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
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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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