Thursday, 24 December 2009
Information and Support for the ME/CFS/FM CommunityDavid S. Bell MD, FAAP, Editor
Volume 6, Number 5: December 2009
Web site: http://www.davidsbell.com
I hope that everyone is able to have a good holiday season.
XMRV: Quiet TimeMy thanks to all those who came to the lecture December 6th on XMRV, and to all those who have kindly donated to the research group. None of the research group is paid from these funds, and if we were to stop working the money will be forwarded to some other group working on ME/CFS, probably WPI. In the spirit of full disclosure, pizzas and other relatively inexpensive luxuries do come from these funds, but no vacations in Maui. I had wanted to write back to persons who have donated but that has proven impossible.The December 6th lecture was well attended. The reason I did not tape it or put it on the web is for two reasons. First I do not know how and we are kind of busy and I didn't want to take time to learn. And secondly, I expect that every few weeks the material will change and I want to keep this talk up to date. I expect that six months from now the talk will be completely different.I have had a few requests to give a talk on XMRV, and I am happy to do so, it is one of the joys of being retired. The material I present will be either published, from very credible public sources, or my own personal opinion. I will not share back room gossip, even if it is the stuff that makes my socks roll up and down. My goal is to insist that good science goes into discovering what role, if any, XMRV has in ME/CFS. I will go anywhere in the US if the supporting group covers costs and offers a small honorarium. I think spin off benefits from these talks will be to re-invigorate support groups. Dr. Klimas said in her last talk that now is the time for people to get active and I completely agree.ME/CFS Essay: Nature Abhors a Vacuum I have a patient in my practice by the name of Sandra Cousins (an obviously false name). She developed CFS somewhere around the age of nine, and I can remember her confusion going from doctor to doctor, occasional visits to the psychiatrist and acupuncturist. Over the years she has been diagnosed with Lyme disease, depression, atypical MS, arthritis, migraine, irritable bowel and lupus, but no one knew what she had. Like many patients, she could tell that, when the medical provider attended to the chart and did not look her in the eye while delivering a diagnosis, the provider had absolutely no idea of what was causing her illness. Same old story.Years went by, and after five years of illness she improved enough to deny the existence of any illness. She was getting by. She could not go out drinking with her college friends because it made her very ill and then have to miss a few days of classes. All she could do was classes and organize her study time well enough to pass. But she was "fine."Work after college was a disaster, as was her love life. But she got by, she was "fine." She stopped going to doctors because they had little to offer except medications that made her feel more ill. She resented being told she was resistant to the obvious truth that she was healthy as a horse.About ten years ago, Sandra went through a change. She decided that she was depressed and that the doctors were right. She took low doses of antidepressants which did little good but made her doctor happy. She joined support groups, went to therapy, and committed herself to accepting the truth. Or at least accepting what other people considered true. Lots of things didn't fit, but at least now she wasn't crazy, she had a legitimate diagnosis, she was depressed. Being depressed and making up somatic symptoms (somatisizing) was a lot better than being crazy. She was no longer lost in the never-never land of no-diagnosis. She belonged. She went on social security disability because she was unable to maintain eight hours a day five days a week because of the depression.When Sandra was evaluated for ME/CFS, she was classic. She did not feel despair, in fact, now that she was "depressed" she felt quite good. Except for the pain, sleep problems, exhaustion, abdominal pain, annoying lymph node tenderness and the foggy memory that is.Nature abhors a vacuum; it is much better to have an incorrect diagnosis than no diagnosis at all. Even when the immunology testing, orthostatic testing, and 2 day exercise testing essentially confirmed the diagnosis of ME/CFS, Sandra was reluctant to believe it. Being "depressed" for the past ten years made her more happy than some unknown diagnosis that doctors didn't believe in.XMRV Study Notes:In a recent note by Suzy Chapman on Co-Cure, she quotes Dr Charles Shepherd as writing "...Not surprisingly, the first stage of the attempt to replicate these results has resulted in various international groups almost entering a race to see who could replicate or refute the WPI results first. And this has meant they have gone for an easy and immediate source of patient material - stored blood samples. I am not aware of any stored blood samples here in the UK that are from patients who meet Fukuda plus Canadian criteria and I doubt if there are any.This brings up really important issues in interpreting the results of studies that will come out over the next six months. In my practice over the years, I have seen the whole range of patients from kind-of tired to bedridden orthostatic intolerance. Despite what the different criteria attempt to prevent, much of the diagnosis is based upon using the "force". There are some clinicians who diagnose CFS and I have absolutely no idea of what their patients are like. Through years of observation, I do have a concept of what Dan Peterson's patients are like.So is XMRV in really severe ME? CFS? Orthostatic intolerance? CFS plus POTS? Mild fibromalgia? Atypical MS? CFS with or without depression? Chronic Lyme disease? Multiple chemical sensitivities? And what about stored samples? Samples taken in EDTA or heparin? And so on.So what does this mean? It means that if someone can't find XMRV in a study, it is either because it is not in the patients they tested, or their lab could not detect it even if it was there. Or the strain might be different, or they used the wrong tubes, or the diagnosis was wrong. And on and on. Again using the "force", I would not be surprised if some of the quickest replication studies fail to confirm XMRV. But as long as people do not jump to conclusions too quickly, science will win out. Truth will win out. That’s all I am looking for.Changing Standards to Establish Cause of ME/CFSDr. J Silver in a review in Journal Watch said, "XMRV might be a cofactor in another infectious process, or the immunologic problems of CFS patients may increase their susceptibility to XMRV infection. Patients with depression also have impaired immune function; could psychiatric illness predispose to XMRV? The 4% prevalence of XMRV infection in the control group might indicate that XMRV infection is a risk factor for development of CFS."I am amazed how mainstream medicine is so fixed in their biases against ME/CFS that the concept of XMRV actually causing the illness almost doesn't enter their consciousness. Dr. Reeves, head of the CDC project on CFS has made only one comment to my knowledge, that he "doubted" this would turn out. What a comment. Why not "Interesting…" or "we will see…"Hillary Johnson made some interesting observations. First, "Why wasn't everyone demanding dozens of replicative tests on the prostate cancer findings?" Yet when CFS is implicated we will need twenty studies which replicate the first. And if some poor studies do not find XMRV, they will be given preferential weight to studies that actually find it.Her second point was that "HIV was hailed as the cause of AIDS in the U.S. in the spring of 1984, after the NCI found isolates in fewer than fifty patients. A few weeks later, an NCI scientist isolated the virus from the blood of a nurse in Los Angeles who fell ill with AIDS after a blood transfusion and the virus was found in the donor blood. That's all it took." Dr. Dan Peterson said at the recent CFSAC meeting that a transfusion case of CFS and XMRV has already been found and traced back to the donor.During the next six months we will know. I am confidant that enough good scientists will try to replicate the WPI study that a bad study here and there will not bury the subject. Meanwhile, what is happening? It is possible that the skepticism is so great that absolutely nothing is happening now. But my hope is that in back rooms across the world scientists are quietly working on this, designing studies to test blood banks, designing treatment studies. Right now is "quiet time"; I hope they are using this quiet time to make some real progress.Question and AnswerQuestion: How does XMRV fit in with slow onset ME?Answer: I have no idea. But in six months to a year we will know. First option is that XMRV has nothing whatsoever to do with ME, it was a fluke, and no one, anywhere, will be able to find it even when they are looking without bias, and in good patients, and with good science. Secondly, XMRV may have either no symptoms, or relatively minor symptoms, and slowly affects NK cells and lymphocytes, permitting reactivation of other viruses over some time.The Australian government and the CDC may have already done the study revealing the answer, the "Dubbo" study (Hickie I, Davenport T, Wakefield D, et al. Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study. BMJ 2006;333.)As you may remember, a small percentage of persons developed ME/CFS after Epstein-Barr virus, Ross River virus or Q fever. They must have saved blood from those who came down with ME/CFS and those who did not. Test the blood for XMRV. If it is in the ones who came down with ME/CFS, but not present in the blood of those people who had regular mononucleosis and quickly recovered, we would have the answer. Ah…if only it were that simple…
To Subscribe: If you wish to either subscribe or unsubscribe to the Lyndonville News, go to http://www.davidsbell.com/DSBJoin.htm and enter your information. The e-mail subscription is free. Disclaimer Any medical advice that is presented in the Lyndonville News is generic and for general informational purposes only. ME/CFS/FM is an extremely complex illness and specific advice may not be appropriate for an individual with this illness. Therefore, should you be interested or wish to pursue any of the ideas presented here, please discuss them with your personal physician.
—————————————————————————————————© 2009 David S. Bell —————————————————————————————————
Tuesday, 22 December 2009
Garth L. Nicolson and Jörg Haier
Cite this article as: BJMP 2009:2(4) 20-28
Chronically ill patients with neurodegenerative, neurobehavioral and psychiatric diseases commonly have systemic and central nervous system bacterial and viral infections. In addition, other chronic illnesses where neurological manifestations are routinely found, such as fatiguing and autoimmune diseases, Lyme disease and Gulf War illnesses, also show systemic bacterial and viral infections that could be important in disease inception and progression or in increasing the number and severity of signs and symptoms. Evidence of Mycoplasma species, Chlamydia pneumoniae, Borrelia burgdorferi, human herpesvirus-1, -6 and -7 and other bacterial and viral infections revealed high infection rates in the above illnesses that were not found in controls. Although the specific roles of chronic infections in various diseases and their pathogeneses have not been carefully determined, the data suggest that chronic bacterial and/or viral infections are common features of progressive chronic diseases.
