelia lonestari, a relapsing fever spirochete, was the cause of STARI or Masters disease - did I miss something?)

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0 Lyme Disease Presents Differently In Women Compared To Men

Recently, Lauren A. Crowder, M.P.H. reported observations on some differences between women and men in response to Lyme disease in a poster at the International Conference on Emerging Infectious Diseases.

The short story: Women with Lyme disease display more clinical symptoms than do men with the disease and also are less likely to seroconvert following treatment, according to findings from a prospective cohort study involving 77 patients.


The study revealed the following observations:

• Significantly more women than men reported joint pain, muscle pain, headache, back pain, heart palpitations, nausea, vomiting, anxiety, numbness and tingling, and changes in vision during at least one of six preplanned study visits with a physician.
• At the initial study visit, a similar proportion of men and women (about 60% of each) tested negative for Lyme disease using the Centers for Disease Control and Prevention’s recommended two-tier testing criteria for serodiagnosis. At the first post-treatment interview, 70% of women who tested negative at the first pre-treatment visit remained negative, compared with only 35% of the men who initially tested negative.

Read more about this Lyme Disease Foundation funded study here:
http://www.internalmedicinenews.com/news/infectious-diseases/single-article/lyme-disease-presents-differently-in-men-and-women/1bf48578d5.html

And see the original source with study here:

SEE page 151 of ICEID 2012 Abstracts
March 11-14, 2012 | Hyatt Regency Atlanta | Atlanta, Georgia
(PDF) http://www.iceid.org/images/iceid_2012_finalprogram_final.pdf

Board 264. Another Difference between Boys and Girls: Sex-Based Differences in Lyme Disease.
L.A. Crowder, A. Rebman, V. Yedlin, M. Soloski, J.N. Aucott; Lyme Disease Research Foundation of Maryland, Lutherville, MD, USA, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.

This isn't the first time, however, that someone observed a difference between men and women's immune responses in relation to Borrelia burgdorferi.

Let's take the time machine back to Sweden, in 2004...

Lyme borreliosis reinfection: might it be explained by a gender difference in immune response?
Sara Jarefors, Louise Bennet, Elin You, Pia Forsberg, Christina Ekerfelt, Johan Berglund, and Jan Ernerudh
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782288/

This study had a different goal than Ms. Crowder's in that it was intended to measure the difference in immunological response between people of both genders who had only been infected once and those who had been reinfected with Lyme disease within a five year period.

The findings relevant to women in this case:

"...for the immunological response there were major differences between men and women. The women displayed higher spontaneous secretion of all cytokines measured, i.e. IL-4, IL-6, IL-10, IFN-γ and TNF-α. Spontaneous secretion, at an infection-free time-point, reflects the habitual immune status and may suggest what type of immunological defence an individual generally displays. For instance, allergy has been considered a Th2-type related condition and, accordingly, atopic individuals have higher spontaneous IL-4 expression than non-atopic controls.

Women of reproductive age are believed to handle infections better than men, having a stronger tendency to show Th1-type responses and expression of higher levels of pro-inflammatory cytokines, and they also develop higher antibody titres than men when vaccinated. However, the female immune response fluctuates with the menstrual cycle. In general, oestrogen has a stimulatory effect on the immune system whereas testosterone acts as a suppressor. When women enter the menopause their levels of oestrogen decrease and thereby the stimulatory effect diminishes, leading to an altered immune status. All except one of the women in our study were postmenopausal, and this could be a factor explaining why more women than men became reinfected with B. burgdorferi."

And...

"Serology was not performed on the individuals in this study because, at the time of EM diagnosis, only 30–40% of patients displayed antibodies to Borrelia. Studies following patients with culture-confirmed EM have shown that, although antibodies can be detected 10–20 years after initial infection, titres decline gradually during the first year."

A paper which cited the previous one discusses the functions of IL-10 in relationship to Borrelia burgdorferi:

Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation.
Gautam A, Dixit S, Philipp MT, Singh SR, Morici LA, Kaushal D, Dennis VA.

Source: http://www.ncbi.nlm.nih.gov/pubmed/21947773

To sum it up: IL-10 (an interleukin) which is produced in higher amounts in women than it is in men, is responsible for inhibiting the actions of some genes in Borrelia burgdorferi - but it is also responsible for empowering the actions of some genes, too.

What implication this has on infection in different genders remains to be seen and requires more study.

But what is already known about the role of inflammation in the presence of Borrelia burgdorferi is important to take note of here: Inflammation facilitates Borrelia burgdorferi's adaptation to its host; it stimulates antigenic variation and it leads to increased spirochetal burden in mice. So if this applies to humans: All that pain, swelling, and inflammation patients feel? It is good for the spirochetes, and it is bad for you.

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1 The Phenomenon Of ‘Chronic Lyme’; An Observational Study

Recently, the results of an observational study on chronic Lyme disease in Norway were published in the European Journal of Neurology. (The full text of the study is behind a pay wall on Wiley - but otherwise you can read the abstract online.) According to the National Institute of Health (NIH) clinical trials database, the purpose of the study was:

"... to chart clinical and laboratory findings in Norwegian patients with symptoms attributed by themselves or their doctor to ongoing chronic Bb infection. Objectives are to assess laboratory findings in relation to established diagnostic criteria and to form a picture of the burden of symptoms and illness perception in this group of patients. The study is essentially exploratory, and is supposed to raise rather than to test hypotheses."

Based on this, it sounds like the authors' original expectations for this study were that the researchers would find out in a given population that among those who either suspect they have chronic Lyme disease and have it - and those who suspect they have chronic Lyme disease and don't have it - that it would be discovered what clinical differences and diagnostic markers would set them apart.

But the abstract doesn't indicate what the criteria are for a case definition of chronic Lyme disease if the researchers had one in mind. Rather, it indicates that of the patients enrolled in the study, there was no evidence that any patient had an existing infection with Borrelia burgdorferi.

The following comments are strictly preliminary and based on the content of the abstract only - a more detailed review is in order once the full text has been read:

First, I was disappointed to find out that the total enrollment expected for this study was a mere 30 participants - and in the actual study, there were only 29 enrollees. This is a very small pool of applicants, and I don't think the data can be extrapolated to fit a large group of people - or even more so, a large group of people from an area which is highly endemic for Lyme disease.

Second, this study in no way set out to solve the problem of whether or not chronic Lyme disease is a real condition - I don't think that was the researchers' goal. Their goal was to characterize those people who either self-reported that they thought they had chronic Lyme disease based on their symptoms or their doctors suspected they had chronic Lyme disease based on their symptoms. Nothing less, nothing more.

It would have been more productive for patients had the researchers taken additional steps to determine what exactly the cause of these symptoms were. But the study was not designed to take those additional steps and just left us with these basic data points:

• Twenty patients (72%) had symptoms of an unknown cause; of them six met the criteria for Post Lyme disease syndrome (PLDS).

• Fourteen patients (48%) had the presence of anti-Borrelia burgdorferi antibodies.

• Eight patients (28%) had other well-defined illnesses.

The researchers stated, "None had evidences of persistent Bb infection, but whether current diagnostic criteria are functional in patients with longstanding complaints is controversial."

Looking at all of this, I'm not sure how to even interpret the initial data shared in the abstract... When those 72% are discussed - of which six patients met the criteria for Post Lyme disease syndrome - are those six patients exclusive of the fourteen patients with anti-Borrelia burgdorferi antibodies or are they inclusive?

If it's exclusive, then twenty of the twenty nine patients have evidence of some relationship to a Borrelia burgdorferi infection. If it's inclusive, then it's only fourteen patients who have evidence of this relationship.

But let's assume they are inclusive, and only fourteen had evidence of anti-Borrelia burgdoferi antibodies. Even if only 48% of the patients studied already have a history of exposure to Borrelia burgdorferi and continue to have persisting symptoms, I think that counts as evidence towards a relationship between Lyme disease and persisting symptoms. Either as a trigger or present causative agent. The researchers themselves state that this is at least partly the case, by reporting that, "sequelae from earlier Lyme disease were probable as main explanatory factor in some cases."

