Monday, 12 September 2016


Testing for Lyme Disease is problematic for several reasons

'Scientifically, sensitivity (% of definite positive patients who test positive by the test in question) and specificity (% of well patients who test negative by the test in question) are measured against another test, such as CDC surveillance pos WB, which is how the patients are determined to be positive in the first place.  As ALL tests for Borrelia lack sensitivity to some extent this makes the sensitivity and specificity of the test in question highly suspect, or limited.  This, of course, means sensitivity and specificity are not really related to % of patients who ACTUALLY have the disease, but % who have been determined by a particular test of limited sensitivity to have the disease, a subset.  As patients who have been definitely determined to have Borreliosis by the CDC criteria for surveillance, and the CDC are measuring the sensitivity of a new test against that, of course the sensitivity of that new test will be inflated, a great advantage if you are the holder of the patent of that new test.  This would be especially so if the new test is measuring some parameter which is related in some way to the baseline test (such as both measuring antibodies to something).
In reality any of the various tests available if positive is a likely indication the patient has Borreliosis, but any one of them will have some false positives.  The false positive rate is not scientifically possible to accurately determine from evidence.  In Borreliosis the sceptics commonly cry "false positive" for any one test which shows positive, but they have no evidential basis on which to ground their claims.  It is certainly helpful to the patient's cause to have 2 separate tests positive, making a false positive far less likely.  In areas of medicine other than Lyme it is usually clinical suspicion plus one suggestive, not necessarily strong positive, test which would be taken as diagnostic evidence.
However, IF the judges (the CDC) are actively trying to protect the health insurance industry (which would appear to be the case, based on the evidence of their judgements), of course their current stance would make a lot of sense.  If they applied the same level of criteria for all other infectious diseases, only a small fraction of patients with infections of all kinds would be diagnosable or treatable.'

I read the above explanation recently and have permission to share, it explains very clearly one aspect of the problems we have with Lyme serology.

Prof Perronne discusses other aspects of Serolgy in this publication 

Calibration of serology

When Lyme serology was developed, no reliable method was available to be used as a gold standard for comparison. As most of the signs and symptoms are non-specific, no reliable clinical diagnostic score could be established. The low yield of culture and the difficulty involved in using the technique routinely were another major obstacle. A pragmatic cut-off level for the serologic tests had to be determined arbitrarily on blood donors (EUCALB, ; Assous, ). In the late seventies, when Lyme disease was first discovered, it was understandably thought to be a rare and regional phenomenon. Therefore, a low prevalence was set as experts were afraid the serologies would produce too many false positive diagnoses (EUCALB, ; Assous, ). Patients and control populations are ill-defined with a high variability in predictive positive and negative values from one test to another. Culture of B. burgdorferi or detection of its genome by polymerase chain reaction (PCR) may occasionally confirm the clinical diagnosis in seronegative patients, however none of these methods are sensitive enough to be considered reliable diagnostic methods, especially in routine practice (Schutzer et al., ; Nields and Kveton, ; Chmielewska-Badora et al.,; Brunner, ; Assous, ; Holl-Wieden et al., ; Aguero-Rosenfeld, ; Dietrich et al.,; Wallet et al., ). As a result, many patients suffering signs and symptoms compatible with Lyme disease, but whose test is negative, are falling by the wayside.

