posted
Has anyone had or heard of Borrelia Miyamotoi? Apparently, this was recently discovered in the US and I am one of the lucky ones (NOT) to have gotten it from a tick bite.
Wish I was just as lucky playing the lottery!
Any information is greatly appreciated.
Thank you
Posts: 9 | From East Coast | Registered: Jun 2015
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posted
Borrelia miyamotoi is a relapsing fever cousin of the Borrelia sensu stricto spirochete responsible for Lyme disease. Its infection is most often caused by a bite from the Ixodidae hard ticks that live worldwide. Its symptoms are similar to Lyme except it appears to have the relapsing fevers during the early stages of the infection due to its immune evading VMP surface protein.
It was first discovered in Japan in the 1990's but forgotten until a rash of people became ill in Russia in 2011 and it was traced to a Bm infection. This is because its slightly genetically different from the more common US B. burgdorferi such that the US nor European test protocols detect it.
Tick testing had seen Bm in the US for at least 15 years but it was thought to not be pathogenic. This is because people with tick bites who were tested always came up negative on the US CDC 2 tied test so the infection went undiscovered. For example, the CA Department of Public Health had been testing ticks and seen roughly half as many ticks with Bb were positive for Bm.
So that suggests many Lyme-like infections were actually Bm infections that tested negative. US researchers went to Russia and realized this and came back and retested blood serum saved frozen and found many undiscovered US infections. This is true throughout the US from the East Coast to California. Its a huge debacle caused by the narrow-minded CDC 2 tiered testing protocol and Bb is the only pathogenic Borrelia in the US dogma.
To date, only an ELISA based on a Borrelia miyamotoi recombinant protein (GlpQ) is able to detect it. If you go into a doctor today and say you were bitten by a tick, the doctor most likely won't have a clue about the Bm or miyamotoi test which is not terribly reliable anyway.
There is a PCR test available but it is only useful during the relapsing fever peaks when the number of spirochetes is high in the blood. Once the immune system or antibiotics bring it under control, it is very hard to detect. I suspect a Western Blot and better test is in development but to date its not available.
I suspect some large percentage of people with Lyme infections actually have Bm infections and were seronegative on the CDC test. The CDC test might pick up a few bands that are similar but won't meet the 5/10 IgG criteria.
Its treated identical to Lyme but just like Lyme, it can become chronic once it disseminates throughout the body. So a Lyme infection and a Bm infection are almost identical except the early fevers.
Posts: 51 | From California | Registered: Aug 2013
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
WOW! Excellent info My Yam!!!! Really impressive. Thanks for sharing. I'm embarrassed to offer my collection of info to STS now, but will offer it just in case there may be something that would help.
Talk about sharing...
Might it be possible I copy and use your info on the TBD site so more folks would have access? As is, or parts? Or if you'd like to add more I'd be even more grateful. Anything you'd care to share I am sure will help those who may have contracted it. The only info so far that I've seen comes from the same crews that have made a mess of Bb, so your info is really nice to have available.
Please let me know!
STS- here is a PR that I wrote last year along with links to more info. Be sure to check the bottom of the page for "subpages" if interested.
posted
Thank you both for providing information. I very much appreciate the assistance and knowledge sharing. Posts: 9 | From East Coast | Registered: Jun 2015
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posted
Thanks. Borrelia miyamotoi is one of those glaring embarassments to the CDC and IDSA. Ths CDC calmly tells a story similar to the one I wrote but with all the backlash from their Lyme debacle, they discuss it like its no big deal.
The CDC has promoted a dogma for many years that B burgdorferi is the ONLY pathogenic species of the Lyme spirochete in the US. So in 1994, at the now infamous "Proceedings of the Second National Conference on Seroligical Diagnosis of Lyme Disease", the CDC 2 tiered protocol based on a single genotype antigen was cast in stone.
They took the Western Blot implementation specifics, the single strain antigen approach and decided to adopt a study done by Dressler et al in 1993 for the IgG criteria. That study had about 250 participants that came to a single New England clinic over the span of one year.