That said, a whopping 72% of patients had symptoms of an unknown cause. So what did they have? It is unknown to me if the issue of seronegativity was considered in patients' reports, whether or not patients with positive antibodies were tested for other conditions with cross reactive antibodies, or whether or not patients were studied for evidence of other tick-borne illnesses.

What is known, however, without having access to the full text is that patients had their blood tested and their CSF studied for any abnormalities and the presence of intrathecal antibodies, as shown in Table 1 of the Supporting Information section. And what is found there leaves me questioning the results - at least in part.

For example, the first patient mentioned in the "unknown causes" category is a 43 year old male who is both IgM and IgG positive for Borrelia burgdorferi antibodies, had 78 weeks of IV antibiotic treatment, and yet is not considered by their definition to have Post Lyme disease syndrome because there was "no documented episode of Lyme disease". This is puzzling - if someone has serological evidence of Lyme disease and they continue to have symptoms - wouldn't this indicate by the most conservative view that the patient at least has Post Lyme disease syndrome (regardless of the controversy over persistent infection)?

That there was no earlier documented acute case of Lyme disease seems to be at the heart of determining whether or not a patient is at least meeting the criteria for Post Lyme disease syndrome. According to this study, it seems that if there was no earlier record of an EM rash and evidence of a tick bite by a doctor, then the patient is disqualified from a Post Lyme disease syndrome diagnosis. Why this is the case when there is evidence patients do not always recall a tick bite, a rash is not always present (and this is even more likely in Europe based on some research), and there are documented cases of patients who are asymptomatic in the early stage - only to be profoundly disabled by symptoms later - is unknown. It doesn't make sense to me.

It would have been interesting had the researchers ran epitope and proteomic analysis of patients' CSF and confirmed earlier research completed by Chandra/Alaedini and Schutzer - so far, I see no evidence this was done; I would expect such an analysis would be included in the abstract. I would also like to know what - if any - immunological factors were examined in each of these patients.

After reading this abstract, what one is left with is are more questions about the nature of chronic Lyme disease than answers.

What is a good starting point for more research of this nature?

What is the relationship between persisting symptoms and infection with Borrelia burgdorferi?

The abstract for this study and its supporting information do not answer these questions. All this study does is begin to examine what relationship there is between Borrelia burgdorferi and persisting symptoms in a small group of people.

References:
http://onlinelibrary.wiley.com/doi/10.1111/j.1468-1331.2012.03691.x/abstract
http://clinicaltrials.gov/ct2/show/NCT01151150
http://www.sciencedirect.com/science/article/pii/S1521661611001914
http://www.plosone.org/article/metrics/info%3Adoi%2F10.1371%2Fjournal.pone.0017287

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10 2011 Guidelines For Treating Lyme Disease...

... from Russia are here. With love.

This past weekend I got into a lengthy discussion with "radicale" on the Embers et al Issues a Statement post, and somewhere along the line, amid over 50 comments there (I highly recommend reading them, too), radicale advised that I check out documentation and research on Lyme disease from Russia and the Balkans.

So I did, and I did in part because he's the one who told me that treatment for both acute and disseminated Lyme disease in Serbia - particularly at two hospitals in the country - is more aggressive by default than it is either in the US or in Canada. He also stated that this treatment is backed by clinical studies (two of which are mentioned in the comments on the above post) - and because it was his home country and had this scientific backing, he went there for treatment for Lyme disease rather than in Canada.

He shared what he said was the standard antibiotic treatment schedule for Lyme disease given to patients in a few hospitals in Serbia:

"It is interesting that in Serbia, where every third tick is infected, amoxicillin is the drug of choice and it is routinely given for 6 weeks for early Lyme Disease.

In addition, disseminated Lyme Disease is treated in the following manner:

1) 4 weeks of ceftriaxone 2g/day plus metronidazole 500 mg bid
or three weeks of amoxicillin 1g tid followed by three weeks doxycycline 200mg bid plus metronidazole 500 mg bid
2) in case of persisting symptoms therapy is extended using pulsed doses up to 6 months

There are open-label control studies to support this type of treatment (in Serbian)."

I found this difference in approach to treatment interesting and I wanted a confirmation with a reliable source - so I have requested more information from him in terms of a citation for official guidelines using this antibiotic treatment.

While awaiting his response, I decided to see if I could find guidelines for other countries in the region and translate them. So far, I have found the 2011 guidelines for treatment of tickborne Borreliosis (they call it SDS) for Russia and ran them through Google Translate.

They are - as you will see - pretty bare bones relative to the guidelines document written up by either the IDSA or ILADS... And oh, OPTIONS... We have OPTIONS... did I say we have options? Yes, only I don't know what all the options actually are yet - I would have to figure out what all the drugs are by name.

Far as I can tell, Azitroks = azithromycin. doksitsi-wedge is, I think, some form of liquid doxycycline that is highly absorbent. klaforan = Claforan. Instructions at the bottom "per os" means "by mouth" or "orally".

I can figure out what some of the other drugs are due to their spelling coming close to the English word - but other drugs are unknown to me by the name being used...

APPROVED
Head of the Department of Health
Tomsk Oblast
O.S. Kobyakov
2011
Lepekhin A.
MD, Professor, Head of
Infectious Diseases and Epidemiology, State Educational Institution SSMU Health Ministry of Russia

Lukashova L.
MD, Professor, Department of Infectious Diseases and Epidemiology
GOU VPO SSMU Health Ministry of Russia

Ilyinskikh EN
MD, Professor, Department of Infectious Diseases and Epidemiology
GOU VPO SSMU Health Ministry of Russia

Zhukov, N.
MD, Professor of Neurology and Neurosurgery
GOU VPO SSMU Health Ministry of Russia

Portnyagina EV
PhD, Assistant Professor of Epidemiology and Infectious Diseases
GOU VPO SSMU Health Ministry of Russia

Dobkin, MN
PhD, chief freelance specialist in infectious
Health Department of the Tomsk region

Guidelines for Physicians
(Third edition, revised and enlarged)

Tomsk - 2011

THERAPY PROGRAM SDS

Schemes of causal treatment for tickborne Lyme Borreliosis

During the acute, manifest form (mild)

(Schema therapy - individual choice of doctor)
A. Amoxicillin 0.5 g three times daily per os (0.375 g of amoxiclav three times daily
per os), 14 days.
 or
Two. Azitroks 0.5 1 g once a day per os, 6 days.
 or
Three. Doxycycline 0.1 g 2 times a day per os, 14 days.

During the acute, manifest form (medium severity)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 1.0 g 2 times a day by intravenous drip, and 7 days, then - Amoxil-
penicillin of 0.75 g 3 times daily per os (0.375 g of amoxiclav three times daily per os),
7 days.
  or
Two. Ceftriaxone 1.0 g 2 times a day by intravenous drip, and 7 days, then - doksitsi-
wedge of 0.2 g 2 times a day intravenous drip, and 7 days.
 or
Three. 0.75 g of amoxicillin three times daily per os (0.560 g of amoxiclav three times daily
per os), 7 days, then - Azitroks 0.5 g of 1 time per day per os, 6 days.
 or
4. Doxycycline 0.2 g 2 times a day intravenous drip, and 7 days, then - Azitroks
0.5 1 g once a day per os, 6 days.

During the acute, manifest form (severe severity)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 2.0 g 2 times a day intravenous drip, and 10 days later - Amoxil-
penicillin at 1.0 g three times daily per os (amoxiclav, 0.625 g 3 times daily per os),
10 days.
 or
Two. Ceftriaxone 2.0 g 2 times a day intravenous drip, and 10 days later - doksitsi-
wedge of 0.2 g 2 times a day intravenous drip, and 10 days.
 or
Three. Amoxicillin 1.0 g three times daily per os (amoxiclav, 0.625 g 3 times a day
per os), 7 days, then - Azitroks of 1.0 g of 1 time per day per os in a 1-day and 0.5 g of 1
once a day per os for the next 5 days.
 or
4. Doxycycline 0.2 g 2 times a day intravenous drip, and 7 days, then - Azitroks 1.0 g of 1 time per day per os in 1-day and 0.5 g of 1 time per day per os for at- the next 5 days.

