Thursday, 25 October 2012


Characterization of Biofilm Formation by Borrelia burgdorferi In Vitro

published 24 October 2012 Plos One here 

Abstract Top

Borrelia burgdorferi, the causative agent of Lyme disease, has long been known to be capable of forming aggregates and colonies. It was recently demonstrated that Borrelia burgdorferi aggregate formation dramatically changes the in vitro response to hostile environments by this pathogen. In this study, we investigated the hypothesis that these aggregates are indeed biofilms, structures whose resistance to unfavorable conditions are well documented. We studied Borrelia burgdorferi for several known hallmark features of biofilm, including structural rearrangements in the aggregates, variations in development on various substrate matrices and secretion of a protective extracellular polymeric substance (EPS) matrix using several modes of microscopic, cell and molecular biology techniques. The atomic force microscopic results provided evidence that multilevel rearrangements take place at different stages of aggregate development, producing a complex, continuously rearranging structure. Our results also demonstrated that Borrelia burgdorferi is capable of developing aggregates on different abiotic and biotic substrates, and is also capable of forming floating aggregates. Analyzing the extracellular substance of the aggregates for potential exopolysaccharides revealed the existence of both sulfated and non-sulfated/carboxylated substrates, predominately composed of an alginate with calcium and extracellular DNA present. In summary, we have found substantial evidence that Borrelia burgdorferi is capable of forming biofilm in vitro. Biofilm formation by Borrelia species might play an important role in their survival in diverse environmental conditions by providing refuge to individual cells.

Dr Eva Sapi link to Utube presentation on Biofilms here

Dr Alan B  MacDonald 'Six years ago,a a Symposium at the University of New Haven I delivered a lecture on biofilms of Borrelia burgdorferi (Bb). The PDF File of the PPT and its Video have been posted on the Web and are freely downloadable.' here

Dr Alan B MacDonald's website here
Dr Alan B MacDonald Alzheimer's Disease here 

Earlier posts on Dr Alan B MacDonald here

Dr Alan B MacDonald will present at 2012 International Lyme and Associated Diseases conference details here

Monday, 22 October 2012


You can read my personal story in the right hand side bar of this blog simply put what started as a Fibromyalgia diagnosis after further deterioration and other diagnoses ended up 4 years later being diagnosed as a bacterial infection and on long term antibiotics I have no Fibromyalgia nor the many Arthritis symptoms or Muscle problems.

I currently follow various sites on Facebook and it concerns me reading the Fibromyalgia sites that few doctors ever bother to look beyond the diagnosis of Fibromyalgia - It is just a name given to symptoms.

What about considering the causes, of which I am sure there will be several?

What about a trial of antibiotics just in case like me it is an underlying stealth pathogen - Mycoplasma, Chlamydia Pneumonia, Bartonella, Borrelia just to name a few. The testing for all these pathogens is poor so negative tests do not always mean you do not have the infection but doctors clearly do not even bother to test.

A trial of say Doxycycline for 3 months in line with guidelines for Lyme disease(Borrelia), there are similar recommendations for Chlamydia Pneumonia, Bartonella, Mycoplasma would it really compromise a person's health as much as some currently prescribed treatments do or can. I was given steroids for 20 months - I wish I knew then what I know now and how damaging they can be to our immune systems if we have any underlying infections bacterial and viral. I was also advised to take anti depressants - although I had no history or symptoms of depression - imagine the consequences of dosing someone up with anti depressants when there is no depression -Zoombie state and a cycle of ups and downs maybe even leading to hyper manic state as the system becomes unbalanced? (Case of a family member whose actually problem turned out to be cancer)

So fellow Fibromyalgia sufferers do your research there is much out there on the World wide web and no longer do we have to just be dismissed with a syndrome and something to suppress our immune systems response - What is it a response to? - do we all really believe the assumption that our immune systems have gone mad and are attacking self, if so why do those of us who finally get diagnosed with an underlying infection such as in my case Lyme Disease get better on long term antibiotics?