So the infections were genotypes that ocurred in and around that New England clinic and the infection durations were less than 6 months or fairly new. The diferent Lyme surface antigens upregulate as the infection proceeds. So which antibodies are found varies over the course of an infections... Duh! They knew the participants had Lyme because they either had an EM or were cultured positive.
They then did some creative statistics known as a ROC analysis of the antibodies found in these people and based on their likelyhood of appearing, chose the magic 10 antibodies and decided on the 5/10 criteria. But what about culture failures or the 50% without an EM. That's called selection bias. Since then, all 40 FDA approved Lyme serological tests used this first positive as its reference - a form of circular reasoning.
But alas, all serological tests that look for antibodies whether they be an ELISA or Western Blot which just looks for the same antibodies but shows them individually rather than luimping them together. But antibodies are produced by B cells based on strings of aminon acids appearing on the various surface antigens like OspA, OspB, OspC, FLA etc.. A typical epitope or string of amino acids is roughly 6-10 amino acids.
That very specific string is called an epitope and the antibodies bind or have an affinity and attach to that amino acid string. A particular surface antigen like OspC may have many epitopes and which ones a particular persons B cells recognize varies from person to person.
But the amino acids in a surface antigen or any protein for that matter is defined by the gene that codes for that protein. So a change or changes in the nucleotides from one strain to strain or worse genospecies to genospecies can and often will change an epitope. So for exanple, B31 OspC can have different eiptopes than say N40 or even worse B. miyamotoi which is genetically more distant.
But the CDC announces the B miyamotoi will be tested seronegative like its a big surprise. Duh!
So the B31 antigens such as OspC used in an ELISA or Western Blot will have its epitopes which might not match the similar but different amino acid string in the N40 or B miyamtoi so that surface antigen lowers the ELISA value or the Western Blot band for OspC doesn't appear because the tests antigen didn't bind to the N40 or B miyamotoi OspC antigen due to slight epitope differences.
The wide variations in OspC has been studied to death but the same is true for most of the CDC magic 10 (18 kDa, 21 kDa (OspC), 28 kDa, 30 kDa, 39 kDa (BmpA), 41 kDa (Fla), 45 kDa, 58 kDa , 66 kDa, and 93 kDa) but alas, here are actually about 2 dozen antigens that could have been chosen.
Vlse is the surface antigen that is similar to B miyamotoi's VMP in it keeps randomly changing epitopes to evade the immune system antibodies and T cells. But Vlse is one of the best antigens to have chosen but it was missed because it occurs later in the infection. Remeneber the Dressler study were all early infections. Ooops.
So as the geographical distance from the US Notheast in New England where the Dressler study was done for say the Midwest,California, Europe or Asia tends to correlate with geentic differences which means epitope differences across strains which will lower the ELISA score or drop a band or a few from the Western Blot.
This problem becomes very serious with genospecies differences such as B garinii, B afzellii or B. miyamotoi. That's why the US B31 antigen based testthat uses the Dressler criteria fails in Europe and Asia but also for distant US strains and surprise surprise B. miyamotoi.
In March of 2013, the California Department of Health's microbiologist Kerry Padgett announced at the LDAC mmeeting that they had seen B. miyamotoi in ticks at half the rate as they had seen B burgdorferi since 2000.
She mentioned this because of the "Oops" realization in Russia that B miyamotoi is pathogenic and is similar to Lyme and was so common in California. Its similar in other parts of the country. So in California, for every 2 tick bites that transmits Lyme, one transmits B. miyamotoi. So on a gross/rough scale, about 1/3 of the infections in California should be B. miyamotoi. But its so gentically different in coding surface protein amino acid sequences, the epitope matches against B31 always cause the CDC 2 tiered test to fail.