8Podostroe for (mild)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 1.0 g of a once-daily intravenous infusion, and 10 days later - doksitsi-
wedge of 0.1 g 2 times a day intravenous drip, and 10 days.
 or
Two. Amoxicillin 0.5 g three times daily per os (amoxiclav, 0.625 g 3 times a day
per os), 10 days later - doxycycline 0.1 g 2 times daily intravenous-drip
10 days.

Subacute (medium severity)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 1.0 g of a once-daily intravenous infusion, and 10 days later - doksitsi-
wedge of 0.2 g 2 times a day intravenous drip, and 10 days.
 or
Two. Ceftriaxone 1.0 g of a once-daily intravenous infusion, and 10 days later - Amoxil-
penicillin of 0.75 g 3 times daily per os (0.375 g of amoxiclav three times daily per os),
10 days.

Subacute (severe severity)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - doksitsi-
wedge of 0.2 g 2 times a day intravenous drip, and 10 days.
 or
Two. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - Amoxil-
penicillin at 1.0 g three times daily per os (amoxiclav, 0.625 g 3 times daily per os),
10 days.

Chronic (phase compensation)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - klaforan
2.0 g 2 times a day by intravenous infusion or intramuscular injection, and 10 days, then -
amoxicillin 0.5 g three times daily per os (0.375 g of amoxiclav three times daily
per os), 7 days.
 or
Two. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - klaforan
2.0 g 2 times a day by intravenous infusion or intramuscular injection, and 10 days, then -
doxycycline 0.1 g 2 times a day by intravenous drip, and 10 days.

Chronic (Stage subcompensation)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - klaforan
2.0 g 2 times a day by intravenous infusion or intramuscular injection, and 10 days, then -
amoxicillin 0.5 g three times daily per os (0.375 g of amoxiclav three times daily
per os), 10 days.
 or
Two. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - klaforan
2.0 g 2 times a day by intravenous infusion or intramuscular injection, and 10 days, then -
doxycycline 0.2 g 2 times a day by intravenous drip, and 10 days.

9Hronicheskoe for (stage decompensation)

(Schema therapy - individual choice of doctor)
A. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - klaforan
2.0 g 2 times a day by intravenous infusion or intramuscular injection, and 10 days, then -
amoxicillin 0.5 g three times daily per os (0.375 g of amoxiclav three times daily
per os), 10 days.
 or
Two. Ceftriaxone 2.0 g of a once-daily intravenous infusion, and 10 days later - klaforan
2.0 g 2 times a day by intravenous infusion or intramuscular injection, and 10 days, then -
doxycycline 0.2 g 2 times a day by intravenous drip, and 10 days.

Scheme of pathogenetic and symptomatic therapy

Universal scheme of pathogenetic and symptomatic therapy
patients with SDS

(Drugs, marked with #, appoint, and the testimony of an individual selection, dosing regimen of drugs - depending on the severity of illness)

- Lineks 1-2 capsules three times daily per os, 30 days;
# 0.9% sodium chloride, 200 ml of intravenous-drip of 5% glucose solution
200-400 ml of intravenous-drip reopolyglukine 200-400 ml of intravenous-ka-
pelno;

# Immunomodulators (including data immunogram).

When neurological manifestations...

# Venotonicheskie tools
- 2.4% -10.0 aminophylline IV-drip, 10 days
or
- Cavinton (vinpocetine) 4-mL intravenous infusion, 10 days
# Neuroprotective drugs
- 10 ml Cerebrolysin intravenous-infusion, 10 days
or
- Actovegin 5-20 ml per day by intravenous drip, and 10 days later - on 0.2 g of 3
times a day per os, 30 days
or
- Cytoflavin 10 ml intravenous drip, in 100-200 ml of 5-10% solution of glucoside
goats, or 0.9% sodium chloride solution, 1 time per day, 10 days later - on 2
tablets 2 times daily per os, 25-30 days
or
- Nootropil 5 ml intravenous drip, and 10 days
or
- Lutset 10 ml intravenous bolus, and 10 days

# Metabolic means

- Mildronat 10% -5.0 (10.0) IV-bolus, 10 days
or
- Panangin 10-20 ml intravenous bolus, and 10 days, then - 1 tablet 3 times a
per day per os, 30 days

# Vitamin
- Milgamma 2 ml daily intramuscular injections of 10
or
1011
- Berokka plus 1 tablet daily per os, 30 days
or
- Benfolipen (combined multivitamin complex) 1 tablet 1.3
times daily after meals per os, 30 days

# Tranquilizers
- Nozepam of 0.01 g per os the night
or
- Grandaksin of 0.05 g 2 times a day per os
or
- Alprazolam 0,025 g per night per os, with a gradual increase in dose
0.025 g in 3-5 days
or
- Phenazepam of 0.005-0.01 g per night per os, 7-10 days
or
- Glycine, 0.1 g 4-6 times a day sublingually, long-term (period-rekonva
lestsentsii)
or
- Adaptol (mebikar) to 0.5 g 2-3 times a day per os, a few days to 2-3
months (the period of convalescence)

# Sedatives
- New-passive 1 tablet or 1 tsp. solution 3 times a day per os, 30 days
or
- Tincture of motherwort (peony, Valerian) or Corvalol (valokordin, valoser-
din)

otvornye tools
- Donormil to 0,015 g per night per os
or
- Radedorm to 0,005 g per night per os
or
- Ivadal of 0.010 g per os the night
or
- Imovan of 0.0075 g per night per os
or
- Sanval to 0,005 g per night per os

# antidepressants
- Amitriptyline to 0,025 g per night per os, with a gradual increase in dose
0.025 g, 30-40 days
or
- Luvox of 0.05-0.1 g per night per os, up to 3 months
or
- Agomelatine 0,025 g per night per os, up to 3 months
When arthrologic manifestations

# Non-steroidal anti-inflammatory drugs
- Diclofenac 3 ml intramuscular injections of 6 or 0.025-0.05 g 3 times
per day per os, up to 7 days
or
- Movalis 1.5 mL intramuscularly or 0.015 g of 1 time per day per os, up to 7 days
or 12
- Ksefokam of 0,008 g 1-2 times daily per os
or
- Celebrex to 0.2 g 2 times a day per os, up to 7 days
or
- Artrozan (meloxicam) to 0,015 g 1 a day per os

# Antispasmodics
- Midokalm of 0.05 g 2-3 times a day per os, with a gradual increase razo-
curve to the dose of 0.15 g (0.1 g 1-2 times a day intramuscularly or intravenously
slowly)
or
- Sirdalud 0,002 g 3 times a day

# With the express pain
- Diprospan 1 ml in 2-4 ml of 0.5% solution of novocaine or lidocaine 2%
an intramuscular injection once a week, 3-5 injections
or
- Combilipen (combined multivitamin complex in conjunction with the Do-
dokainom) 2 ml intramuscularly daily for 5-7 days, then - 2
ml 2-3 times a week for 2 weeks

# Massage, therapeutic exercise, physical therapy (in the period of convalescence)

When cardiac manifestations...

# Metabolic means
- 10% mildronat -5,0-10,0 intravenous bolus, and 10 days (myocarditis, myocardial-
odistrofiya, ECG signs of repolarization, disturbances of rate)
- Panangin 10-20 ml intravenous bolus, and 10 days, then - 1 tablet 3 times a
per day per os, 30 days (arrhythmias and conduction)

# Sedatives
- New-passive 1 tablet or 1 tsp. solution 3 times a day per os, 30 days
(Syndrome of vegetative dystonia)
or
- Tincture of motherwort (peony, Valerian) or Corvalol (valokordin, valoser-
din)

# Antihypertensives
- Atenolol to 0.05-0.1 g per day, 20-30 days (arterial hypertension syndrome-
sion, cardiac arrhythmias, the syndrome of vegetative dystonia, stenokardicheskie
syndrome)

---

Comments? Questions? Thoughts?

My first thought on these guidelines are that the first thing I notice is that they are broken down into certain stages and conditional stages of Lyme disease/Borreliosis that are not defined here - perhaps they are defined in another document I have yet to locate, but just at first glance, medical professionals in Russia seem to break the stages down into finer grades of distinction with treatments to match.