The most interesting presentation was one I saw of Richard Horowitz on M.S.I.D.S Multi systemic Infectious Diseases Syndrome I posted about it here 

Do your research and then discuss with your doctors, but remember Doctors are humans to, they make mistakes, but we live with the consequences - they do not necessarily learn or even know when they make a mistake but continue on and on to the next and the next patient believing that because that is what they do then they must be right - science is emerging to turn many misconceptions upside down but medicine is slow to follow the lead of science.

Good luck in finding treatment that works for you and maybe even the underlying causes to your condition.

Sunday, 21 October 2012


Kristin Mehre, a director in the Research Council of Norway acknowledges that we don’t know enough about tick-borne disease. 

Kristin Mehre  in a TV interview link here  says 'Directorate of Health now recognizes that the tests taken in Norway to affect disease ticks, is uncertain.'    It is not enough to do a test. It must be tested and, in addition, there must be a thorough clinical evaluation, says Department of Health, Kristin Mehra to TV 2 We recognize that there are many who have chronic ailments. Also we do not know if it's a chronic Lyme disease because we do not know whether it is a bacteria or a reaction to the disease, says Kristin Mehra.

Directorate of Health admits that Norway knows too little about the long-term disease after tick bites.
- It's still not enough knowledge to be able to give a general recommendation for those with long-term ailments, said department director of the Health Directorate.
Comment from Lyme Disease Action Facebook page 
'If people would only read the small print, European guidelines said this 2 years ago: we don’t know the best drug, dose or duration. EFNS guidelines are based on what they call “good practice” ie habit - not evidence. Time this was more widely acknowledged.'

From Lyme disease Action website here 

EFNS (The European Federation of Neurological Societies)
November 2009 – EFNS guidelines on the diagnosis and management of European Lyme neuroborreliosis. Mygland A, Ljøstad U, Fingerle V, Rupprecht T, Schmutzhard E, Steiner I. Eur J Neurol. 2010;17:8-16.
Points to note:
  • Deals with neuroborreliosis only.
  • Contains recommendations on treatment but points out the lack of European treatment studies and controlled trials on treatment length.
  • Most recommendations are based on opinion because of the lack of evidence.
  • Recognises that studies show significant treatment failure rates, but makes no recommendation as to further treatment.

Link to European Federation of Neurological Societies  guidelines here 

 'Man has in a way not seen or realized, that chronic Lyme disease is a real problem, says Norwegian doctor at Lyme Center, Rolf Luneng.'

Sunday, 14 October 2012


The Open Neurology Journal

The previous post came from the above link here

Also included are the following with links to the full papers.

Chronic or Late Lyme Neuroborreliosis: Present and Future 
Judith Miklossy*, Samuel Donta, Kurt Mueller, Oliver Nolte and George Perry 
Alzheimer Research Center,
 Prevention Alzheimer International Foundation, 1921 Martigny-Croix, CP 16, Switzerland
This special issue gives a framework of an international effort, to critically and constructively overview the clinical
and pathological aspects of Lyme neuroborreliosis and show directions for future practice and research.
The issue in the diagnosis and treatment of Lyme neuroorreliosis is assessed followed by a comprehensive analysis
of the involvement of connective tissue and associated clinical manifestations. A critical review shows that both the
meningovascular and meningoencephalitic forms, which define chronic or late neurosyphilis also occur in Lyme
neuroborreliosis. Clinical and pathological confir-mation of these tertiary forms and detection of Borrelia burgdorferi in association with tertiary brain lesions were reported by many authors. These observations indicate that similarly to Treponema pallidum, Borrelia burgdorferi infection is directly involved in the late or chronic manifestations of Lyme neuroborreliosis. Chronic or late Lyme neuroborreliosis both refer to tertiary neuroborreliosis, therefore, the use of these terms as different entities is not justified and may lead to