Possible causes of seronegativity

Several factors leading to seronegativity have been identified in confirmed cases of Lyme disease: (i) the arbitrary cut-off level of tests, (ii) the sequestration of antibodies in immune complexes, (iii) the wide variety of species and subspecies of Borrelia that co-exist in different parts of the world, and (iv) coinfections with other pathogens which may be responsible for some or all of the symptoms or which may alter the immune response (Schutzer et al., ; Brunner, ). The complex B. burgdorferi sensu lato includes (Table (Table1):1): B. burgdorferi sensu stricto (including genetic diversity), B. afzelii, B. garinii (several serotypes) and additional species isolated in different parts of the world (Rudenko et al., ; Ogden et al., ). Some of these species have been isolated in symptomatic patients (Varela et al., ; Lopes de Carvalho et al., ; Rudenko et al., ; Stanek and Reiter, ; Branda and Rosenberg, ; Clark et al., ; Lee et al.,; Margos et al., ). B. spielmanii may cause early skin disease (Stanek and Reiter, ). B. bavariensis, B. bisettii, B. valaisiana, B. americana, B. andersonii, B. lonestari and more recently B. kurtenbachii have been isolated from patients with Lyme-like diseases (Varela et al., ; Rudenko et al.,; Rizzoli et al., ; Stanek and Reiter, ; Clark et al., ). The pathogenic role of B. lusitaniae, isolated in a case of vasculitis, remains to be substantiated (Rudenko et al., ). Despite such diversity in strains, most of the commercially available tests still rely on the original 1982 Massachusetts B31 isolate of B. burgdorferi. No diagnostic tool is available for routine detection of B. miyamotoi (Branda and Rosenberg,; Lee et al., ). Coinfections with other microbes add to the complexity of these illnesses (Table (Table1).1). Among patients with early Lyme disease in the USA, 2–12% were found to also have human granulocytic anaplasmosis, and 2–40% babesiosis (Wormser et al., ). In Brazil, a Lyme-like syndrome, due to the tickAmblyomma, has been described and mobile non cultivable spirochetes could be visualized in patients' blood using a dark field microscope (Mantovani et al., ). A new tick-borne bacterial pathogen, CandidatusNeoehrlichia mikurensis, was reported in Switzerland (Fehr et al., ). An illustration of the limits of serology is the Scottish example: the sensitivity of the immunoblot was improved by using local Scottish strains of Borrelia (Mavin et al., ).

Conclusion and perspectives

The numerous complexities of Lyme disease make it an extremely difficult illness to fully comprehend. It remains a diagnostic challenge even for the best informed of clinicians. The lack of a gold standard for diagnosis renders the management of patients difficult and seriously hinders our ability to produce accurate statistics, especially as very similar syndromes could be due to other species of Borrelia. In some patients suffering from syndromes of unclear origin, following tick bite, other microbial agents could also be playing a role.
To read Prof Perronne full paper

Saturday, 3 September 2016


Published on Aug 25, 2016
Green fluorescent Borrelia interacting with the walls of a skin postcapillary venule of a live mice after injection of bacteria into the blood stream. Blood vessel walls are stained with a red dye. Posted by lab of Tara Moriarty ( From: Norman et al 2008:

Fascinating research from the Moriatry Lab which has just published the following paper

Biomechanics of Borrelia burgdorferi Vascular Interactions

Rhodaba Ebady, Alexandra F. Niddam Anna E. Boczula Yae Ram Kim Nupur Gupta Tian Tian Tang Tanya Odisho

Hui Zhi Craig A. Simmons Jon T. Skare Tara J. Moriarty


  • Biomechanical characterization of bacterial-vascular interactions
  • Identified catch bond-mediated bacterial vascular adhesion mechanism
  • Conserved vascular interaction strategies in bacteria and host cells


Systemic dissemination of microbes is critical for progression of many infectious diseases and is associated with most mortality due to bacterial infection. The physical mechanisms mediating a key dissemination step, bacterial association with vascular endothelia in blood vessels, remain unknown. Here, we show that endothelial interactions of the Lyme disease spirochete Borrelia burgdorferi under physiological shear stress mechanistically resemble selectin-dependent leukocyte rolling etc... ................................................

These findings provide insight into the biomechanics of bacterial-vascular interactions and demonstrate that disseminating bacteria and circulating host immune cells share widely conserved mechanisms for interacting with endothelia under physiological shear stress.
To read the paper go to 
This paper is causing a great stir in the media rocketting the paper up to -
  • top 2% of all research papers of same age
  • top 4% of Cell Reports papers of same age
  • top 3% of all Cell Reports papers ever!!!!!
with a growing list of media interest  that can be read from

David Michael Conner  explains so well in the Huffington Post why this paper is being read so widely.
For more information and videos visit the Moriatry Lab website

Friday, 2 September 2016


Ticks found on 'one third' of dogs, researchers say

Tuesday, 9 August 2016


My early morning walk in 'Tick Land' prior to being interviewed on BBC Surrey about Tick awareness. I am well booted and covered and Meg wears her tick collar which so far has been successful.