My second thought is it seems their approach is to vary the kind of antibiotic used, and use the most bactericidal antibiotic first, followed by progressively less bactericidal and more bacteriostatic antibiotics. I am wondering if this is done for any specific reason.

My third thought is that the IDSA would probably not like part of these guidelines because they recommend using vitamins, massage therapy, and a little alternative medicine. That tincture of motherwort would probably be troubling to them. (Personally, I found valerian root to be a useful sleep aid, but it smells like dirty socks so I don't use it.)

My fourth thought is that this is pretty thorough in terms of intensive treatment for patients with cardiac and neurological manifestations of disseminated and late stage Lyme disease/Borreliosis, and I like that it offers ideas for supportive treatment for not only pain, anxiety, and depression - but for irregular heart rhythms.

There are some things that didn't translate well and I'm wondering what they are. "8Podostroe" for one thing."9Hronicheskoe" for another... I don't know what that is, either. Readers are invited to guess.

One thing I have learned while looking at various Russian and Balkans regional web sites on Lyme disease: They take it seriously.

You are considered an early mild case only within the first few days of a bite. After that, there is concern the disease has moved to the disseminated phase and it is treated more intensively. They also believe in relapses, and will give additional antibiotics if the initial course fails. In a number of places, you are expected to visit an infectious disease doctor as an outpatient 1, 3, 6, and 12 months after treatment in order to get follow up testing, report any relapsing, ongoing, or new symptoms, and give doctors more data for them to collect to understand how Lyme disease affects people.

There's more I've learned, but I'll share it later. Right now I just wanted to put these out here for you to see what other countries are doing to treat Lyme disease.

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6 Washington Post Article On Chronic Lyme Disease

The Washington Post has an article on chronic Lyme disease which is well written and touches upon not only how the disease can be insidious and slowly creep up on people with a wide range of symptoms - it also touches upon the science and the controversy around chronic Lyme disease. 

I consider an article such as this one to be a far better one than "Chronic Lyme: a dubious diagnosis" which was published in 2010 in the Chicago Tribune, because this one focuses on patients, their symptoms, and outcomes of their treatment in the face of information which contradicts their reality. 

These two paragraphs tidily sum up the sort of information chronic Lyme disease patients are faced with when they first receive their diagnosis and begin treatment:

"I began my research on the Web site of the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. “Lyme disease can usually be successfully treated with 3 to 4 weeks of antibiotic therapy,” it stated. “After being treated for Lyme disease, some patients still report non-specific symptoms, including persistent pain, fatigue, impaired cognitive function . . . . These patients . . . may be diagnosed with post-Lyme disease syndrome. Studies have shown that more antibiotic therapy is not beneficial and the risks outweigh the benefits.” 

I was puzzled. Why did the NIH say long-term antibiotic therapy was not effective? Although it was only one case, my friend’s daughter had apparently been cured by it. And at this point, Pat had been taking a single antibiotic for about six weeks and was clearly getting better. After a week on the drug, the numbness in his hands started to recede. After a month, he stopped gagging while he drank. But he was still extremely sick, and it seemed clear that stopping the treatment would be a disaster."

This is, as they say, where the rubber meets the road.

Once you begin antibiotic treatment and your symptoms begin to improve, the decision to stop them earlier doesn't make sense. When your symptoms are so severe that you cannot function and other alternatives you have tried have not worked, what else are you doing to do?

I have stopped treatment during the course of my disease - only to find my symptoms returning within a few days after antibiotics were stopped. Even after the worst of my symptoms began to fade, I have also gone without treatment for months, where I hovered back and forth between a state of flu and arthritis to fibromyalgia and functional fatigue - never living, just vaguely existing - only to improve when I began antibiotics again.

Inbetween the antibiotics, I tried painkillers and sleeping pills. I tried trigger point release therapy, gentle massage, and acupuncture. Of these, acupuncture worked the best. But beginning antibiotics again often not only brought the pain down - it gave me some energy and focus back.

As one person without a control version of myself, I can't really tell you how my control version would have fared without antibiotic treatment. But it's not a thought I want to contemplate, because I do remember just how much more worse off I was when I first found myself ill with Lyme disease and how I declined without treatment:

I could not understand what I read even if I read it multiple times and could not follow conversations around me. I remember crawling on my hands and knees to the bathroom, and not being able to wash my own back. Raising my arms became impossible. They were too heavy to lift. And at one point, I would fall asleep sitting up against many pillows and try hard not to move even the slightest amount because even that would send severe pain jolting through my entire body. From my head down to my fingertips; from my neck down to my toes. Every.single.joint. Every.single.muscle.

With antibiotics, I went from nearly bedridden to being able to walk. At first to the front door. Then to the mailbox. It was slow going. Agonizing.

But eventually, I did manage to get out more and walk further, and have life become at least a little closer to something resembling normal. Not in every respect - but not the hell it was when I first contracted Lyme disease, either. And I still have some distance to travel before I am more or less back to my old self.

This is just one report from one person. It's anecdotal. It's not the result of a clinical trial or published in a peer-reviewed well-established journal - unless we consider Rita, TicksSuck, Joanne, Heidi, Claudia, and others who comment here to be peers and this blog to be the journal.

I wish I had evidence I could give everyone to tell people that they helped me. That I improved, and when I went off of them for extended periods of time, it was like turning the clock back. Progress could be undone.

But I don't have hard scientific evidence to hand you on this one. I can say, though, that I went from doing next to nothing and wanting to die from severe pain to beginning to think again, read and write again, and sleep through the night without stabbing pain waking me. That, for me, was evidence enough that more antibiotic treatment helped. That's why I continued when I did.

Anyway... quit hanging out around here and go check out the entire Washington Post article, "The doctor diagnosed chronic Lyme disease, but many experts say it doesn’t exist": http://www.washingtonpost.com/national/health-science/the-doctor-diagnosed-chronic-lyme-disease-but-many-experts-say-it-doesnt-exist/2012/02/06/gIQA4aMHtR_story.html

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6 Viral Genetics Issues Latest Report On Chronic Lyme Clinical Trials Status

Recently, Viral Genetics posted an update on its move towards testing its product, VGV-L, for treating chronic Lyme disease.

Research for this product was funded by two Lyme disease advocacy organizations, Time For Lyme, Inc. and the Turn The Corner Foundation.

You might be familiar with the project lead, Dr. Karen Newell Rogers, whose research was mentioned at the LDA-Columbia University Lyme 2011 Lyme and TBD Conference.

I previously wrote about Dr. Newell Rogers research, and highlighted the following excerpt from a summary report on her conference presentation:

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

She pointed out: 

"[...]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."

So what is VGV-L, and what does this soon-to-be-tested product supposedly do? It would seem to fall more in line with Dr. Newell Rogers' research addressing chronic inflammation than addressing chronic infection, based on what I've read thus far.

According to Viral Genetics' web site, VGV-L seems to be related to Targeted Peptide Therapy (TPT), a therapy which uses synthetic peptides to "trick" cells that may be responsible for harmful symptoms and makes these cells vulnerable to the body's natural immune response mechanism.

What exactly are targeted peptides? According to Viral Genetics (VG), targeted peptides are custom-designed protein fragments that work to modify certain immune system reactions that they believe cause or worsen some inflammatory diseases.

More about Targeted Peptide Therapy is found on its own VG page:

 "Autoimmune diseases occur when the body reacts to itself or self-tissues. In some cases, an external threat from disease-causing organisms activates too many of certain types of immune cells which in turn cause damage the body. A physical trait of those cells also makes them impervious to the body's natural defense system that would ordinarily limit their numbers.  

TPT works by tricking those impervious cells into dropping their defenses. They can be fooled into releasing their protective shields, swapping the shield for a synthetic TPT-polypeptide instead. Those peptides, created by our research team, have been engineered to make the cell susceptible to the body's natural defenses. We expect our TPT drug compounds to enable the body to destroy the cells that help trigger the symptoms of autoimmune diseases." 

 So what this sounds like is it a treatment for chronic Lyme disease which lessens inflammation by modifying the immune system in some way.