Chronic infections appear to be common features of various diseases, including neurodegenerative, psychiatric and neurobehavioral diseases, autoimmune diseases, fatiguing illnesses and other conditions.1-4 Neurodegenerative diseases, chronic degenerative diseases of the central nervous system (CNS) that cause dementia, are mainly diseases of the elderly. In contrast, neurobehavioral diseases are found mainly in younger patients and include autism spectrum disorders (ASD), such as autism, attention deficit disorder, Asperger’s syndrome and other disorders.5 For the most part, the causes of these neurological diseases remain largely unknown.2 Neurodegenerative diseases are characterized by molecular and genetic changes in nerve cells that result in nerve cell degeneration and ultimately nerve cell dysfunction and death, resulting in neurological signs and symptoms and dementia.2,3 On the other hand, neurobehavioral diseases are related to fetal brain development but are less well characterized at the cellular level and involve both genetic and environmental factors.6, 7 Even less well characterized at the cellular and genetic level are the psychiatric disorders, such as schizophrenia, paranoia, bipolar disorders, depression and obsessive-compulsive disorders.
Genetic linkages have been found in neurodegenerative and neurobehavioral diseases, but the genetic changes that occur and the changes in gene expression that have been found are complex and usually not directly related to simple genetic alterations.2, 6-8 In addition, it is thought that nutritional deficiencies, environmental toxins, heavy metals, chronic bacterial and viral infections, autoimmune immunological responses, vascular diseases, head trauma and accumulation of fluid in the brain, changes in neurotransmitter concentrations, among others, are involved in the pathogenesis of various neurodegenerative and neurobehavioral diseases.2, 3, 5-16 One of the biochemical changes found in essentially all neurological, neurodegenerative and neurobehavioral diseases is the over-expression of oxidative free radical compounds (oxidative stress) that cause lipid, protein and genetic structural changes.9-11 Such oxidative stress can be caused by a variety of environmental toxic insults, and when combined with genetic factors could result in pathogenic changes.14
In the British Jounal of Medical Practitioners well worth accessing the link above and reading the full article.
Friday, 18 December 2009
Dr. Stephen Barthold and Dr. Ben Luft
I was rather dissappointed at first when I read the details of the above study.
I remember Pam Weintraube mentioning in her book Cure Unknown that Tigecycline was a new antibiotic that was found to be more effective than others in treating Lyme. Somewhere else I read that it was thought to be 100x more effective than other antibiotics but can't for the life of me remember where. I recently read the latest Brorson research, not widely available and again Tigecycline was considered to be very effective in treating Lyme.
So initially I was dissappointed to read about this above research but then I thought if nothing else it does add to the growing evidence that Borrelia can persistent even after what is considered to be an effective antibiotic treatment.
Then Phyllis Mervine (the founder of CALDA) kindly pointed me to Lorraine Johnson's post and as usual Lorraine puts things so much more clearly. Recognizing the problem is the first step—Persistence
"Under The Eightball"
This film documentary investigates the human and animal experiments in 1951 at Fort Detrick, Maryland under a hollow metal sphere nicknamed the "Eight Ball". Fort Detrick was the center for the United States biological weapons program from 1943 thru 1969. Is it possible that some diseases of today are a result of uncontrolled experiments gone wrong? From Andalusian Dogs' press releases
The independent film examines heartbreak and corruption in the often misunderstood world of Lyme disease. Under the Eightball chronicles author Lori Hall-Steele's battle with the devastating illness and delves into the alarming origin of the disease and its roots in the US Government's Bio-warfare Program. In their search for answers the filmmakers interviewed top experts in the field including micro-biologist, physicist, M.D.s and P.H.D.s The film includes live footage, historical documents, original animation and archival military footage.
Grey and Russell have included never-before released information gathered throughout the eighteen month production. The soundtrack includes music from The Faint and Orenda Fink, of Azure Ray, both on Saddle Creek Records. The original score was written and recorded by Grey.
Under The Eightball was produced by Michigan based film company Andalusian Dogs and was written, directed and edited by Timothy Grey and Breanne Russell. Executive producers are Justin Blake and Rasheed Ali of Traverse City and New York City.
Through the above link you can click on the trailer to this shocking revelation in this documentary film.
However remember that ticks and Lyme Disease have been around since soon after the Ice Age according to some sources and there are ticks with DNA for Lyme disease found dating back to 1900 in the Natural History Museum.
Could this type of experimentation have contributed to increased incidence as the film suggests but more importantly could it be another reason for the denial seen amongst our Government Health Departments which hinders diagnosis and treatment when so much evidence supports seronegativity and persistent infection.
Under the Eight BallDocumentary
Review by Joseph RobinsonNovember 18, 2009
Every so often a documentary film comes along that is so surprising and inspiring that it has the nagging affect of entering into the deepest hallows of a post-modern cynical mind and acknowledging all that is there. But what ends up so shocking is how in this treatise to expose the evil doing of mankind at its worst is a love so profound as to move your soul despite the horrors of "the truth."Tim Grey and his girlfriend/film partner Breanne Russell direct this documentary tour de force in as a personal of a journey as one can image. This is true documentary story of the bonds of love within a family during the tragic discovery and untimely illness and demise of Mr. Grey's Sister – Lori HallSteele. The tragic illness and unfortunate end is told and filmed as unflinching and honest as one can bear. As witnessed by Grey/Russell' s most telling camera, you travel through an earnest and personal review of her life, the struggle to determine the illness that has its grips on her, and then ultimate journey to the end of her life – and beyond. Grey/Russell and Lori Hall Steele's family are then left in the grief stricken state of asking why?Why indeed.
From this tragic inspiration is born the question of why? Why did this illness occur? What caused the health concerns from the beginning? What was the troubled medical industry responsible for? What role did the environment play? What role did the fact that Lori Hall Steele ran out of insurance play in this tragedy? And finally, what role did pre-communist China, Nazi Germany, the Cold War, and the United States Government have in all this? That's right, from this simple question of a grief stricken "why?" Grey/Russell launch into a line of questions many don't wish to have asked.
In a highly stylized flourish of personal creativity, this documentary art piece dares to take a personal, private, family matter and dig ever so gently and then more aggressively into all that is truth in the manufacture and testing of bioweapons in America.
As told in linear fashion this true-to-life script could easily play out like a courtroom drama in a compressed 2 hour and 4 minute burst of emotional, edge-of-your- seat drama. This line of events is exposed over a period of nearly ten months as the exploration of Lori Hall Steele's illness and what could becausing her to head so fast into unrecoverable sickness. We find out very quickly what ails her is Lyme disease and that this is the reason she is made to struggle so.
From failure to diagnose, to withdrawals of treatment, to refusals to issue known medications that could have prolonged or even saved her life, the tragic first act is rife with head shacking witnessing of just how bad the healthcare system is and what levels of denial we are all willing to accept in the name of capitalism and personal freedom to chose an insurance-based healthcare system.
Then, She dies.
In what has to be the most courageous act of film making I've ever watched, Grey/Russell turns the camera on their own and the family's grief and we are witness to it all. Unflinchingly, we move from hospital to hospice, to final hours as treated by Grey/Russell with a ghostly telling of the time we live with those we love as they live out their end of time. We then are witness to a cinematic requiem in honor of Lori, with a love poem in image to his dear Sister in what is a fantastic musical and ethereal call of a Spirit Home as told through film. In a homage, unsurpassed in recent memory, this scene alone is worth taking the journey, no matter how painful the steps.
As act three unfolds, the tone shifts as Grey/Russell try to get to the bottom of the question of "why." The directors stand on the shoulders of the greatdocumentarians: Michael Moore with Fahrenheit 9/11 and Morgan Spurlock withSuper Size Me, in telling a personal story with an honest and courageous eye while including credible witnesses from a huge cast of supporters. Experts include doctors, professors, medical scientist, government historians, and the like. In the role of character, along side the family and girlfriend Breanne,Tim Grey, filmmaker as partner to the story, uses this modern documentary style to add accessibility and connection to the material. If the audience gets any closer to Tim Grey as filmmaker and the emotional witness in this tragedy, he'd have to adopt us all into his family and hope we brought enough food to pass at his poor sister's memorial reception.
This is all very heavy stuff. It is technical in nature, and at times hard to swallow. But it is worth it. What works with the film is the way the detail is explained in a nicely stylized fashion without patronizing nor "dumbing-down"the material for a "lesser audience." Under the Eight Ball is an intelligent film with a critically important message that could affect us all. If you watch this documentary you won't think of a wood tick, our government, or your family in the same way again.
The climax note to us all involves the town of Lyme, CT. Grey/Russell interview the Mother of two long-ago suffering children of the yet unnamed Lyme disease.