Monday, 8 August 2016



Enactment of mandated insurance coverage for Lyme disease treatment in Massachusetts.
Passage of H4491 showed how advocacy groups, activists, Lyme patients, and their supporters can work with legislators to bring about real change.
to read further go to 
I copy below an important letter that Dr Neil Spector sent to Governor Baker - this letter is a lesson for all those who deal with patients with Lyme Disease.

"Governor Baker,
It is with great concern for the welfare of the residents of the Commonwealth that I urge you to support Bill H4491.
I have been an academic medical oncologist and cancer researcher who led the development of two molecularly targeted cancer drugs. I have published basic and clinical research in the top tier, peer reviewed journals. My cancer research and clinical oncology career was launched at the MGH and Dana-Farber Cancer Institute. I am also a survivor of a devastating case of Lyme disease that was misdiagnosed for several years.
I have been in clinical and basic for 25 years. As a scientist, I understand there are relative absolutes when it comes to human biology. The real world experience changes medical practice. When I was a resident in training, the dogma was that peptide ulcer disease was caused by stress and increased acid production. The notion it could be caused by a bacterial infection was considered by mainstream medicine as being ludicrous and representing quackery. Scientists who proposed that a bacteria, h. pylori, was an underlying cause of peptic ulcer disease were laughed at. Well, two scientists who were laughed at by the medical community ended up winning the Nobel Prize in Medicine for demonstrating that h. pylori caused peptic ulcer disease. That "wacky" idea changed the practice of medicine in terms of how we treat peptic ulcer disease. There are many other examples of how dogma in our medical system thwarted and delayed seminal discoveries that changed medical practice.
People in your state and around the country are suffering, falling through the cracks of our medical system. These folks have Lyme disease and the co-infections that accompany Lyme disease. Similar to the days before the acceptance of h. pylori as a cause of peptic ulcer, there is a dogmatic approach that says that chronic problems from Lyme or co-infections that persist beyond the IDSA algorithm of care does not represent persistent infection. However, based on excellent research from prestigious institutions such as Johns Hopkins Medical Center, hardly a bastion of quackery, we know Borrelia burgdorferi, the bacteria that causes Lyme disease, becomes resistant to the standard antibiotics prescribed according to Infectious Disease Society of America (IDSA) guidelines. We know there is persistent infection in primate studies based on peer reviewed research from scientists at Tulane and other institutions. Some may 'poo poo' preclinical research. The reality is, we as scientists rely on research in the laboratory to model human diseases. We would not have made the transformative strides in Cancer if we had turned our backs on preclinical research.
Studies suggesting that prolonged antibiotic therapy is not effective, the basis for the dogmatic approach denying access to additional antibiotics to patients who are physically suffering, are grossly flawed in their methodologies.
The truth is, we have failed our fellow human beings who are suffering by accepting a dogmatic approach that is not founded on solid science. In 2016, where cancer patients are afforded cutting edge genomic science to guide diagnosis and treatment, Lyme disease diagnostics are still rooted in less than cutting edge and low sensitivity indirect immune response diagnostics (ELISA and Western blot, the latter I have performed hundreds to thousands in my own research so I'm very familiar with the strengths and weaknesses of the assay). This doesn't take into account the fact there are different variants of Borrelia that might not be detected by current diagnostics.
I am not a Lyme disease physician. I had to learn more than I ever cared to know about this disease(s) due to my own misdiagnosed case that necessitated a heart transplant and nearly cost me my life.
As a physician- scientist, there are more unanswered than answered questions. For example, does everyone with chronic symptoms after antibiotic therapy for Lyme disease have active, persistent infection or some other pathology triggered by the infection? We currently DON'T have the tools to make that determination. There are numerous examples of infectious diseases that require prolonged antibiotics and cocktails of antibiotics.
I fully understand the dangers of unnecessary antibiotic therapy on the development of resistant organisms and on the all important protective normal gut microbiome. Having said that, there are folks whose lives were ruined by Lyme disease until they found compassionate and licensed physicians, many trained in infectious diseases and rheumatology but not members of IDSA who treat these folks with cocktails of antibiotics. Many of the people have their lives restored. Does that prove they have persistent infection as credible peer reviewed published research supports? I'll let you decide.
I've met so-called LLMDs [Lyme Literate MDs] who have more practical experience with Lyme disease and co-infections than IDSA counterparts. These LLMDs are thoughtful, read the latest literature, and as best they can, try to improve the lives of people in need.
We don't restrict treatment of diabetes MRI endocrinology, or treatment of asthma to pulmonary specialists. Why deny people suffering with Lyme disease access to care from highly experienced clinicians?
If you want to focus your attention on the many unanswered questions surrounding Lyme disease and co-infections, I would suggest you look to the State of Texas for innovation. Texas established a $3 billion fund called CPRIT (Cancer Prevention and Research Institute of Texas). CPRIT funds researchers in the state of Texas, in a peer reviewed process, to conduct transformative research. I consider the Commonwealth of Massachusetts to be a highly progressive state when it comes to innovative biomedical research and healthcare delivery. Massachusetts is at the epicenter of Lyme disease. What an innovative move for the state government to establish a research fund, which is sadly lacking at the federal level, to help its citizens and ultimately those around the country by funding research at Mass institutions to develop better diagnostics and therapeutics and greater insight into this disease that for many is not so easy to diagnose and cure.
Thank you for your time and consideration.
Neil Spector, MD
Sandra Coates Associate Professor Medicine
Duke University Medical Center
Durham, NC 27705"