And judging from the content above, I am wondering if the "certain types of immune cells" of which there are too many could be referring to the overabundant low quality plasma cells that were found in lymph nodes in Tunev and Barthold's study, "Lymphadenopathy during Lyme borreliosis is caused by spirochete migration-induced specific B cell activation."?

So what is the status of getting VGV-L's TPT to the clinical trial stage?

Excerpts from its letter to shareholders indicated that due to the time required for coordinating schedules, screening clinicians, and presenting the data, that it was only "recently that we neared finalization of securing a clinician to act as lead on this program. We expect to be able to discuss this in much more detail very soon, but I am very confident that we will be filing our pre-IND for our Lyme disease candidate this year."

 For those who are reading along who do not know what a pre-IND is, "IND" stands for Investigational New Drug, and any clinician who wishes to begin clinical trials to test a new drug must file for approval from the FDA.

From the FDA's own site:

"During a new drug's early preclinical development, the sponsor's primary goal is to determine if the product is reasonably safe for initial use in humans, and if the compound exhibits pharmacological activity that justifies commercial development. When a product is identified as a viable candidate for further development, the sponsor then focuses on collecting the data and information necessary to establish that the product will not expose humans to unreasonable risks when used in limited, early-stage clinical studies.

FDA's role in the development of a new drug begins when the drug's sponsor (usually the manufacturer or potential marketer) having screened the new molecule for pharmacological activity and acute toxicity potential in animals, wants to test its diagnostic or therapeutic potential in humans. At that point, the molecule changes in legal status under the Federal Food, Drug, and Cosmetic Act and becomes a new drug subject to specific requirements of the drug regulatory system."

(For more specifics, see: http://www.fda.gov/drugs/developmentapprovalprocess/howdrugsaredevelopedandapproved/approvalapplications/investigationalnewdrugindapplication/default.htm)

I am finding this all very interesting and will continue to watch Viral Genetics as they move towards the trial phase.

I wonder what requirements will need to be met for study participants - and how many chronic Lyme disease patients would be willing to sign up?

Would you?

Additional Information: http://www.viralgenetics.com/investors/2012-Letter-to-Shareholders.pdf

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2 Blog Post: A Letter To A Patient With Chronic Disease

This blog post from Dr. Rob Lambert got passed on to me by a friend.

Although the blog post is from 2010, the advice given of how to approach a doctor when you have a chronic illness is good advice any time.

And with over 250 comments, those who posted and exchanged comments with the good doctor had their own advice and concerns to share.

 I highly recommend checking out Dr. Rob's post in Musings Of A Distractible Mind blog:

A Letter To A Patient With Chronic Disease:
http://distractible.org/?p=3912

You also might want to check out Dr. Rob's new blog, too:

More Musings (Of A Distractible Mind):
http://more-distractible.org/

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0 News: New Molecular Test Could Detect Early Lyme Disease

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

Excerpt that will be of interest to readers:

"Q: In years to come, is this something that could be available in hospitals? 

That's the hope we have. The first clinical trial is on the detection of Lyme disease. A fraction of patients get a skin rash but for those without the rash it is very difficult to diagnose. So with the particles we are able to capture the antigens that come from the spirochaete that is the causative agent of Lyme disease. If we see in the urine a piece of the bacteria of the spirochaete, we are sure that the patient has Lyme disease. We are gathering all the evidence and then we will need to go first for FDA approval before it is available in clinics. 

Q: How much earlier will you be able to detect Lyme disease? 

Lyme disease has a window of two to three weeks before seroconversion [production of antibodies in the host blood, indicating infection]. With our tests, we're able to detect it before seroconversion, because we're not looking for the antibodies, we just look for the spirochaete. I would say here, yes, by weeks, and earlier diagnosis would be beneficial for the prognosis."

Comment: One thing this does make me wonder about is how similar this test is to Temple Douglas' hydrogel nanoparticle test for early detection of Lyme disease. Maybe it's time to do a compare and contrast of patent application content?

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

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0 News: New bacterium found causing tick-borne illness ehrlichiosis in Wisconsin and Minnesota

 ScienceDaily (2011-08-03) -- A new tick-borne bacterium infecting humans with ehrlichiosis has been discovered in Wisconsin and Minnesota.

Experts say the new species from the Ehrlichia genus can cause a feverish illness in humans.

The new bacterium, not yet named, has been identified in more than 25 people and found in black-legged ticks, also known as deer ticks (Ixodes scapularis), in Minnesota and Wisconsin. Researchers used culture and genetic analyses.

Citing from the article, this is important to know:

"Doctors need to know to test for ehrlichiosis in the two states so the diagnosis is not missed. However, traditional blood antibody tests may offer misleading results and fail to accurately identify the new species. A specific antibody test for the new bacterium has been developed by the CDC but isn't widely available. Instead, a molecular blood test that detects DNA from the new Ehrlichia species is the preferred method for detecting this disease in symptomatic patients."

READ MORE: http://www.sciencedaily.com/releases/2011/08/110803174745.htm#

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16 Abstract: Chronic Tick Associated Poly-organic Syndrome

Diagnosis and treatment challenges in patients with chronic Tick Associated Poly-organic
Syndrome (TAPOS) - Case series
A. Radulescu, M. Flonta, D. Tatulescu
University of Medicine and Pharmacy, Cluj, Romania,
The Teaching Hospital of Infectious Diseases, Cluj, Romania
Int J Infect Dis 2010;14

Background: Chronic Lyme disease is often considered in case of long lasting miscellaneous symptoms after tick bites. Despite new codified diagnosis algorithm and treatment persistent signs and symptoms frequently occur. The aim of the study was to assess the diagnosis of Tick Associated Poly-organic Syndrome (TAPOS) and to evaluate the treatment’s efficacy.

Methods: A consecutive case series of patients referred to the Cluj-Napoca Teaching Hospital of Infectious Diseases (January 2006 -October 2009) revealed 52 patients with TAPOS. Inclusion criteria were: more than 18 years of age, chronic symptomatology, positive Borrelia burgdorferi serology and/or tick-bite. Data was collected through chart review and medical observation. We used two clinical scores classifying the diagnosis of TAPOS. All patients were seropositive for IgM and/or IgG antibodies to Borrelia burgdorferi (EIA and western blotting). Treatment regimen was established according to the literature data. They received intravenous ceftriaxone, 2 g daily for 21-28 days and doxycyline 200 mg daily for 21 days. Patients with persistent symptoms were retreated with the same regimen.

Results: The baseline assessment documented that the most frequently reported symptoms were neuropsychological (90%), systemic (98%) and articular (23%). The sex ratio was 0.26 (41 women, 11 men), the average age was 43.2 ±12.6 years. Only 7 patients experienced erythema migrans, 57% had tick exposures and Borrelia burgdorferi serology was 92% positive [44 (84%) IgM positive, 19 (36%) IgM and IgG positive]. According to both clinical scores all patients were classified as “very probable” or “probable”. All patients were evaluated at 3 months showing a decrease in the number and intensity of signs and symptoms and the same serologic pattern. Ten patients were 2-3 times retreated due to persistent clinical picture, all presenting mood disorders or depression. No case of clinical aggravation or serious adverse events was reported and Jarish-Herxheimer syndrome was observed just in two cases. Most of the patients remained with at least one neuropsychological complaint.

Conclusion: Diagnosis of miscellaneous Borrelia burgdorferi chronic infection is challenging but should be always considered if prolonged symptomatology or tick related. Treatment regimens are not standardized, we appreciate as reasonable shorter 6 week regimens.

---

Comments: 

First of all, "Tick Associated Poly-organic Syndrome" or TAPOS - is this a new name Romanian doctors have come up with for what Dr. Benjamin Luft was referring to as a "Lyme Borrelia Complex" at the IOM workshop in October 2010 - or instead of Chronic Lyme disease? It's an interesting name, and I'm wondering where the "Poly-organic" part comes in.

The statements "Ten patients were 2-3 times retreated due to persistent clinical picture" and "All patients were evaluated at 3 months showing a decrease in the number and intensity of signs and symptoms and the same serologic pattern", caught my eye. Presumably, those ten patients also experienced a decrease in the number and intensity of symptoms as well as in their serologic pattern - so retreatment was a benefit for them.