As she explains her children's journey, we are brought full circle to the tragic impact of how fear can kill on and on into the future. The fear we weak humans possess that allowed us to make this nasty germ and unwittingly (or not) unleash it on our own. We learn that her family suffered when the disease was first"discovered. " The facts become ever clear as she tells her story. We realize it is horribly and hauntingly familiar to the one we just watched. And we are all then left with the question: Why is this allowed to happen over and over again?
Wednesday, 16 December 2009
"Inappropriate illness beliefs" is itself a type of ideology, a type of belief system. It requires the assumption that if there is no APPROVED objective test for a medical condition, then the condition must belong in the domain of psychiatry. In the history of medicine, the reverse has always been the case. Charcot's hysterics were epileptics and victims of third-stage syphillis. Women with hysterical paralysis turned out to have Multiple Sclerosis. "Cold Mother Syndrome" is now called autism.
Well worth a read and I find this blog interesting to follow.
I decided to respond :-
Such an excellent and informative post. I like to follow ME/CFS developments as this was my original diagnosis until it was found to be Lyme Disease.
There are so many parallels with these two illnesses and some patients may indeed have both how many of the sickest Lyme patients also have XMRV or visa versa.
However my reason for commenting is that the President of ILADS a psychiatrist presented at the Lyme Disease Action conference last year and what he had to say should be of interest to all Psychiatrists and also ME/CFS as well as Lyme patients. He is not the only Psychiatrist at the forefront of Lyme Disease research and developments. Dr Brian Fallon being another one. What a pity more don't follow their example. Please take time to look at the whole presentations through the following links.
• Chronic infections and immune reactions contribute to causing mental illness.
• Diagnosing and treating Lyme/tick-borne diseases and other infections and immune reactions from them are new treatment opportunities for mental illness.
• Since interaction between infections, the immune and nervous systems can cause mental illness, greater interaction is needed between infectious disease physicians, immunologists and practicing psychiatrists to more effectively treat mental illness.
From Controversy to Collaboration
• Psychoimmunologists don’t have to be convinced that infections cause immune dysfunction that in turn causes mental disorders. Some don’t understand brain physiology and need to listen more attentively to psychoimmunologists.
• Since interaction between the immune and nervous systems can cause mental illness, greater interaction is needed between immunologists and practicing psychiatrists.
• It is time to stop fighting each other and direct all our efforts towards fighting these diseases instead
This is a very interesting U tube presentation.
Many Lyme patients have problems with teeth jaw pain and nerves around that area of the face.
A friend and fellow Lyme Patient being treated by an LLMD having reached a plateau on her current treatment had occasion to need dental treatment which was metronidazole this treatment miraculously lifted her constant head fog, improved her energy and relieved her aching arms and legs. One comment back from her LLMD was one wonders how often dentists are unknowingly treating Lyme symptoms.
Monday, 14 December 2009
After being diagnosed by a top London Rheumatologist (not ME/CFS specialist) as having ME/CFS I was lucky that my GP and private specialist did not accept his diagnosis and believed my illness to be Lyme Disease. With antibiotics and only antibiotics I have recovered to nearly 100%.
I still take an interest in ME/CFS and have followed the developments recently over XMRV retrovirus with great interest, but also started to look into the politics of the illness and surprise, surprise they are as bad if not worse than they are over Lyme Disease.
Margaret Williams statement of concern is of particular interest.
I never quite understood what was going on over the Judicial Review into the NICE guidelines and probably never will.
However it was good to read these statements from so many good doctors prepared to support the patients cause. What a pity the Judicial Review didn't get to consider them. One day science will no doubt prove what mistakes were made by those writing the NICE guidelines and condemning patients to even worse problems than they had already fighting not just the illness but the denial of a physical condition.
I was even more surprised to read this post about Medical Research Council secret files. Or was I?
'As one puzzled ME sufferer recently noted: “why on earth have a 73 year embargo on these documents on an illness where a load of neurotic people, mostly women, wrongly think they are physically ill ill?”'
Was there some big medical cock up? If not then there certainly appears to be now!
Also this report of the APPG (All Party Parliamentary Group on ME) makes you wonder whose working for who.
So the most important thing I have learned from my experience is to get informed, get to know your symptoms and keep a log and be your own best advocate, guided by our doctors but not blindly following their advice, they are only human after.
Thursday, 10 December 2009
Wilske B. Diagnosis of Lyme borreliosis in Europe. Vector-Borne Zoonotic Dis 2003;3:215-27.So far I have only seen the abstract.
However I have been looking at this Wilske
There is much here that doesn't support HPA stance. Just a few extracts.
6.4. Sources of error in serodiagnosis False negative results. False negative results can be caused both by the test itself or biologically. Thus the high background reactivity of first-generation tests may lead to a lack of specificity, with sensitivity being comparable to that of second or third-generation tests. Differences between the test antigen and the strain causing infection in the patient may occasionally play a role, but also expression of diagnostically relevant proteins in the strains used for antigen production may be lacking(cf. Chapters 5.3.10 and 5.3.4.). Of utmost importance, however, are thediagnostic gaps due to the localisation and stage of the clinical manifestations (detailed in Table 7).
However, these criteria cannot be adopted for diagnostics in Germany or Europe because they were developed using B. burgdorferi s.s. and American sera only. Dressler et al. have shown in an immunoblot study that the immune response of European patients is obviously restricted to a narrower spectrum of Borrelia proteins , compared with that shown by American patients. Using different serum panels (first serum panel from Germany, second serum panel from various European countries) Hauser et al. demonstrated in two studies that interpretation rules must be defined strain-specific [22, 24]. Thus different interpretation rules are required in order to achieve equal sensitivity and identical specificity values, resp., when different strains are used. The criteria established by Hauser have been re-evaluated by Kaiser and Brauer [31a], who also believe that they are more suitable for application to the European situation than the American rules .
Therefore, the rules for the whole-cell lysate immunoblot established by Hauser et al. are cited here as reliable interpretation criteria [22, 24].
5.4 Fig 10
Step 2 confirmatory assay Igg immunoblot and Igm immunnoblot
Report as a negative serologic result
If short duration Lyme Borreliosis is suspected clinically serological follow up control
If a long course Lyme Borreliosis is still suspected clinically
Check special indications for
1 for serological follow up control
2 use of additional serological methods (eg use of another Borrelia species as a blotting antigen)
III 90-100% Usually solely IgG sensitivity (WHAT OF THE POSSIBLE 10% THEN!)
Extensive interlaboratory tests conducted in the United States reveal that the average specificity of commercial tests has even diminished over the past decade. Use of the immunoblot not only lacks standardisation in the form of established minimum requirements, but also goes without thoroughly evaluated interpretation rules. This deficiency results in diagnostic uncertainty and lack of comparability of results obtained by different laboratories.
During my search I came across this hypothesis
The 100% figure we all dispute. My understanding is that the US CDC produces panels of blood that are 'known to have Lyme disease' mixed with 'false positives' such as lupus and people who had Lyme but are now 'cured'. All serological tests are tested against these panels. Of course, I wish life were so simple as to say that the 'false positives' are truly false positives and people are definitely cured.
If a researcher requests a panel of blood (often they come in groups of 40) somewhere in the neighbourhood of 30 would be 'true positives' and the remaining 10 would be a mix of true negatives and false positives. Of course the exact mix has been double blinded and the 'key' is only released after the experiment is run. This allows the researcher to give percentages of 'my test gives 100% accuracy for Lyme arthritis'. Of course, I doubt that it's as simple as that. Lyme is truly a 'shape shifting superbug' and has more plasmids than any other bacterium yet described, so it defies easy answers.
I would really appreciate comments and thoughts on both the Wilske and the hypothesis.
One other interesting extract from Wilske is
4. Clinical Picture of Lyme Borreliosis
In the majority of cases the infection is self-limiting. However, even after antibiotic treatment, B. burgdorferi may persist in the tissue . Persistence of the pathogen may be associated with clinical symptoms
39. Preac-Mursic V, Weber K, Pfister H-W, Wilske B, Gross B, Baumann A, Prokop J (1989) Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme borreliosis. Infection 17:355-359
Seems to me yet more examples of our Health Authorities cherry picking research to support their opinions.
Wednesday, 9 December 2009
Volume 141, Number 6, November/December 2009ISSN 1918-3240
Lyme borreliosis in Canada: biological diversity and diagnostic complexity from an entomological perspective Janet L.H. Sperling and Felix A.H. Sperling
Only just published I do hope everyone will download as it will help give greater publicity, it is open access for two months.
The Sperling's son Ed was on the recent CTVW5 program posted about on my earlier post LYME ON CANADIAN TV.
Also Janet Sperling wrote the response to AMMI posted on Canlyme recently and featured in my earlier post CANADIAN LYME DISEASE GROUP TELLS IT AS IT IS.
Thank you to the Sperling family for all their work in the field of Lyme Disease Research and advocacy.
Tuesday, 8 December 2009
At least that is one landowner in the UK thinking of doing something about ticks and at least acknowledging there is a problem which is more than most do and certainly much more than most doctors do here in the UK.
I can't get the registration to work for the Times On Line, but Lyme Disease Action Chair woman Stella Huyshe says it all very well. Thank you Stella.