A critical assessment of clinical trials will guide the design of future clinical studies and a detailed analysis of various factors influencing PCR detection of Borrelia specific DNA would be precious to improve the sensitivity of this potentially important diagnostic tool.
*Address correspondence to this author at the International Alzheimer Research Center, Alzheimer Prevention Foundation, 1921 Martigny-Croix, CP
16, Switzerland; Tel: + 41 27 722 0652, +41 79 207 4442;
An update on the virulence determinants of Borrelia burgdorferi and the pathomechanisms involved in Lyme disease is discussed followed by a review showing the importance of co-infections in the diagnosis and treatment of Lyme disease.
Evidence for an infectious origin of various neuropsychiatric symptoms of tick-borne diseases and various psychiatric disorders are also discussed. The involvement of immune system reactions, chronic inflammation, genetic and environmental factors are also considered. Finally an update on the perspectives on Lyme Borreliosis in Canada closes the special issue.
The majority of authors are internationally recognized neurologists and scientists with extensive experience and
complementary expertise in clinical and/or basic research on Lyme disease. The exchange of knowledge at an international level and between experts in various branches of medicine and in basic research is the way to advance faster in this new, promising and important field of medicine. The aim of this special issue is to contribute to this process. This approach motivated the authors at the annual meeting of the German Borreliosis Society (Deutsche Borreliose-Gesellschaft, DBG) in 2011 at Wuppertal, Germany to initiate and realize this special issue.
This issue is dedicated to the memory of Mark A. Smith whose untimely death has left a void for those looking to
novel ideas to solve chronic diseases.

A Reappraisal of the U.S. Clinical Trials of Post-Treatment Lyme Disease Syndrome, 2012; 6: Pp. 79-87
Brian A. Fallon, Eva Petkova, John G. Keilp and Carolyn B. Britton
Published Date: (
05 October, 2012)

Four federally funded randomized placebo-controlled treatment trials of post-treatment Lyme syndrome in the United States have been conducted. Most international treatment guidelines summarize these trials as having shown no acute or sustained benefit to repeated antibiotic therapy. The goal of this paper is to determine whether this summary con-clusion is supported by the evidence.

Methods: The methods and results of the 4 U.S. treatment trials are described and their critiques evaluated.

Results: 2 of the 4 U.S. treatment trials demonstrated efficacy of IV ceftriaxone on primary and/or secondary outcome measures.

Conclusions: Future treatment guidelines should clarify that efficacy of IV ceftriaxone for post-treatment Lyme fatigue was demonstrated in one RCT and supported by a second RCT, but that its use was not recommended primarily due to adverse events stemming from the IV route of treatment. While repeated IV antibiotic therapy can be effective, safer modes of delivery are needed.

The Psychoimmunology of Lyme/Tick-Borne Diseases and its Association with Neuropsychiatric Symptoms, 2012; 6: Pp. 88-93
Robert C. Bransfield
Published Date: (05 October, 2012)

Disease progression of neuropsychiatric symptoms in Lyme/tick-borne diseases can be better understood by greater attention to psychoimmunology. Although there are multip
le contributors that provoke and weaken the immune system, infections and persistent infections are significant causes of pathological immune reactions. Immune mediated effects are a significant contributor to the pathophysiological processes and disease progression. These immune effects include persistent inflammation with cytokine effects and molecular mimicry and both of these mechanisms may be present at the same time in persistent infections. Sickness syndrome associated with interferon treatment and autoimmune limbic encephalopathies are models to understand inflammatory and molecular mimicry effects upon neuropsychiatric symptoms. Progressive inflammatory reactions have been proposed as a model to explain disease progression in depression, psychosis, dementia, epilepsy, autism and other mental illnesses and pathophysiological changes have been associated with oxidative stress, excitotoxicity, changes in homocysteine metabolism and altered tryptophan catabolism. Lyme disease has been associated with the proinflammatory cytokines IL-6, IL-8, IL-12, IL-18 and interferon-gamma, the chemokines CXCL12 and CXCL13 and increased levels proinflammatory lipoproteins. Borrelia burgdorferi surface glycolipids and flagella antibodies appear to elicit anti-neuronal antibodies and anti-neuronal antibodies and Borrelia burgdorferi lipoproteins can disseminate from the periphery to inflame the brain. Autism spectrum disorders associated with Lyme/tick-borne diseases may be mediated by a combination of inflammatory and molecular mimicry mechanisms. Greater interaction is needed between infectious disease specialists, immunologists and psychiatrists to benefit from this awareness and to further understand these mechanisms.