So, let's look at the treatment: "They received intravenous ceftriaxone, 2 g daily for 21-28 days and doxycycline 200 mg daily for 21 days." Should one assume based on their report that those ten patients were treated with up to 4 months of  IV ceftriaxone plus 84 days of doxycycline - or is that off? Two to three times the baseline treatment seems to put the upper range in that ballpark.

"No case of clinical aggravation or serious adverse events was reported and Jarish-Herxheimer syndrome was observed just in two cases."

Boy, does that sound very different from the other reports from the American clinical trials on extended antibiotic treatment for chronic Lyme disease. One of the reasons extended treatment with IV antibiotics was recommended against was because of serious adverse events such as line infections. On a large scale, how often do line infections occur in thousands of patients worldwide? It's a risk, but is it that difficult to prevent with proper care?

I find it interesting that these case studies were shown at a poster session at the 14th ICID. An international professional infectious disease conference - pretty much showing a conclusion where chronic infection treatment is mentioned as not being standardized and setting 6 week regimens as being reasonable.

Wait a minute... doesn't this case series treatment study sound very similar to one of the American clinical trials on extended antibiotic treatment for chronic Lyme disease?

[Camp Other goes to new window, googles...]

I guess it is somewhat similar to the 2001 Klempner trials, but the fact that multiple retreatments were permitted under the case studies are a noted difference among other differences. I think for me, I'm wondering what the full text stated, and not just the abstract - in order to see the authors' line of reasoning on the dosage and regimen - but also wondering why there was only a three month followup on patients after treatment? Where are these post-treatment Romanians today, and how are they doing?

I have more questions...

Patients had the following serology at the start of their studies: [44 (84%) IgM positive, 19 (36%) IgM and IgG positive. How was it IgM positive-only patients were included in the study, when other researchers have stated that a sustained IgM response to Bb with no IgG response means the test was a false positive? (I'm not pushing this idea, as I am still working on the whole "how are new and newly intense IgM bands significant" issue - just putting it out there for the overview.)

"All patients were evaluated at 3 months showing a decrease in the number and intensity of signs and symptoms and the same serologic pattern."

Two questions here: What symptoms and signs did they have to begin with, and what changed, objectively and subjectively?

What does it mean to state in the above sentence, "the same serologic patterns"? Did all patients serological results remain the same across the board despite treatment?

"Most of the patients remained with at least one neuropsychological complaint."

What is the cause or what are the causes of the neuropsychological complaints?

Also, even if the authors reported a decrease in the number of signs and symptoms of infection three months post-treatment, how close were patients to their pre-infective state of health? This is always the question for which I want an answer - especially after reading through the results of treatment trials mentioned in the IDSA 2006 Lyme disease treatment guidelines - results which did not always post a clear outcome of cure.

There are a lot of unanswered questions on this abstract - hopefully getting the full text some time will help in answering them.

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9 Recap Of Dr. Zemel and Dr. Cameron Chat

ZEMEL VS. CAMERON

I'm going to be posting comments here during the course of the chat, then offer additional feedback here afterwards.

So far, this is off to a slow start. I don't know if it's the live chat software or if the servers are flooded with Lyme disease patients, but it's 10 minutes in and we barely have introductions. Dr. Cameron apparently wasn't logged in or having trouble logging in.

Okay, now things are moving along, and questions about testing are being posted by the audience. Questions on how to test for Lyme disease and on seronegative Lyme disease.

(I think that the servers are really busy - huge lag time on my end. I emailed my questions in advance, and I don't know if they are taking a combination of emailed questions or live - what is the deal here?)

Not that Milton! We said
Milton Carrero!

Milton Carrero, live chat moderator just wrote, "Because the questions are so many, and often similar I'm trying address the most prevalent topics associated with Lyme disease" - I suspect only a small fraction of questions and comments that got emailed or posted are showing up here and they may not ever pick mine. Or yours.

Okay, now we're getting a mix of questions and answers on different topics, some personal and some general. One man asks about the relationship between lipogranuloma cysts and late stage Lyme disease, a good question about the existence of chronic Lyme disease being investigated by an NIH study, the ineffectiveness of oral antibiotics for neurological Lyme disease, one mother's question about the relationship between her daughter's symptoms of anxiety and depression after Lyme disease...

Is Lyme disease underreported, why not continue to treat the patient if he is suffering, what is the role of coinfections, treatment approach by each organization, question about neurological testing... It's hard to keep up now, and the questions and answers are a jumble.

Okay, it looks like it's wrapping up now... Dr. Zemel has to leave even though Milton said an extra 15 minutes could be extended for the live chat.

My questions never made it into the chat - did any of yours?

In case you're wondering, here is a copy of what I sent out:

---

Mr. Carrero, I'd like to ask the following questions of Dr. Zemel and Dr. Cameron for Friday, July 1, chat on Lyme disease:

For Dr. Zemel, I have the following questions:

1) Since there is evidence that Borrelia burgdorferi can be intracellular and studies indicate a small number of spirochetes can survive antibiotic treatment, what further studies can be conducted to provide evidence of persistent post-antibiotic infection in human hosts? Are there any currently being done which address these issues?

2) What mechanisms does Borrelia burgdorferi use which lead to immune dysregulation in the human host, and what research do you know of being conducted now that could determine how to prevent immune dysregulation in the infected human host?

For Dr. Cameron, I have the following questions:

1) Do you and other members of ILADS compare case studies and have you been working on conducting your own clinical trials based on those case studies? Lyme patients are sorely in need of more research for effective treatment and hopefully shorter term treatment.

2) Have you and other members of ILADS considered writing a detailed, scientific book with citations that explains for both public and medical professionals why your treatment guidelines are more in line with the state of the science on Lyme disease? If not, would you? It would be great to have a better understanding why long-term treatment is an effective approach for a number of patients beyond their own success stories.

Thank you,

Camp Other

---

My general thoughts about the chat:

I think that a live, in-person presentation of the material would be more effective than the live chat presentation. One thing which kept happening is that even with leaving audience participation limited, questions and answers to those questions were being posted out of sync and hard to follow.

The answer to a previous question asked minutes ago would show up directly after a question which was just posted, making it difficult for the audience to line up questions and answers.
In a real time, in-person presentation, an answer would immediately follow a question. I would have preferred something along the lines of streaming video with a split screen that looked like a Presidential debate if I have to watch something like this again.

It's not clear to me from where Milton was drawing his questions at all times. Sometimes they seemed to be taken from email, and at other times from the live chat box. I wish that the Morning Call could put together a page showing all of the questions they'd been asked because I (and I'm sure others) are curious about what they are - and perhaps leave it up to Dr. Zemel and Dr. Cameron to address them in writing at a later time either for the Morning Call or elsewhere.

At any rate, my questions did not get asked. I'm wondering how much success I would have if I wrote the doctors directly.

Okay, comments on what was said:

"Dr. Lawrence Zemel: Approximately 10 percent of people who have had Lyme Disease will develop persistant symptoms following appropriate treatment. Most of these patients are no longer considered infected. Previous research has shown that at least 50 percent of people with "chronic Lyme Disease" never had Lyme Disease in the first place. We as physicians are obligated to treat these patients in the most humane and safe way possible."

Dr. Zemel, please provide references and citations for your statements. Up to 10 percent of early cases of infection have resulted in treatment failure and by extension, persisting symptoms. In a number of studies, the authors retreated individual patients - in some cases, with IV antibiotics when the study was based on oral antibiotics. They went on to improve, when they hadn't improved earlier. Do you call this a discrepancy, or is this a case where a garden variety Lyme disease infection became neuroborreliosis and researchers decided to give the patient additional treatment? Consider the real life scenario of a patient who fails early oral antibiotic treatment and does not go on to receive additional treatment when symptomatic. How do you differentiate between an individual case which requires more treatment versus one which has immediately become an autoimmune case?

Can you please cite evidence and research on how many patients with Chronic Lyme disease never had Lyme disease to begin with? I'd like to know more about that research.

It seems to me that between the IDSA Lyme disease guidelines panel's article in the NEJM and your comments that you tend to focus on this group of patients who never had Lyme disease in the first place. I know nothing about this group. Please focus on those of us who have had it and conduct more research for effective treatment for us. We deserve humane, safe, and effective treatment.