'We at the charity Lyme Disease Action (www.lymediseaseaction.org.uk) are very encouraged to learn that HRH Prince Charles is both concerned about and aware of Lyme disease. We shall be watching the results of the 'tick mop' trial with interest. We agree whole-heartedly with Jenny O'Dea of Tick Talk Ireland, who says: "Lyme is most certainly NOT a mild illness - UNLESS you get very fast treatment. Getting any treatment at all - let alone fast treatment - is, however, the biggest challenge". The recent announcement that bushcraft expert Ray Mears has just been diagnosed with Lyme disease 10 years after contracting it is just one example of the problems of awareness and diagnosis. Many people have struggled, while suffering hugely from a wide range of symptoms, to find out what is wrong with them and how to treat it. Lyme Disease Action offers a patient enquiry service for advice and help by email and also has posters/advice on how to remove ticks at www.lymediseaseaction.org.uk. We hope Times Online readers will look at our website to brief themselves more fully on Lyme disease and to protect themselves from long-term Lyme problems.'
Stella Huyshe - Chair - Lyme Disease Action
Monday, 7 December 2009
Press Release [published in the Canadian Health Reference Guide Nov. 25th, 2009] Copy To: Gwen Lovagi, Association of Medical Microbiology and Infectious Disease (AMMI) Canada From: Janet Sperling, Canadian Lyme Disease Foundation Re: CTV W5 Story – Lyme disease Debate (press release of 20 November 2009) It is encouraging to see that the AMMI is willing to keep the debate over Lyme disease open in a public forum like a press release. The Canadian Lyme Disease Foundation has been struggling for years to increase the transparency of the debate. Similarly, working with the investigative reporters of CTV’s W5 has been an opportunity to work with some of the best investigative journalists in Canada and we have welcomed their incisive input. We are in complete agreement that our ultimate goal is to protect and educate the public through the promotion of accurate diagnosis, prevention and treatment of human disease. We also agree with the statement that there is no need to alarm the public needlessly. Working with W5 allowed us to demonstrate that there is hope for the many Canadians who are struggling with Lyme disease. Among the three cases highlighted by the W5 documentary, one showed a full recovery and one showed a partial recovery, both of which responded well to antibiotics under medical supervision. These cases showed that there is hope and that education about Lyme disease is the key to recovery. The importance of such education was clear throughout the W5 documentary, as all the featured patients were faced with disbelief by their Canadian physicians that they were suffering from Lyme disease. Since the AMMI is in agreement that Lyme is much more treatable in its early stages, it is logically obvious that widespread education is essential to early diagnosis and treatment. For late stage Lyme disease, W5 documented that some Canadians have recovered from serious Lyme-like illnesses that responded positively only when treated by those educated in the complexities of Lyme disease. We do not believe that it is helpful for the AMMI to deflect attention away from antibiotic-treatable late stage Lyme disease by highlighting an old hypothesis that such illness is purely an induced autoimmune disorder. Not only has no useful treatment been developed on the basis of this hypothesis, but the weight of recent peer reviewed research has failed to support it. If the AMMI has reason to believe that we are wrong in this assessment of the autoimmune theory of late stage Lyme disease, then we would welcome a rebuttal supported by evidence.We are pleased to see that the AMMI has emphasized the importance of ‘epidemiologic findings about the likelihood of exposure to ticks’. However, it is important to remember that this logic may be mistaken to mean that people living outside of restricted areas should not have their Lyme symptoms taken seriously, which would allow them to progress to a stage that is more difficult to treat. Ground cover with oak leaves is only partially correlated with vector distributions, and dispersal of Ixodes ticks on birds migrating to areas distant from oak forests has been well documented. In the interests of accuracy, we note that the 2008 AMMI conference (1) referred to by the AMMI press release included only a single talk, not a symposium, on the epidemiology of Lyme disease. This plenary talk was presented by an American doctor. There was also a single poster presentation on Lyme disease at this conference. Interestingly, this poster demonstrated that Lyme disease was found in a dog in Alberta as well as in an Ixodes cookei tick removed from that dog. Thus the AMMI is aware that Borrelia burgdorferi (which is spelled with only one i, not two as in the press release) can be found in a putatively non-endemic areas of Canada and that tick vectors other than I. scapularis or even I. pacificus may be involved.We also wish to correct the AMMI press release statement that ‘One of the issues raised in the W5 story is the stated “fact” that 19,000 cases of LD have been seen in US Border States’. W5 did not say that, neither in the episode that was aired which gave the number as "closer to 15,000 a year" nor in the accompanying website text where it was given as 'nearly 13,000’ (2). We were surprised to see the AMMI suggesting possible over-reporting of Lyme disease in the United States. To our knowledge, this is the first such indication by a professional organization that US government Centers for Disease Control statistics on Lyme may have been tainted by interference 'engendered by a medical system that pays substantial dividends to both laboratories and physicians for the diagnosis and management of purported “chronic” LD'. In contrast, the CDC’s Morbidity and Mortality Weekly Report for May 7 2004 (3) states that 'Studies from the early 1990s suggested that LD cases were under reported by six to 12-fold in some areas where LD is endemic; the current degree of underreporting for national data is unknown'. In this light, we believe that it would have been more appropriate for the AMMI to claim biases in US CDC statistics in the presence of supporting evidence. Finally, we are glad to know that 'AMMI Canada doctors are at the forefront of antibiotic resistance issues and are confronting the over-use and misuse of antibiotics'. Antibiotic resistance is a serious problem in Canada and it is arguable that the largest component of this problem is due to the extensive use of antibiotics in animal feed at sub-therapeutic levels for economic gain (e.g. 4). We certainly support continued research into the responsible use of antimicrobials. We’re grateful that W5 journalists were willing to discuss the difficult situation that surrounds Lyme disease, particularly in the Canadian context. We look forward to continued discussion with AMMI Canada, whether in a public or private forum. 1) AMMI Canada Annual Conference 2008 Final Program http://www.ammi.ca/annual_conference/AMMI_Final_Prog2008_rev5.pdf last accessed 23 November 2009. 2) http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20091113/w5_lyme_091114/20091114?s_name=W5 last accessed 23 November 2009, audio statement at 7:20 3) Morbidity and Mortality Weekly Report 53 (17): 365-369. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5317a4.htm last accessed 23 November 2009 4) CIPARS 2007 Farm Surveillance Preliminary Results http://www.phac-aspc.gc.ca/cipars-picra/pdf/2007pr_fs-sf-eng.pdf last accessed 23 November 2009 TOP
Friday, 4 December 2009
A Tale of Two Spirochetes: Lyme Disease and Syphilis.
Halperin JJ.Department of Neurology, Madison Avenue, Mount Sinai School of Medicine, NY,USA; Department of Neurosciences, Overlook Hospital, 99 Beauvoir Avenue, Summit,NJ 07902, USA.
Only two spirochetal infections are known to cause nervous system infection and damage: neurosyphilis and neuroborreliosis (nervous system Lyme disease). Diagnosis of both generally relies on indirect tools, primarily assessment of the host immune response to the organism. Reliance on these indirect measures poses some challenges, particularly as they are imperfect measures of treatment response. Despite this, both infections are known to be readily curable with straightforward antimicrobial regimens. The challenge is that, untreated, both infections can cause progressive nervous system damage. Although this can be microbiologically cured, the threat of permanent resultant neurologic damage, often severe in neurosyphilis and usually less so in neuroborreliosis, leads to considerable concern and emphasizes the need for prevention or early and accurate diagnosis and treatment.
http://eutils. ncbi.nlm. nih.gov/entrez/ eutils/elink. fcgi?dbfrom= pubmed&id= 19932386& retmode=ref& cmd=prlinks
PMID: 19932386 [PubMed - as supplied by publisher]
However thanks to Renee of Renee's Reflections I see that Connie Strasheim has posted several interesting updates on Lyme treatments that she learned from the LLMD's speaking at the annual ILADS Conference this fall. You can read them on her blog, LymeBytes at http://www.lymebytes.blogspot.com/.
Many of you will remember the trailer for this film which promised a very revealing look at Lyme, much like Under Our Skin. Unfortunately the film makers ran out of funds I believe and I hadn't heard much else about it...until recently, A2Z Media posted a clip on You Tube, to be found here:http://www.youtube.com/watch?v=EE8gK_cR8VQ
Monday, 23 November 2009
Saturday, 21 November 2009
(DVD available and worth every penny from http://www.ilads.org/ )
I had the privilege to hear Dr Bransfield present at the Lyme Disease Action conference in the UK in 2008
Thus I was aware of his work with Lyme Induced Autism foundation
and therefore found his presentation particularly interesting
Details of presentation at ILADS conference removed.
Friday, 20 November 2009
Excellent news from Under Our Skin. This documentary so accurately represents our experiences. Our struggles for diagnosis and treatment of chronic Lyme Disease.
The Academy of Motion Picture Arts and Sciences today announced that UNDER OUR SKIN was selected as one of the 15 finalists competing for “Best Documentary Feature” in the 82nd Academy Awards®.