The Lymphocyte Transformation Test for Borrelia Detects Active Lyme Borreliosis and Verifies Effective Antibiotic Treatment, 2012; 6: Pp. 104-112
Volker von Baehr, Cornelia Doebis, Hans-
Dieter Volk, Rüdiger von Baehr
Published Date: (05 October, 2012)

Borrelia-specific antibodies are not detectable until several weeks after infection and even if they are present, they are no proof of an active infection. Since the sensitivity of culture and PCR for the diagnosis or exclusion of borreliosis is too low, a method is required that detects an active Borrelia infection as early as possible. For this purpose, a lymphocyte transformation test (LTT) using lysate antigens of Borrelia burgdorferi sensu stricto, Borrelia afzelii and Borrelia garinii and recombinant OspC was developed and validated through investigations of seronegative and seropositive healthy individuals as well as of seropositive patients with clinically manifested borreliosis. The sensitivity of the LTT in clinical borreliosis before antibiotic treatment was determined as 89,4% while the specificity was 98,7%. In 1480 patients with clinically suspected borreliosis, results from serology and LTT were comparable in 79.8% of cases. 18% were serologically positive and LTT-negative. These were mainly patients with borreliosis after antibiotic therapy. 2.2% showed a negative serology and a positive LTT result. Half of them had an early erythema migrans. Following antibiotic treatment, the LTT became negative or borderline in patients with early manifestations of borreliosis, whereas in patients with late symptoms, it showed a regression while still remaining positive. Therefore, we propose the follow-up monitoring of disseminated Borrelia infections as the main indication for the Borrelia-LTT.

Diagnosis of Infectious or Inflammatory Psychosyndromes, 2012; 6: Pp. 113-118
Karl Bechter
Published Date: (05 October, 2012)

Before an outline of the process of diagnosis and differential diagnosis in infectious and/or inflammatory psy-chosyndromes is given, a more general overview onto the approach to organic psychosyndromes seems useful, b
ecause in both entities similar principles of causality conclusion are applied. Correlation does not demonstrate causality. Therefore the principles and consensus recommendations, and limitations of causal inference to categorize psychosyndromes as be-ing ‘organic’, is to be discussed in detail.

How do Lyme Borrelia Organisms Cause Disease? The Quest for Virulence Determinants#, 2012; 6: Pp. 119-123
Steven J. Norris
Published Date: (05 October, 2012)

Lyme disease Borrelia are invasive, nontoxigenic, persistent pathogens, and little is known about their mechanisms of pathogenesis. In our laboratory, a signature-tagged mutagenesis (STM
) library of over 4,000 Borrelia burgdorferi transposon mutants has been constructed and is being screened for infectivity in mice. In this manner, a global view of the virulence determinants (factors required for full infectivity) is being developed. Additionally, the mechanisms of immune evasion involving the VMP-like system (vls) are under analysis, and cryo-electron microscopy is providing a detailed view of the three-dimensional structure of B. burgdorferi. These approaches will contribute to the improved understanding of how Lyme disease Borrelia cause disease.

All really fascinating articles go to the link above to read in full.


I have posted below details of an excellent publication on Evolving Perspectives on Lyme Disease - although written on the Canadian perspective certainly in respect of the Abstract and the Conclusion the words United Kingdom can be substituted wherever the word Canada is written. 

As the authors so rightly pose we need International and Transcontinental perspectives which also include patients in the process. For too long the IDSA small cohort who wrote the IDSA Lyme disease guidelines have held too much control and power Worldwide, using their narrowly held beliefs to dictate policies to our Health Authorities. There is now far too much scientific evidence that shows their restrictive view to be no longer valid for many people with Lyme Disease complex.

Evolving Perspectives on Lyme Borreliosis in Canada 

J.L.H. Sperling, M.J. Middelveen, D. Klein, and F.A.H. Sperling
Link to the full paper here


With cases now documented in every province, Lyme borreliosis (LB) is emerging as a serious public health risk in Canada. Controversy over the contribution of LB to the burden of chronic disease is maintained by difficulty in 

capturing accurate Canadian statistics, especially early clinical cases of LB. 

The use of dogs as sentinel species demonstrates that potential contact with Borrelia burgdorferi spirochetes, as detected by C6 peptide, extends across the country. Dissemination of infected ticks by migratory birds and rapid establishment of significant levels of infection have been well described. 