"Dr. Lawrence Zemel: Dr Cameron is correct: early treatment with antibiotics may blunt an antibody response, but at that point, no further treatment is needed."

But what about early treatment which is inadequate? Dr. Zemel, you're making an assumption that everyone who gets treated early has had enough antibiotics for a long enough duration of time. If a patient only receives 10 days of doxycycline - which is what some patients receive from their doctors (and not 21-28 days of oral antibiotics) is that enough? What if the patient has neuroborreliosis and they only receive a short course of doxycycline? What if they are allergic to doxycycline - could they have treatment failure from having had a shorter course of a third line choice which was not the most effective antibiotic to use for Borrelia burgdorferi?

A patient, Steve Hollingworth, had this to say:

"The NIH's study brief at http://www.clinicaltrials.gov/ct2/show/NCT01143558?recr=Open&cond=lyme+disease&cntry1=NA%3AUS&cntry2=EU%3AIE&age=1&rank=1 actually says "It is currently unknown why some patients continue to have symptoms. One possibility is that the antibiotics have not successfully gotten rid of all of the bacteria. Current tests for Lyme disease cannot tell whether the bacteria have been successfully eliminated from the body." Care to comment on that government statement?"

and

"In particular, how does the doctor expect an infection in the brain by the Lyme spirochete to be eradicated by oral antibiotics, when no appropriate oral antibiotic is capable of crossing the blood-brain barrier?"

Go Steve! Please keep asking these kinds of questions! This is the line of questioning which is sorely needed in these discussions.

Sadly, they never did answer your question about the NIH, did they? But you got this response from Dr. Zemel on your second one:

"Dr. Lawrence Zemel: Steve, CNS infections are treated with intravenous antibiotics. Thank you for sharing the other information."

Steve, I take it that this answer was inadequate for you? It was for me. While Dr. Zemel is technically correct, he is answering the letter of the question and not the spirit of it. His response didn't address my concern that a number of cases of neuroborreliosis are missed in diagnosis and not treated adequately. Dr. Brian Fallon has cited research which shows a relationship between neuroborreliosis and the development of chronic, persisting symptoms. Diagnosing and treating neuroborreliosis early on seems key to me in preventing persisting symptoms.

Backtracking a bit, I'd like to make a comparison here on the responses both doctors gave:

"Dr. Lawrence Zemel: There are at least 3 studies that demonstrated the lack of benefit from the use of long-term antibiotics, suggesting that persistent symptoms are no longer antibiotic sensitive.

Daniel Cameron: Dattwyler published several papers on Late Lyme disease with success. Donta also described successes, The original Logigian papers on neurologic LD also described successes. The Krupp clincal trial supported treatment."

Dr. Cameron, you get points for citing names for research. Dr. Zemel, given my knowledge and experience in the Lyme world, I know which studies you are likely to be referring to - but for the sake of the audience, please give names and citations for your studies.

I often wonder why in mentioning any studies on long-term antibiotic use, most of the media does not mention Dattwyler's research - given he is a member of the IDSA and has done a lot of Lyme research. Same goes for Logigian, who has cowritten work with Dr. Steere.

Biostatisticians such as Alison Delong have analyzed the raw data and data reporting on the clinical trials and studies related to the 2006 Lyme disease guidelines and came to the conclusion that while the studies were well designed, the data could be finessed in different ways and extended antibiotic treatment did, in fact, help a sub-population of the groups studied.Her team concluded that more research is necessary - something I've been saying all along.

Further discussion by both of you about the data on this sub-population would be very insightful for us all.

"Daniel Cameron: The three trials -Klemner's and Fallon describe patients ill an average of 4.7 to 9 years after treatment failures. Patients this severe for this long need much more support and treatment than was offered in the trials."

Dr. Cameron, where are these patients now? How are they doing? Were they on any treatment after the trials? Has anyone followed up on them?

Time for another comparison, this time on the issue of if Lyme disease is underreported:

"Dr. Lawrence Zemel: Most likely under reported. Estimates are that Lyme Disease may be two to three times more prevalent than the CDC data

Daniel Cameron: There are at least 10 time more cases than the 30,000 cases reported to the CDC per epidemiologist projections. The chief epidemiologist in Connecticut estimate in testimony there are 24 times the numbers in their state."

So, guys, you both agree on something: Lyme disease IS underreported, anywhere from 2 times the reported number of cases are out there on upwards of 10 times. What about the citation by the CDC of there being 6-12 times the number of reported cases in highly endemic areas?

Could we please hire more epidemiologists and expand surveillance? I noticed it's getting the lowest amount of funding from the NIH. Can you shift funding from another area even if funding isn't increased for 2012? I'd like to aim for a more accurate estimate here if nothing else.

"Dr. Lawrence Zemel: Dr Cameron's data is pure speculation. Current testing for the Lyme bacteria picks up all spirochetes in North America, at all commercial labs. One lab in California has not been shown to produce reliable results."

Dr. Zemel, please provide citations and research to support your claims. Last I checked, research indicated that Borrelia lonestari is not picked up by standardized lab tests for Lyme disease, and according to Durland Fish, neither is Borrelia miyamotoi. There may be other strains which have yet to be discovered which are not picked up.

I'm hoping that Dr. Ben Luft's research will lead to better testing in the future.

"Dr. Lawrence Zemel: Chris: Persistent symptoms may represent earlier tissue damage even though the bacteria is gone. Futher more, antibodies to the Lyme bacteria may be toxic. Persistent symptoms do not necessarily mean ongoing infection."

Dr. Zemel, can you explain how to detect evidence a patient has tissue damage, persistent infection, or a combination of both?

In stating that "antibodies to the Lyme bacteria may be toxic", could you explain more to me and everyone else reading along? This sort of statement requires clarification and sounds off a cause for concern in everyone not knowing what you mean.

"Daniel Cameron: Many of these chronically ill patients remain sick. Symptomatic treatment with pain medication, Lyrica, Neurontic etc often fail. Antibiotics have helped many of these patients."

Dr. Cameron, do you have a record of case studies on these patients? Have you conducted any larger scale studies on the treatment of post-treatment Lyme disease patients (to use Dr. Maloney's term, which is growing on me) which show which patients receive benefit from pain medication and which fail?

I'd be curious to know, because some subset of patients I know of have received some relief from pain medication while others have not. Do they have different conditions? I have also found some people have had abdominal pain and other pain is relieved by use of small doses of specific antidepressants and tranquilizing medications such as Ativan. Any comments on this?

"Daniel Cameron:
Krause first introduced the concept that Babesia and Lyme together can lead to a severe presentation."

True. Krause also wrote the Babesiosis treatment guidelines for 2006, if I recall correctly, and acknowledges that Babesia can relapse and may need additional treatment - especially in immunocompromised patients.

"Dr. Lawrence Zemel: Coinfections do not interfere with diagnostic testing. If patients have high fever and other flu like symptoms, then tests for anaplasma and Babesia are indicated."

You know what? This is a good response. But time and again, what I have noticed is that the reasonable response the ID doctor gives is not what is happening with people who are showing up to their primary care physician or urgent care clinic. Based on patients' own self reporting, what I hear about are people who were not accurately diagnosed early on by their family doctor and went on to develop more severe symptoms

If the agreed upon mantra between ILADS and IDSA doctors is "early treatment usually leads to success", Dr. Zemel, what is your organization doing to ensure patients get diagnosed and treated early on for both coinfections and Lyme disease, since coinfections can increase the severity and duration of symptoms?

"Dr. Lawrence Zemel: IDSA recommends oral antibiotics for 10-21 days for early Lyme Disease, one month for Lyme arthritis, and intravenous antibiotics for CNS disease or persistent arthritis."

Dr. Zemel, why is the treatment range such a wide number of days? How does a clinician make the decision to use 10 days versus 21 days? What if 10 days doesn't work - is retreatment advisable then?

If someone takes the recommended 2 tabs of doxycycline after a tick bite as prophylaxis, does that prevent a seropositive test from developing later if the prophylactic treatment fails and the patient goes on to develop Lyme disease later? This is important to know, and to let doctors know not to rely to heavily on tests and look at the clinical picture.