Unfolding like a real-life thriller, UNDER OUR SKIN exposes the hidden epidemic of Lyme disease and reveals how our corrupt medical system is failing to address one of the most serious illnesses of our time. Open Eye Pictures is thrilled that the Academy has honored the courageous Lyme patients and physicians whose stories are told in this film. And we hope that this nomination will help spread awareness about this devastating disease and serve as a catalyst for fixing our country’s broken health care system.
The Documentary Branch Screening Academy Committee viewed all eighty-nine qualifying documentaries during the preliminary round of voting. Academy members will now select five nominees from among the 15 titles on the shortlist, and Academy Awards nominations will be announced on Tuesday, February 2, 2010.
Wednesday, 18 November 2009
In the past I have sent many e mails to all the national newspapers and spoken with reporters from most of them they are disinterested to the point of rudeness. One day they will be all over this like they were when HIV first broke into the news, but sadly people and children will continue to suffer unnecessarily because of lack of good investigative journalism of the calibre of Pam Weintraube ( links on my side bar).
When someone in the media realises that they or their loved ones are ill with Lyme Disease and the scandal that surrounds diagnosis and treatment then the brakes will start to come off.
Meanwhile I will continue to feed them information. Do feel free to comment constructive criticism always welcome.
This is what I sent.
There is much controversy about diagnosis and treatment of Lyme Disease. Our Health Protection Agency follows Infectious Disease Society of America Guidelines. These Guidelines are currently under review and at a presentation in July 09 available at IDSA website http://www.idsociety.org/Content.aspx?id=15026
Presentation number 15. highlights 25 studies on Seronegativity and persistent infection. There is considerable evidence that IDSA/HPA restricted guidelines are causing patients to continue with chronic ill health and be denied treatment that can help them. For many years now in USA doctors specialising in treating Lyme Patients developed ways of treating successfully with controversial long term antibiotics. Alternative Guidelines to IDSA were developed by International Lyme and Associated Disease Society.
UK Charity http://www.lymediseaseaction.org.uk/ has provided much needed support to UK sufferers of Lyme disease. This charity holds annual medical conferences details available on their website. This charity has for some time tried to engage HPA in dialogue to discuss the problems that IDSA/HPA rigid guidelines have caused several thousands of patients here in UK but their work is falling on closed ears.
'MP Oliver Letwin says he gives his full support to this charity on his website he says:- 'It is an interesting and important feature of the scene that, when these medical disputes occur, there is no joy to be had from lobbying ministers – because, no matter how many meetings you hold at Westminster, and no matter how many letters you write, you inevitably just get the answers written for ministers by the Health Protection Agency.'
My own MP Anne Milton Shadow Health Secretary has also been very supportive in trying to raise awareness of this awful disease but sadly her efforts result in the same denial from just a handful of people who advise the HPA, cherry picking science and playing with words to support their OPINIONS.
http://www.lymediseaseaction.org.uk/seminar2008/index.htm Following a meeting held at the House of Commons in November 2008 there were further developments, not as you might expect further discourse (especially as Dr Sue O'Connell from HPA actually said at the meeting 'Not everything is hunky-dory, but we have to work from the best available evidence.') but no the two doctors presenting at that meeting, supporting alternate treatment guidelines that of International Lyme and Associated Disease Society, were reported by Sue O'Connell to the GMC for using unorthodox treatments. Since when was long term antibiotics for complex bacterial infections unorthodox and by whose say so on what evidence? How many other zoonosis are difficult to diagnose and difficult to treat? Not content with shutting down those pioneering doctors who have helped many patients, there has now been issued a letter from the Chief Medical Officer to all our doctors. This is whilst the IDSA are still reviewing all their evidence and still not made their decision, although anyone reading or watching the presentations in July can see that nothing is simple to diagnose or easy to cure with Lyme and both parties agree that if not treated early people often go on to have chronic illness. http://www.lymediseaseaction.org.uk/releases/cmoupdate.pdf The above was a response to CMO from LDA with a link to CMO letter included. I was fortunate that I was treated by my GP but suffered 4 years of chronic arthritis before being diagnosed and was retired early on ill health grounds. For 2 1/2 years I could not walk up or down stairs and was at one point housebound, I am now 100% recovered and can actually cycle again. Quite a miracle but it took many months of simple antibiotics to recover my health, treatment which because of HPA schinanikens is denied most patients. In the USA there is a documentary film doing the circuit Under our skin http://www.underourskin.com/ Take time to watch the trailer and look under press at various other extracts. Seems rather melodramatic but I assure you the same is happening here in the UK. Who ever would have believed it possible! Recently Canadian TV showed the following, make sure you watch both parts.
We have our own list of tragic cases too here in UK, a Widow I know whose husband suffered psychiatric problems in his 70's as well as other Lyme Disease symptoms, diagnosed on NHS but was refused further treatment after the initial short courses. He went into his garden in the middle of the night doused himself with petrol and set fire to it, he died the next day of his injuries. His widow and family believe it was due to his Lyme Disease not adequately being treated.
There are parents of young children also struggling for adequate treatment possibly the saddest being Lewis Jeynes
Finally diagnosed but still medics do not know how best to treat him and although he is on antibiotics privately and made some significant progress his constant seizure spells are very worrying. Will they be able to help him or has it been too late getting his diagnosis?
Borreliosis and Associated Diseases Awareness UK charity produced their own DVD you can see their trailer here.
The following interviews, patients in UK and arguments from both sides.
Or a link to A2Z media site which is a bit slower to access
All the above just scratches the surface of what is considered by those specialising in it's treatment as a formidable bug. Those who advise doctors in UK that it is simple to treat and remaining symptoms you live with, there is no treatment, are wrong for many of us because on adequate treatment we do get better.
I would hope that an in depth documentary would help get to the route of the problems and would if nothing else expose what one doctor I met described as a 'Medical disgrace' her son ill with Lyme disease was taken to America for treatment, but from being in a wheel chair after many months antibiotics is now back at school, playing sport. She is not the only doctor I have met who has travelled to USA for treatment, what hope for those none medical people with restricted finances and now refused by NHS.
Tuesday, 17 November 2009
This was posted recently I had missed part of this testament when I watched the CFSAC meeting.
I watched it again and felt moved to e mail him my support.
I have heard of so many good doctors supporting Lyme Disease patients who have been hounded and are still being hounded by IDSA supporters in the USA and now it seems we are having similar problems here in UK. Who would have believed such evilness.
This was the reply to my e mail.
Indeed you are one of the few and one of the fortunate!
In the United States, two studies indicate that approximately 30 percent of CFS/ME patients actually have Lyme Disease.
Getting physicians to re-check their patients is not easy.
I sincerely appreciate your support and your taking the time to write to me.
My hope is that eventually the number of patients willing to speak up will be sufficiently large that we will be heard.
This was the e mail I sent:-
Many thanks for your courage in speaking out at the SFSAC meeting and all the work you do.
It is disgraceful what happens to you and other doctors for your pioneering work.
I was diagnosed with ME/CFS by a top London Rheumatologist! it turned out to be Lyme Disease and on antibiotics I have my health and my life back.
Who ever would have dreamt that such controversies are ongoing with ME/CFS and also Lyme Disease when there is so much science supporting a bacterial/viral illness.
One day science will prove the nay sayers wrong, but it is wonderful to have such brave pioneering doctors prepared to put their careers at risk for us chronically ill patients while our health authorities do nothing.
Well done Canada for doing a program on Lyme Disease in two parts it has covered the subject well and goes some way to highlighting problems that we have in USA, Canada and Europe but also other parts of the World because physicians follow IDSA discredited guidelines which are currently under review.
Now available on You tube part one here and part two here
Below are just some of the extracts from the meeting found on Medscape
Medscape Conference Coverage, based on selected sessions at the:Infectious Diseases Society of America (IDSA) 47th Annual Meeting.
From Medscape Medical News
Infectious Disease Treatment Guidelines Weakened By Paucity of Scientific Evidence
Daniel M. Keller, PhD
November 13, 2009 (Philadelphia, Pennsylvania) — Two separate analyses presented here at the Infectious Diseases Society of America (IDSA) 47th Annual Meeting revealed that most of the society's treatment guidelines are based on expert opinion, nonrandomized trials, and case studies.
Between 1994 and April 2009, IDSA issued 68 guidelines on 52 different topics .
Dr. Lee summarized his presentation, saying that of the 1408 guideline recommendations he reviewed, "more than half were based on level III evidence, which is from expert opinion or not supported by properly controlled trials. Level I evidence was only 15%." He said his study should help to point out where evidence is lacking and to suggest areas for further research.
Physicians and trainees should not just look at guidelines, but should also examine the strength of the evidence on which they are based, he advised. "When clinicians are using the guidelines, they should not assume that they are all based on well-designed studies. . . . Clinicians should remain cautious when using current guidelines as the sole source for guiding patient care."
A second presentation supported the findings of Lee and coworkers. Abdur Khan, MD, assistant consultant at King Fahad Medical City in Riyadh, Saudi Arabia, presented his results in a poster session. Of the 65 IDSA guidelines, encompassing 6667 recommendations, issued between March 1994 and July 2009, he and his colleagues evaluated the 44, comprising 4206 recommendations, that were posted on the IDSA Web site at the end of July.