Now 1/3 or even 1/4 of the infections not being diagnosd by the standard ELISA or Western Blot ( it may be missed by the IGenex 2 strain 297/B31 although the double strains broaden the epitope matching) would on its face seem a debacle. So thye debacle proofed it. Clever sleazy bureaucrats. If the CDC and IDSA really believed ( and they did and do) that the CDC 2 tiered test was 90% sensitive, this discovery or realization instantly drops that 90% to about 60% without any arguing. Its just an arithmetic fact or BooBoo.
So to protect their beloved 23 year old Dressler based 2 tiered test, they gave the B. miyamotoi a different disease name other than Lyme as a sematics trick to avoid the facts. This is even though its transmitted by the same ticks, closely related to the Lyme spirochete with similar symptoms and treatment. So by not calling a B. miyamotoi infection Lyme, they get to protect their test with semantics without breaking a smile. Borreliosis = Borreliosis = Borreliosis PERIOD!
Now in the meantime, much more quietly, Bob Lane from UCB had discovered infections based on a new genospecies in California named B bissettii in 2011. And Kerry Clark from the University of North Florida had found 2 new genospecies infections due to B. lonestarii and B. andersonii in 2013.
The lesson here is that if you design a test specific to a strain and spread that across the nation to all doctors, when someone with a tick bite comes in the office ill, the B burgorferi only dogma will persist because the other strains and genospecies will always be missed. Ads has happened. An existence proof.
This will go on and on until a universal Borrelia test is developed that detects all genospecies. When that is positive, the doctor has the choice of treatment or moving to a more genospecies or strain differentiating test if desired. You can think of it like a pyramid.
The test should catch anything across the wide base of the pyramid ( all Borrelia) and not only detect a peak ( New Englands B31 B. burgdorferi) defined by one study in New England that defined that peak. This is logic 101. But getting a PhD does not require a logical mind, all one need to do is focus and kiss up to the professor and you too might ruin lives after you go to work for the CDC.
Its so ridiculous. I'm wondering if they are really that stupid or if group think and peer pressure have locked dogmas in place until some brave souls break up the group party.
Sorry for the long RANT! But its the sad truth.
Sorry for the Rant! Posts: 51 | From California | Registered: Aug 2013
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
While the Daytona race is under yellow again- yes, it is still going, and into the last laps at 3 AM- I stopped in here to visit.
Want to thank you Mi Yam for your explanation, and say I can't read it through right now- way too head-spinning tired- but, I am anxious to check it all out when I am rested tomorrow night.
This looks like it took a lot of thought and time, so thank you again for your effort.
posted
Dr MacDonald has been detecting, using extremely accurate Molecular beacon DNA probes, BOTH Borrelia miyamotoi and Bb in numerous chronically neurologically ill patients. These include the autopsy brain tissue of Alzheimer patients.
Interestingly, he also found a chimeric Borrelia - part miyamotoi, part Bb - in Alzheimer brain tissue.
Elena
-------------------- Justice will be ours. Posts: 786 | From UK | Registered: Oct 2007
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
DONE! Finally had a brain to read and absorb. Thanks for sharing that info My Yam- Eight Legs too.
My Yam- you made me smile and get sick too, so good job!
I remember the exact day I said to someone years ago that we need to start saying "CHRONIC" Lyme in everything we publish. We are not getting our point across with the early, acute, naming various stages and the late-stage designations.
It worked to bring attention to Lyme disease and has been used since that time, even cursed by the IDSA/CDC gangs.
I am seeing this same approach could be useful for the various strains, subspecies, etc., at least in print. It has a lot of advantages for our educational efforts. The science can keep sorting out the details, but lumping it all in one Borellia category (Lyme disease) with the public makes sense.
This way the tests are even more wrong than we already know they are- but this opens the door for more public scrutiny. The vaccine would be less effective, the treatment less effective and so on. More types of meds would be needed, for varying times in varying combinations when all the little names are lumped into one big CHRONIC LYME category.
When writing for a newspaper your audience level should be about 5th grade level. (NOT my rules, the newspapers rules.)
Your explanation helps get me from heavy science wording regarding testing to the 5th grade level and I appreciate your efforts very much.