Canadian public health response has focused on identification of established populations of the tick vectors, Ixodes scapularis and I. pacificus, on the assumption that these are the only important vectors of the disease across Canada. Strains of B. burgdorferi circulating in Canada and the full range of their reservoir species and coinfections remain to be explored. Ongoing surveys and historical records demonstrate that Borrelia-positive Ixodes species are regularly present in regions of Canada that have previously been considered to be outside of the ranges of these species in recent modeling efforts. 

We present data demonstrating that human cases of LB are found across the nation. 

Consequently, physician education and better early diagnoses are needed to prevent long term sequelae. An international perspective will be paramount for developing improved Canadian guidelines that recognize the complexity and diversity of Lyme borreliosis.


An International and transcontinental perspective on LB is needed to better understand the complexity of this disease as it currently exists in Canada. 

With diagnostic options narrowly focused on those appropriate to the eastern USA, Canadian patients have been restricted in their access to health care. 

Development of better testing and emphasis on patient outcomes is needed, including more opportunity for adaptive approaches and more comprehensive documentation of outcomes. 

Such conditions allow better clinical diagnoses and treatments that take into account the diversity of  Borrelia genotypes as well as their coinfections and regionally variable ecological circumstances. 

These improvements are particularly important in the context of government funded healthcare where avoidance of chronic illness is more consciously tied to broader economic as well as societal benefits. 

 Difficult-to-diagnose diseases are not only a challenge to our current paradigms for medical research and administration. 

Much is at stake in resolving such problems, since successful public healthcare is considered by many Canadians to be a defining characteristic of the Canadian state [99]. 

Consequently, Lyme patients who abandon the Canadian medical system are a sign of a fundamental incompatibility between their perceived needs and what the current Canadian system provides, and in doing so they are part of the thin edge of a wedge that may alter this system in fundamental ways. 

Successful resolution of these conflicts will depend on action by both patients and physicians, ideally  via cooperation rather than conflict. But for hundreds and perhaps thousands of Canadians the means matter less than the desired endpoint,which is timely treatment and effective care for people who suffer from the debilitating conditions that characterize Lyme borreliosis.  

Pub med   here

Thursday, 11 October 2012


For the past 30 years Dr. Alan MacDonald has worked to revive the Model of Syphilis and draw attention to clinical and laboratory parallels between 

Treponema pallidum infection and Lyme Borreliosis. 

Dr. MacDonald hypothesized that Alzheimer's disease might be the late neural borreliosis equivalent of General paresis of the insane. 

He further hypothesized that syphilitic Tabes Dorsalis might have a "spinal cord only" neurodegenerative equivalent In borreliosis, namely Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease). 

He hypothesized that syphilitic Temporal arteritis might have a Borrelia equivalent in Temporal arteritis of unknown cause.

 In addition to the ongoing Alzheimer's studies, which would occupy the remainder of his research career, Alan made basic new observations in pathobiology. He was the first to publish evidence for a cystic form of Bb, granular forms of Bb, and cell wall deficient forms. 

Although officially retired now, Dr. MacDonald has started a research collaboration with Dr. Eva Sapi of University of New Haven.

Dr MacDonald and many other distinguished researchers and doctors will be presenting at this years ILADS Conference in Boston details here  

Dr MacDonald's hypothesis are slowly becoming acknowledged and researched elsewhere we have a lot to thank him for.

Judith Miklossy has also found Borrelia in the brains of patients with Alzheimer's here

Dr Martz found patients with ALS linked to Borrelia and with appropriate antibiotics some recovered and some stabalised  here 

Three cases of neuroborreliosis misdiagnosed as giant cell arteritis.  here 

Link to Dr MacDonald's website here

link to Borreliosis Spirochetes imaged from Human Blood -- Case studies  here  

Wednesday, 3 October 2012



Thanks to artist Buba Touray. 

Buba describes himself - 'I am a Gambian artist who creates paintings using my own hand-made colours.

A link to his artwork here 

In The Gambia people are well aware of the dangers of infections passed from ticks and have locally grown treatments which Western medicine is only just learning about. 

Perhaps one day I will pursued Buba to farm  Cryptolepis in the Gambia. 

link here to Planet Thrive for details of Cryptolepis

 How sad that people in the UK are left so ignorant of the dangers of tick borne diseases that we have here in the UK.