They, too, found that, overall, the strength of the recommendations did not correlate with the available evidence. Level I evidence was the basis for only 15% of the guidelines, which is in agreement with the findings that Lee and colleagues reported. Thirty percent of the evidence was level II."
Around 55% of the guidelines had a level of evidence of III, which was based on expert opinion," evel II; 37.8% on level III).
Neither of these studies received funding. Dr. Lee and Dr. Khan have disclosed no relevant financial relationships.
Infectious Diseases Society of America (IDSA) 47th Annual Meeting: Abstract 1324. presented November 1, 2009; Abstract LB-31, presented October 31, 2009.---------------------------------
Monday, 16 November 2009
The Whittemore Peterson Institute has many links into news articles.
I have followed this because there are many people with Lyme disease who struggle with ME/CFS type symptoms and like me are often diagnosed with ME/CFS before being diagnosed with Lyme. Conversely I have met other patients on line who have an ME/CFS diagnosis but also have Lyme Diagnosis.
Whether XMRV will be found in some patients with Lyme remains to be seen.
What also interests me is the politics that surround ME/CFS and where best to read about that but through Oslers web blog by Hillary Johnson. I came across Hillary Johnson as she wrote the forward in Pam Weintraube's book Cure Unknown a must read for anyone with Lyme Disease. One day I look forward to reading Osler's web.
Who would have believed that these two illnesses could have been skewed so by medical politics, so that thousands of patients suffer undiagnosed for years and are denied adequately treated, because a handful of people in powerful positions dictate their OPINIONS and do not consider all available science or even try to further available science to the benefit of those patients.
A good place to start is by watching the Chronic Fatigue syndrome advisory committee video cast day 1 especially but also day 2
Dan Peterson and Annette Whittemore present to the committee.
Another interesting link is through the Huffington post to a TV interview with Judy Mikovits and Annette Whittemore.
One of the blogs I follow has posted many interesting articles about developments going on with XMRV My Life as I StandUP2ME I recommend this blog for further reading.
Thursday, 12 November 2009
Borrelia burgdorferi – en unik bakterie
Borrelia burgdorferi - a unique bacterial
Background. Lyme borreliose is a tick transmitted disease caused by Borrelia burgdorferi. Number of reported cases is rising steadily in both Europe and the United States. Tick as vector for the disease spreading to ever new areas. The disease is now called "the new great imitator disease. The possibility of fault diagnosis and fault management can be significant.
Materials and methods. The overview is based on articles found by searching on the properties of "Borrelia burgdorferi" in PubMed, as well as their own research in the field for the past 20 years.
Results. In recent years, has discovered many new characteristics of Borrelia burgdorferi. It turns out that bacteria can survive even if the host has an intact immune system. The bacterium can be disseminated early in the course of the disease to remote areas, be anaerobic, hiding in the niches, be intracellular and express multi-drug resistance. It can cover itself with the host material, make antigenic changes, manipulate the host's immune system and change to the inactive cyst forms.
There may be clinical treatment failure by any suitable antibiotic. Without appropriate treatment the infection can lead to multi-systemic chronic infection. Erythema migrans is a clinical diagnosis. If chronic illness is the clinical diagnosis is uncertain. Antibody development is slow and negative serological test is frequent, particularly in early disease phase.
Interpretation. Borrelia burgdorferi have many opportunities to escape the host's defense mechanisms and it has the ability to multi-drug resistance. There is a need for better diagnostic methods.
The bacterium Borrelia burgdorferi is named after the zoologist sveitsiskamerikanske Willy Burgdorf (b. 1925). Spirochaete was isolated and recognized as the cause of Lyme borreliose in 1982 (1).
Lyme borreliose has in recent years increased sharply in incidence in both the U.S. and Europe. This is probably due to several factors, both gjengroing of the cultural landscape, increase in hjortedyrbestanden, milder climate and the fact that people spend more time outdoors (2). It can not be excluded that some of the reason for the frequently reported cases is more awareness about the bacteria and better tests.
The purpose of this overview article is to provide an update on the various properties of B. burgdorferi.
Materials and methods
The overview is based on articles about the properties of the bacteria found by searching for "Borrelia burgdorferi" in PubMed, as well as their own research in the field for the past 20 years.
The bacterium Borrelia burgdorferi
B. burgdorferi sensu Lato divided into at least 13 different genospesies. Lyme borreliose typically caused by the four genospesies of B. burgdorferi sensu Lato: B. afzelii, B. garinii, B. burgdorferi sensu stricto and the recently discovered B. spielmanii (3, 4). The bacterium is a gram negative moving spiroket (Fig. 1) which measures 0,18-0,3 x 15-30 microns, are helical and have 7.11 periplasmatiske flag or. Movement related genes occupy more than 6% of the genome of the bacterium. The unique flagellene allows it to move in the viscous fluid and rapidly disseminated (5). The bacterium can be mikroaerofil or anaerobic, depending on genospesies and type. It is also fakultativ intracellular (6-9).
Figure 1 Borrelia burgdorferi grown in BSK-H medium and stained in akridinoransje. UV-microscopy, 2 000 times larger. Photo Øystein Brorson
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One of the most striking features of B. burgdorferi is unusual genome, which consists of a linear chromosome of 910 kilobasepar (KBP) and at least 12 linear and nine circular plasmids that vary in length from 5 to 54 KBP KBP. It is not known other bacteria with as many plasmids per cell. Many of the plasmids can be lost in culture, but the remaining are considered very important for the bacteria and are often called "mini-chromosomes". In all DNA ends of chromosomes are the telomeres that are closed at one end - like a hairpin. It is not known from other prokaryotes. Linear genome is also very unusual among microorganisms. Bacterial genome contains genes for hemolytic and DNA repair and antibiotikaeffluksproteiner. The bacterium contains no genes for cellular biosyntesereaksjon, and it must therefore have a very complex medium for growth. Some plasmids code for proteins that are important virulensfaktorer, including the linear plasmids lp-28, which codes for antigen variation.
Many bacterial genes are encoded to produce more than 100 lipoproteins. This is more than in other known bacteria. These genes are mostly located on plasmids. The proteins are located on the bacterial surface, where they can come in contact with the host. Some of these outer membrane antigens are important for the bacteria - they are called aspen-F protein and 100 (10).
Lyme borreliose is a vector-transmitted disease. Generally, infected people by infected ticks. In Europe, the Ixodes ricinus is the source of Borrelia infection. In Norway, ticks (Fig. 2) particularly widespread in the coastal areas from Whales to Helgeland, but in recent years of mild winters has now led to a permanent population in some places inland. Lund Lusen Ixodes Uriah can also be carriers of B. garinii. It is therefore possible that infected birds can spread the infection in the Arctic via the grove lice (11). Tick saliva contains proteins that are stupefying, vasodilaterende, immunomodulatory and prevent coagulation (12). This increases infeksiøsiteten. Other insects horsefly and mosquito stick can also be carriers of Spirochaete (13).
Figure 2 Full sucked female that spring has added eggs. The size of the tick is about. 1 cm. Photo Øystein Brorson
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Particularly virulent strains seem constantly increasing in prevalence in both Europe and the USA (14).
The surest evidence of a Borrelia infection is the expanding red circular rash called erythema migrans, but the characteristic rash may occur and cause problems with the diagnosis of the disease. It may also be delayed development of the rash from the normal (2-30 days) to 100 days (15), which can result in a late treatment. Most often it is skin, muscle, central and peripheral nerves, brain, heart and joints that affect, but the bacteria can be disseminated to all tissues and organs (5, 16).
B. afzelii and B. spelmanii leads often to different hudmanifestasjoner, B. garinii to neurological symptoms and B. burgdorferi sensu stricto to joint problems, but the three genospesies B. afzelii, B. garinii and B. sensu stricto can give all the symptoms (3 , 4). The bacterium is now often called the "the new big sykdomsimitatoren".
Establishment of infection
Two of bacterial lipoproteins (decorinbindende protein A and B) binds to decorin, a proteoglycans that "decorates" collagen fibers (17). The bacterium also has the ability to bind to dermatansulfat, heparin, inte grin and fibronectin. B. burgdorferi increases their ability to invasivitet by degrade soluble and insoluble components of the host's extracellular matrix (18). It is also shown that Lyme Spirochaete use pheromones as an important mechanism for communication, to control the protein production and to coordinate different functions (19).
B. burgdorferi produces a variety of so-called Erp proteins on its outer membrane that can bind factor H and factor H-like protein (complement inhibitory molecule) and thus circumvent the alternative komplementvei (20). It applies to B. afzelii and B. spielmanii and all or part B. burgdorferi sensu stricto, whereas B. garinii is predominantly sensitive (3, 4). The different Erp proteins have affinity for complement inhibitors in various animal species, and bacteria can therefore withstand komplementmediert murder and fagocytose at any of the potential hosts it infects.
During the antibody can attack B. burgdorferi mutate and make rearrangement of DNA, which can lead to antigenvariasjon. It is particularly OspE undergoing major antigenic variations (21). Modification and lower regulation of other outer surface proteins (aspen, C), so they do not bind to protective antibodies, is also a feature that the bacterium can use to circumvent the host's defense. This is especially important for the bacteria in early infection phase.