Thomas Grier Executive Director
Dr. Paul H Duray Pathology Research
902 Grand View Ave
Duluth MN 55812
TO: Editors of Arts and Patient magazine
Dear Editors: I am writing to express a concern about the article you recently published, written by Professor Jan Keppel Hesselink. The article was a position paper about how patients and the lay-public have exaggerated concerns or misrepresented the seriousness of Lyme disease and modern vaccines.
As someone who has been involved with Lyme disease and Lyme disease research since 1990, I have concerns about academics who express strong opinions on this subject, but offer little or no scientific support or research of their own to support that patients are trying to influence medicine in a negative direction.
Since 1991 I have fought for pathology based Lyme disease research to put certain myths and misinformation about Lyme-Borreliosis to rest. For over 25 years the lay-public has been told facts about Lyme disease that quite frankly are not true and were never true. Many of these untrue facts are still being propagated by major physician groups and medical institutions; but lets look at the facts from a position of human pathology. Then decide who is misleading whom?
We were told that only the Ixodes dammini tick could carry Lyme disease and that it was only found in the NE USA therefore Lyme disease was only in the NE USA. The truth is there never was an Ixodes dammini tick, Dr. Andrew Spielman of Harvard misidentified the Black Legged tick which is found throughout North America and several close cousins of this tick all carry the Lyme spirochete and B. burgdorferi is found all through the Northern Hemisphere.
We were told that Borrelia burgdorferi was never intracellular. In truth Lyme disease is very much an intracellular disease and I have attached our own research photos to support that Lyme disease enters the brain and then enter both glial cells and human neurons. We urge every country to do human-brain autopsies as we have done, to see the whole truth of this disease.
We were told for over two decades that Lyme disease is not transferred from mother to fetus. (2006 Dr. Gary Wormser Yale in Under Our Skin documentary.) Once again we have the pathology evidence from 1989 of eight fetal autopsies showing Borrelia in the umbilical fluid, in the placenta, and in almost every fetal organ at necrotopsy. (See attach images)
What else did they get wrong? (When I say they I generally mean in my opinion that the misinformation about Lyme was most damaging from those that had the most influence on the Medical Community which includes the CDC, Yale, SUNY, Harvard and Mayo Clinic, the ACP and the IDSA)
Another untrue truth we were told was that only one species of Borrelia causes Lyme disease. Did they learn nothing from Relapsing Fevers? Borrelia changes and evolves like no other bacteria. It is constantly changing and evolving. We now have 12 species that cause Lyme disease and several species that we call Lyme-Like.
Another non-fact is that we were told that there was only one reservoir host – the white footed mouse. Of course now we know many rodents and birds are carriers of the disease and transmit it to feeding ticks. The range of these animals is far beyond the NE USA where we were told was the only place Lyme disease could exist.
In the Yale medical Report by Marc Voortman it says that patients with a positive ELISA test but a negative western blot can ignore symptoms like a bull’s-eye rash, Bell’s Palsy, and swollen joints and no treatment is necessary, but if the Western Blot test is positive you can treat up-to 2 weeks with doxycycline. I have attached pathological proof that two weeks is not sufficient for late Lyme symptoms.