"Dr. Lawrence Zemel: Dr Cameron, while physicians have a right to treat with antibiotics, they have a responsibility to practice medicine in the safest way possible, following established scientific principles. Avoiding science is not in society's best interest."

I agree with this statement on face value. But I don't always agree with the implied statement behind it, which is, "long-term antibiotic treatment is not safe and is not scientifically supported".

I think that more research is required on this issue, in terms of efficacy, and I think that long-term antibiotic use confers the same kinds of risks for many different kinds of infections. One has to weigh the risks and benefits in any medical treatment, and recognize there will always be risks. For example, I had to get a colonoscopy and sign a paper before the exam, a paper telling me there was a small chance I could die from the procedure - miniscule - but the benefits outweigh the risk. Do you make sure you don't have colon cancer or do you avoid the small chance of death? Most people would go for the colonoscopy. (No cancer was found, thankfully!)

"Dr. Lawrence Zemel: Medicine should be practiced by physicians and not by politicians. Physicians should engage in a dialogue with their patients."

Microbiologists and molecular biologists will hopefully split the difference for you all.

I'm really tired of your infighting. Jane! Stop this crazy thing! I want to get off!

"Daniel Cameron: We need many more physicians to diagnosed and treat chronic Lyme disease. We will have less chronic LD if they are recognized early. Finally, more physcians will offer more options for patient within HMO's"

Dr. Cameron, I'm going to emphasize this bit: We need many more physicians to diagnose and treat Lyme disease, period. Early on, along with coinfections, so that people can avoid persistent symptoms.

Saying that more physicians and HMOs should be participating in increased early diagnosis and treatment is a positive statement on your end for both patients and for how it reflects on ILADS, because critics have stated that as long as ILADS stands to profit from their position there is no reason for the current situation to change.

"Dr. Lawrence Zemel: Insurance companies respond to evidence based medicine. Since there is no evidence, that IV therapy beyond 4-6 weeks is effective, they should rightfully deny coverage."

Dr. Zemel, what do you do about insurance companies denying patients access to any IV therapy to begin with? Let alone beyond 6 weeks?

"Dr. Lawrence Zemel: A small vocal group of constituents should not be dictating medical care."

Oh, I agree. But what does science have to say about this? If all we have is a hypothesis and not a proven and accepted theory, is it ethical to base treatment guidelines on a hypothesis or is more research required?

"Daniel Cameron: We need more dialogue among physicians to come to common ground for the increasing number of patient who fail treatment."

Yes, I agree here, too. But first and foremost, we need more research, more meticulously reported case studies, and clinical trials using antibiotic and non-antibiotic treatments. If you've got a hypothesis you want to provide evidence for, I'd like to see both sides actually do something about it to help patients.

More treatment studies, please? And more scientific research on Bb pathogenesis, please?

Are you familiar with William Burgdorfer's "thirty years quote"? I want to hear Dr. Zemel's response to it.

"Dr. Lawrence Zemel: Lois: Most physicians are now testing for Lyme Disease if there is a reasonable likelihood that Lyme disease is present. It is probably not accurate to say that Lyme Disease is still underdiagnosed in most Lyme areas."

Do you have references and evidence to support your statements? What about patients in the southeast US? The midwest? The west coast? Canada? There are many reports patients have given of being told by doctors that Lyme disease is rare and not in their area when according to what limited epidemiological data is on record and their state health departments, Lyme disease is not rare. How do you recommend closing this gap between doctors' knowledge and knowledge of other institutions?

More Q & A:

"[Comment From Dedee]
Is it common for scientific principles to not be challenged? New discoveries cannot be made without challenging science."

"Dr. Lawrence Zemel: Dedee: I entirely agree with you. This is why scientific guidelines are continually updated. The problem occurs when the public and wayward physicians ignore the science."

It's a good question, Dedee. And Dr. Zemel, it's a good answer.

The problem is, I think treatment and diagnosis is lagging behind the science at the moment, and that right now, not enough is understood about chronic Lyme disease and Lyme disease's pathogenesis to effectively treat everyone in a timely fashion.

When one makes the statement, "We don't know what causes persisting symptoms", what that should mean is "We don't know what causes persisting symptoms". Period. The rest is speculation, and what the cause is may not be a uniform, one-size-fits-all answer. This is why I ask for more research, and I want to see more independent research from parties not invested in either "side", if there have to be sides at all.

Ah, look! This sounds like consensus. Sorta...

"[Comment From Ellen] My insurance will not cover the antibiotics my doctor prescribes and I can not afford them out of pocket. What are your thoughts on homeopathic and herbal treatments?"

"Dr. Lawrence Zemel: Ellen: I'm not aware of evidence to support alternative treatments in place of antibiotics. Can you please educate me?"

"Daniel Cameron:
Many of my patients with chronic issued try many different alternative medications. We need more research on new strategies."

I initially found it amusing that Dr. Zemel is asking for a patient to educate him on the use of alternative treatment. But then I got pissed off. As someone who is supposed to be upholding his own guidelines, if that patient needs antibiotics, he could be providing advice as to how to get authorization for antibiotics if they are medically necessary and/or advise further testing to substantiate her diagnosis for treatment. Instead, he is humoring her.

But in the end, the message I'm getting out of this: Alternative treatments are currently not evidence-based treatments for Lyme disease. Sure, people try them, and some may help with some symptoms - but we need more research on them.

"Daniel Cameron: ILADS published an evidence based guideline in 2004 reviewing the evidence. See our website at ILADS .org. We expect a new guideline soon. Many of our members are now publishing. The publication should help the dialogue."

I hope that you are providing more peer-reviewed-from-established-journal citations and references to support your guideline, and that we get to see it soon. I eagerly await the outcome of all this work you've been doing.

"Dr. Lawrence Zemel: The ILADS guidelines were reviewed by the British Health Agency and found to lack scientific credibility. Most major specialty organizations in North America and Europe have endorsed the IDSA guidelines."

Dr. Cameron, there's a reason why I said what I did above.

Interesting, Dr. Zemel. Could you please explain why each of these countries overseas have adopted IDSA's guidelines and not written their own, given that they have historically had somewhat different diseases and disease presentations? (This is becoming less the case with bird migration affecting infection distribution and rate.)

And then there are these differences in approach. Why is it in much of Europe doctors are trained to look for more cases of neuroborreliosis and treat them earlier on, whereas in the US they aren't? Recent evidence from EUCALB and your not-cited organizations state that the percentage of American-based Bb infected patients in Europe show a percentage of neurological symptoms equal to those found in European-based Bb infected patients. (It's in that recent Institute of Medicine report that was posted in April.)

Another patient weighs in...

[Comment From Julia Wagner]
Actually - while a dialogue will help, it is not uncommon in medicine to have multiple schools of thought that inform a physician, who can make the call that is best for that patient - the same approach should be used with Lyme - and physcians need to be educated that 2 schools of thought. Any scientist who vociferously opposes other thinking, is limited the potential for progress in medicine - we need to follow the science as it emerges, and not ignore or disparage this. The science just evolving last year was significant in explaining "chronic lyme" from the 13 subtrains genotyped by Dr. Luft with some having serious neuro sx and others a more limited easy to cure disease, to lymphadenopathy study finding spirochetes hiding in the lymphs as another means to evade the immune system. I so no reason why the IDSA should fight other points of view - physicians should be informed about emerging science period, and treat their patients to get them well. Chalking up all remaining symptons to "aches and pains of daily living" is not acceptable when other viable options have not been explored."

I've bolded what I particularly would want to emphasize of your good points - thank you for contributing to this discussion. We need more people to ask questions referring to the science related to Lyme disease.

PS Julia: Please have someone proofread your question or type it into Word or some other text editor to run it through spell check first. I know you didn't mean to post typos, but it makes it harder to read.

---

So after this, Milton asked questions about vaccines, but they went unanswered as the chat was shut down at 1 pm EST.

This is all I have to say on this for now.

What are your thoughts about it?

Refer to the original chat transcript here:
http://www.courant.com/health/mc-health-chat-lyme-disease,0,4675217.htmlstory

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