Virulensegenskapene leading to infection is considered to be strongly linked to one of the outer surface protein (OspC) (22).
One of the many challenges that the bacterium is exposed to the highly toxic oxygen and nitrogen compounds that are formed in the infected organism in response to bacterial invasion. The bacteria can respond to oxidative stress by activating stress-related genes for the production of enzymes that protect against oxidation (23).
Circulating immune complexes was one of the earliest immunological phenomena that were described by Lyme disease (24). Immune complexes can be found both in serum, cerebrospinal fluid and synovialvæske. When circulating immune complexes are not well-NOK removed by the retikuloendoteliale system, deposited in the tissues and organs and enable komplementer, and this may lead to local inflammatory vevsdestruksjon (25). Immune complexes may also contribute to alter the host's defense mechanisms by defective Fc-receptor, so that opsoniserte B. burgdorferi can not be eliminated by monocytes.
B. burgdorferi is known to produce liposomliknende vesicles (blebs) which repels from the outer membrane. Anti genes aspen, B and D and protein-100 is incorporated into these "blebsene" and its affinity for endothelial cells. In order for bacteria to survive in the circulatory system is probably the removal of surface antigens beneficial. Bacteria "blebser" will be incorporated into the Cytosol and in the nucleus to dendritic cells, lymphocytes and fibroblasts. This leads to the generation of CD8-positive T-cells, which will be able to kill certain cells, and thus stand behind an autoimmune-like state (26). "Blebsene" also contains a mitogen factor for B lymphocytes, which stimulates IgM production. They are also essential penicillin binding proteins.
Much attention has been focused on aspen. This is a special protein that is not found elsewhere in nature. It can, among other things activate nukleærfaktor-kB and induce many cytokines, adhesjonsmolekyler and nitric oxide. Aspen is also a plasminreseptor, and the proteolytic activity on the cell surface can protect against both komplementer and specific antibodies. A marked increase in aspen-reactive CD-positive T-cells are also identified in inflammatory joint with antibiotic resistant patients with Lyme arthritis and in the cerebrospinal fluid in patients with neuroborreliosis.
It is shown that B. burgdorferi isolates from patients can be converted to cyst forms in vivo under the influence of penicillin (27). It has also succeeded in converting cyst forms (Fig. 3) back to moving Spirochaete, both in vitro and in vivo, and cysts have been shown to be infectious for mice (28-30). Cysts have upgraded VlsE (VMP-like sequence, expressed) and aspen-proteins, and they have at least 20 new antigens (31). It is shown that Borrelia can form cysts when exposed to pencillin or doksysyklin in concentrations corresponding to the MIC (minimal inhibitory concentration). It nedreguleres many proteins, including p-66 (an important Porin), and it is expressed more until recently unknown proteins that are important for energy, aminosyresyntese, enzymatic activity and cell division (32). Recently it has been shown by studies in cell culture and in biopsies from the brain tissue of neuroborreliosis patients that Borrelia cysts can be found both extra-and intracellularly and cause apoptosis (33).
Figure 3 Borrelia Burgdorf-cysts from distilled water that is transferred to BSK-H medium and cultivated two weeks at 33 ° C. Cyst forms in the sharing phase (large arrow). It is also seen many normal regular Spirochaete (thin, long arrow) and "blebser" (small, thin arrow). 15 000 times larger. Photo Sverre-Henning Brorson
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Host response to infection
Lipoproteins, Peptidoglycan and circulating immune complexes contribute in large part to the pathogenesis of Lyme borreliose. The bacteria activate different cells to produce betainterleukin-1-beta (IL-1-β), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8). When neuroborreliosis is in the spinal fluid demonstrated increased secretion of the Borrelia-specific gamma interferon (INF-γ) and extremely reduced secretion of interleukin-4 (IL-4) (34). This can lead to vevsdestruksjon secondary to the immune response.
B. burgdorferi can induce a four times increase in the number of CD 16-NK-cells (natural kill cells), but also a serious inhibition of NK-cell cytotoxic capacity (35). This is in contrast to other bacteria, which are known to activate NK cells.
Neutrophil granulocytes are important for fagocyttering of promotional organisms, but OspB-production with B. burgdorferi can inhibit the fagocytterende ability of the neutrophil granulocytes and the ability to oxidative killing. Neutrophil granulocytes are the fastest moving fagocytterende cells in the body, but recently it has been shown that B. burgdorferi can move several times faster than them and thus avoid fagocytose (36).
Serological analysis are important tools to make a clear diagnosis of Lyme borreliose, but sensitivity is low in the early stage of the disease. Medical history and clinical examination is therefore important to be able to make a clear diagnosis.
However, it appears increasingly new and improved methods - eg. "Focus floating microscopy (both horizontal and vertical microscopy) of biopsy material, as the erythema migrans has a sensitivity of 98% and as high specificity of polymerase (PCR). There are also recently shown that by detecting 16S rRNA gene from the serum polymerase will be increased sensitivity. Borrelia antibody specifically bound in circulating immune complexes may contribute to the low diagnostic sensitivity in early course of the disease. Detection of specific immune complexes may therefore be useful where there is clinical suspicion and negative serological test and can possibly say anything about whether there is active infection (37). Validated surveys for the detection of specific immune complexes is not yet available.
The antigenic heterogeneity of the different tribes are great. This can give rise to the low diagnostic sensitivity, since often only one strain of B. burgdorferi sensu Lato is used in ELISA and Western blot tests. It was recently developed an ELISA test in which one uses a synthetic peptide from the conserved part of the OspE (IR6) at Spirochaete. This test has high sensitivity and specificity, but the analysis results are also here depending on the strain causing the infection.
Causes of low antibody production may be that the bacterium actively adheres to, invades and kills the human T-and B-lymphocytes (38), is fakultativ intracellular (6-9, 33) and has the ability to cover himself with the host material (19) .
A study of culture positive spinal fluids showed that there was a large difference in serological and other laboratory markers if the infectious strain was B. garinii or B. afzelii (39). New tests can be useful for spinal fluid is the detection of cytokines CXCL13, which has been shown to be elevated early in the course of neuroborreliosis (40). A new lymfocyttransformasjonstest (LTT-Melis) seems to correlate with Borrelia infection and could possibly say anything about clinical improvement.
Antibiotic resistance mechanisms
Treatment of Lyme borreliose early sykdomsforløper is usually successful if you follow the recommended guidelines, but chronic infection may be difficult to treat.
Mechanisms of bacterial survival is insufficiently understood, but that the bacterium covers himself with the host material, the intracellular localization and lavbiologiske bacteria and cyst forms may be of importance (6-9, 33). Polymorfnukleære leukocyte production of calprotectin, which removes the accessible sink and thereby inhibit cell division, can make bacteria resistant to b-laktamantibiotika (41).
Bacterial antibiotic sensitivity differs from both gram positive and gram negative bacteria. It has natural resistance above aztreonam, teikoplanin, fucidinsyre, fluorokinoloner, aminoglukosider, cefaclor, loracarbef, nalidiksinsyre, trimethoprim-sulfamethoxazole, fosfomycin and rifampicin (42). The strains investigated so far, shows very variable sensitivity to different antibiotics. The minimum concentration of penicillin G to inhibit growth of B. afzelii (MIC) is 100 times higher than that of B. garinii (42).
Efflukssystem bacteria can evolve to include utpumping from the bacterial cell by many different antibiotics, and can thereby contribute to the lack of efficacy and persistent infection (43). New antibiotics that are resistant to bacterial efflukssystem can perhaps be a solution.
It is a controversial question about cysts may be the cause of persistent infection and reactivation of the disease. Hydroxychloroquine and metronidazole, however, has proven to be cyst active in vitro (44, 45). It is also controversial whether persistent symptoms after undergone Lyme borreliose originate from persistent infection or are immunologically related (46), but few studies show that there are effects of repeated and prolonged treatment (47-49).
It developed an aspen-vaccine for B. sensu stricto, but due. bacterial aspen-heterogeneity was not the vaccine is effective against B. afzelii and B. garinii. It also gave more side effects and were withdrawn from the market. Working, however, continued to develop an effective vaccine that can cover the usual genospesies. A new recombinant tetravalent vaccine based on multiple OspC types, which are under development, will cover the sydomsfremkallende genospesies.
Declared conflicts of interest: None
Borrelia burgdorferi is a unique bacterium that has developed many defense mechanisms
It has the ability to survive all types of antibiotics
The current diagnostic tests are inadequate and are only a supplement in the diagnosis
See also Laboratory Diagnosis of Lyme borreliose See also Borrelia - serological studies to use and trouble
1. Burgdorf W, Barbour AG, Hayes SF et al. Lyme disease - a tick-borne spirochetosis? Science 1982; 216: 1317-9.
2. Barbour AG, Fish D. The biological and social phenomenon of Lyme disease. Science 1993; 260: 1610-6.
3. van Dam A, pools H, Vos K et al. Different genospecies of Borrelia burgdorferi are associated with distinct clinical manifestation of Lyme borreliosis. Clin Infect Dis 1993; 17: 708-17.