The list of misinformation shows that the medical experts from the very discovery of this disease got over a dozen major-critically important facts about Lyme Borreliosis completely wrong, and perpetrated misinformation long after pathology had proved them wrong.
The most damaging untruth about Lyme disease was the insistence that Lyme disease does not persist in the human body after antibiotic treatment.
Attached are photos from a patient that lives just a few miles from me. He was a logger who was sick for 30+ years. He was diagnosed with Lyme disease and treated with aggressive antibiotic combinations for over seven years. When he died we found both Borrelia burgdorferi and Borrelia miyamotoi in his brain, and we found live B.burgdorferi and B. mayoni in his testicle.
Lyme disease does persist. It gets into the brain and inside brain cells. (Attached pathology photos from brain autopsies) In addition we have cultured B. burgdorferi out of Alzheimer’s brains.
It is unfortunate to see a position paper like this in 2016 considering that this is the year that many major Universities are clamoring to be the first to publish that they have found an infectious etiology to Alzheimer’s disease, and Borreliosis is the front running contender as a brain pathogen. While we have been using pathology for over twenty-years to prove Borrelia and Alzheimer’s are related, others are just now waking up to the fact that having both a cause and a potential treatment for Alzheimers, is worthy of major recognition.
2016 is the year that the race for the Nobel Prize has begun in earnest, and the group that gets accepted recognition of Borrelia in human brain causes Alzheimer’s pathology will most likely win the prize. You will see papers by Harvard and other major Universities vying for the pole position to prove Alzheimer’s has an infectious etiology.
While others live in the past and criticize patients for their efforts to use pathology to prove their illness has been mismanaged, the medical community has moved on and accepted that the facts they once thought were true are now part of history, and that the Lyme patients were in fact more right than the experts.
Lyme disease persists in the brain, the serology tests are missing brain infections, pregnant mothers can transmit the disease to their unborn child, sexual transmission is likely now that we documented Borrelia in human testicles even after antibiotics, and Lyme disease is found through-out the Northern hemisphere caused by more than a dozen species of Borrelia and carried by many ticks, and Lyme disease can kill as it did in the New York man who had Borrelia in his heart.
So when a patient disagrees with their doctor and explains that they are still sick after treatment. Who is right? The doctor citing 30 year old dogma, or the patient that died and had a brain-autopsy done that revealed a persistent brain infection despite years of antibiotics?
Thomas M. Grier (Exec Director)
Dr. Paul H. Duray Pathology Research Foundation

To read further on the work done by The Dr.Paul H. Duray Pathology Research Foundation go to this link :-

Thursday, 28 July 2016


Published on Jul 28, 2016
Interviews from the Worldwide Lyme Disease Protest on the 24th May 2016 held in Parliament Square.

For more information please visit :

Excellent Video produced from interviews at 2016 Lyme Disease Protest