4. Herzberger P, Siegel C, Skerka C et al. Human patogenic Borrelia spielmanii sp. now resist complement-mediated killing by direct binding of immune regulators Factor H and Factor H-like protein 1 Infect Immun 2007; 75: 4817-25.
5. Luft BJ, Steinman CR, Neimark HG et al. Invasion of the central nervous system by Borrelia burgdorferi in acute disseminated infection. JAMA 1992; 267: 1364-7.
6. Ma Y, Sturrock A, Weis JJ. Intracellular localization of Borrelia burgdorferi within human endothelial cells. Infect Immun 1991; 59: 671-8.
7. Wang P, Gartenhaus R, Sood SK et al. Detection of Borrelia DNA in circulating monocytes as evidence of persistent Lyme disease. Journal of Spirochetal and Tick-Borne Diseases 2000; 7: 16.9.
8. Georgilis K, Peacock M, Klem opens MS. Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro. J Infect Dis 1992; 166: 440-4.
9. Peters DJ, Benach JL. Borrelia burgdorferi adherence and injury two undifferentiated neural cells in vitro. J Infect Dis 1997; 176: 470-7.
10. Casjens S. Borrelia genomes in the year 2000. J Mol Microbiol Biothechnol 2000; 2: 401-10.
11. Larsson C, Comstedt P, Olsen B, et al. Firest record of Lyme disease Borrelia in the Arctic. Vector Borne Zoonotic Dis 2007; 7: 453-6.
12. Hovius JW, de Jong MA, the Dunne J, et al. Salp15 binding to DC-SIGN inhibits Cytokine expression by impairing both nucleosome remodeling and mRNA stabilization. PLoS pathogen 2008; 4: E31.
13. Magnarelli LA, Anderson JF, Barbour AG. The etiologic agent of Lyme disease in deer flies, horse flies, and mosquitoes. J Infect Dis 1986; 154: 355-8.
14. Qui WG, Bruno JF, McCaig WD, et al. Wide distribution of a high-virulence Borrelia burgdorferi clone in Europe and North America. Emerg Infect Dis 2008; 14: 1097-104.
15. Carlson SA, Granlund H, Jansson C et al. Characteristics of erythema migrans in Borrelia afzelii and Borrelia garinii infections. Scand J Infect Dis 2003; 35: 31.3.
16. Wormser GP. Hematogenous dissemination in early Lyme disease. Wien Klin Wochenschr 2006; 118: 634-7.
17. Fischer JR, Parveen N, Magoun L, et al. Decorin-binding proteins A and B confer distinct mamma Lian cell type-specific attachment by Borrelia burgdorferi, the Lyme disease spirochete. Proc Natl Acad Sci USA 2003; 100: 7307-12.
18. Coleman JL, Roemer EJ, Benach JL. Plasmin-coated Borrelia burgdorferi degrades soluble and insoluble components of the mamma Lian extra cellular matrix. Infect Immun 1999; 68: 3929-36.
19. Stevenson B, von Lackum K, Wattier RL et al. Quorum sensing by the Lyme disease spirochete. Microbe Infect 2003; 5: 991-7.
20. Hellwage J, Meri T, Heikkilä T, et al. The complement regulator factor H-volume to the surface protein OspE of Borrelia burgdorferi. J Biol Chem 2001; 276: 8427-35.
21. Sung SY, McDovell JV, Carylon JA et al. Mutation and recombination in the upstream homology box-flanked ospE-related genes of the Lyme disease spirochetes results in the development of new antigenic variants during infection. Infect Immun 2000; 68: 1319-27.
22. Xu Q, Seemanapalli SV, McShane K et al. Constitutive expression of outer surface proteinC diminishes the ability of Borrelia burgdorferi two evade specific humoral immunity. Infect Immun 2006; 74: 5177-84.
23. Boylan JA, Posey JE, Gherardini FC. Borrelia oxidative stress response regulator, Bozrah: a distinctive Zn-dependent transcriptional activator. Proc Natl Acad Sci USA 2003; 100: 11684-9.
24. Hardin JA, Steere AC, Malawista SE. Immune complexes and the evolution of Lyme arthritis. Dissemination and localization of abnormal C1q binding Activity. N Engl J Med 1979; 301: 1358-63.
25. Theofilopoulos AN, Dixon FJ. The biology and detection of immune complexes. Adv Immunol 1979; 28: 89-220.
26. Beermann C, Wunderli-Allenspach H, Groscurth P et al. Lipoproteins from Borrelia Burgdorf applied in liposomes and presented by dendritic cells induce CD8 + T-lymphocytes in vitro. Cell Immunol 2000; 201: 124-31.
27. Preac Mursic V, Wanner G, Reinhardt S et al. Formation and cultivation of Borrelia burgdorferi spheroplast L-form variants. Infection 1996; 24: 218-25.
28. Brorson Ø, Brorson S-H. Transformation of cystic forms of Borrelia burgdorferi to normal, mobile spirochetes. Infection 1997; 25: 240-6.
29. Brorson Ø, Brorson S-H. In vitro conversion of Borrelia burgdorferi two cystic forms in spinal fluid, and transformation two mobile spirochetes by incubation in BSK-H medium. Infection 1998; 26: 44-50.
30. In shallow, Malovrh T, Murgia R et al. Conversion of Borrelia garinii cystic forms two motile spirochetes in vivo. APMIS 2001; 109: 383-8.
31. Alban SP, Johnson PW, Nelson DR. Serum-starvation-induced changes in protein synthesis and morphology of Borrelia burgdorferi. Microbiology 2000; 146: 119-27.
32. Hunfeld KP, Burg S, Hanssen-Hübner C, et al. Changes in the expression pattern of structural proteins after exposure of Borrelia burgdorferi two penicillin G and doxycycline. Int J Med Microbiol 2008; 298 (suppl 1): 325-32.
33. Miklossy J, Kasas S, Zurna AD et al. Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis. J Neuroinflammation 2008; 5: 40
34. Eker Field C, Ernerudh J, Bunikis J et al. Compartmentalization of antigen specific Cytokine responses to the central nervous system in CNS borreliosis: secretion of INF-g predominates over IL-4 secretion in response to outer surface proteins of Lyme disease Borrelia spirochetes. J Neuroimmunol 1997; 79: 155-62.
35. Hartiala P, Hytönen J, Suhonen J, et al. Borrelia burgdorferi inhibits human neutrophil functions. Microbe Infect 2008; 10: 60-8.
36. Malawista SE, ChevanceAB. Clocking the Lyme spirochete. PLoS ONE 2008; 3: e1633.
37. Schützen SE, Coyle PK, Reid P et al. Borrelia burgdorferi-specific immune complexes in acute Lyme disease. JAMA 1999; 282: 1942-6.
38. Dorward DW, Fischer ER, Brooks DM. Invasion and cytophatic killing of human lymphocytes by spirochetes causing Lyme disease. Clin Infect Dis 1997; 25 (suppl 1): 52-8.
39. Strle F, Ruzic-Sabljic E Cimperman J et al. Comparision of findings for patients with Borrelia garinii and Borrelia afzelii isolated from cerebrospinal fluid. Clin Infect Dis 2006; 43: 704-10.
40. Ljøstad U, Mygland A. CSF B lymphocyte chemoattractant (CXCL13) in the early diagnosis of acute Lyme neuroborreliosis. J Neurol 2008; 255: 732-7.
41. Lusitania D, Malawista SE, Montgomery RR. Calprotectin, an abundant cytosolic protein from human polymorphonuclear leucocytes, inhibits the growth of Borrelia burgdorferi. Infect Immun 2003; 71: 4711-6.
42. Hunfeld KP, Brade V. Antimicrobial susceptibility of Borrelia burgdorfri sensu Lato: What we know, what we do not know, and what we need to know. Wien Klin Wochenschr 2006; 118: 659-68.
43. Bunikis I, Denker K, Östberg Y et al. S. An RND-type efflux system in Borrelia burgdorferi is involved in virulence and resistance to antimicrobial compounds. PLoS pathogen 2008; 4: e1000009.
44. Brorson O, Brorson S-H. An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi two metronidazole. APMIS 1999; 107: 566-76.
45. Brorson O, Brorson S-H. An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi two hydroxychloroquine. Int Microbiol 2002; 5: 25-31.
46. Clamp opens MS, Hu LT, Evans J et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N Engl J Med 2001; 345: 85-92.
47. Dont ST. Late and chronic Lyme disease. Med Clin North Am 2002; 86: 341-9.
48. Oksi J, Marjamäki M, Nikoskelainen J et al. Borrelia burgdorferi detected by culture and PCR in the clinical Relapse of disseminated Lyme borreliosis. Ann Med 1999; 31: 225-32.
49. Cameron D. Severity of Lyme disease with persistent symptoms. Insights from a double-blind placebo-controlled clinical trial. Minerva Med 2008; 99: 489-96.
The manuscript was received 2.7. 2008 and approved 20.8. 2009. Medical Editor Erlend Hem.
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Borrelia burgdorferi - a unique bacterial
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