Now, can I share your explanations at other sites, or do you have this somewhere that I can link to?
LisaK
Frequent Contributor (1K+ posts)
Member # 41384
posted
good info.
how do you find out what "kind" of lyme you have?
if this is a dumb question, sorry.
-------------------- Be thankful in all things- even difficult times and sickness and trials - because there is something GOOD to be seen Posts: 3558 | From Eastern USA | Registered: Jul 2013
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Its very difficult if not impossible to determine what kind of Lyme you have.
From a methodology point of view it would not be very difficult but its not practical.
To determine what kind of Lyme you have, you need one of the spirochetes or enough of its genes to look it up at NCBI.
The Lyme spirochete has about 1 million base pairs in its genome. By contrast, humans have about 3 billion.
If you were able to culture your spirochetes, they could be sent to a lab for sequencing. That means they would read all 1 million nucleotides in the genome and that includes all the genes.
Then one could take about eight housekeeping genes and run a search at NCBI Nucleotide and it would find strains or species of Borrelia that had the same eight housekeeping gene nucleotides.
Hundreds of Borrelia strains and species have been fully sequenced or partially sequenced such that their genes are in the NCBI database.
A perfect match or the closest match would tell you both the strain and species you were infected with.
Advanced Laboratory Services formerly had an option to culture and sequence one gene called the pyrG gene. That one gene is enough to determine the species and get close to the strain.
I had it done and was sent the gene listing. I looked it up on NCBI and it was very close to a CA B. burgdorferi strain. I live in CA so that made sense. They are under FDA pressure after some bashing by the CDC and no longer offer the pyrG gene sequencing.
So their is no longer a way commercially for the average doctor to determine the strain. A research lab with culture capability could do it but I doubt they would be interested.
Given all the turmoil and discovery of 4 new US species, its very sad this isn't available. The 4 new species are not caught by the current CDC 2 tiered ELISA and Western Blot because of genetic differences that change the amino acid sequence epitopes to which antibodies bind. If a nucleotide changes in the epitopes amino acid sequence, the antibody stops binding and the ELISA and Western Blot fails.
So knowing the species would be VERY VALUABLE but the CDC fears the embarrassment that would occur so don't expect any progress soon.
Posts: 51 | From California | Registered: Aug 2013
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posted
Miyamotoi, why do you feel the vlsE is so good? I don't.
Dr Allen Steere, (in Liang et al 1999), reported that the C6 ELISA detected only 62% of "post-treatment Lyme" patients who had continuing symptoms in the US.
His interpretation - they didnt have Lyme anymore, they were all "cured" even though their illness marched on.
Steere, Wormser etc are greatly pushing the vlsE at the moment.
Elena
-------------------- Justice will be ours. Posts: 786 | From UK | Registered: Oct 2007
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
I think you'll find this poster by Dr MacDonald fascinating. It describes the chimeric Borrelia he found in the brain of a patient who died of Alzheimer's. There was BOTH miyamotoi and b. burgdorferi DNA in ONE Borrelia spirochaete. These images were the result of testing with the most accurate method of identifying bacteria known- Molecular Beacon DNA probes.
It's staggering that this was found in Alzheimer's, a disease affecting tens of millions of people worldwide.
posted
Eight Legs Bad, I tracked down that 1999 Steere study.
The neat thing, for me, at least, is that it actually says close to two-thirds of PLDS patients test positive for continued infection according to the C6. That admission is unheard of these days.
The other third could be explained away by Borrelia species not covered through having the IR6, like B miyamotoi, or strains that don't have it, like strain N40 may not.
I share your reservations about who is promoting it. But it is a little bit interesting that they have changed their collective stance on the utility of the C6 for late stage or PTLDS - and I cannot nail down why.
Maybe part of the reason is because they are having difficulty explaining away results like the 1999 study, with almost 2/3 of confirmed (2T or EM) Lyme patients, post-treatment, testing positive.
I know there are reasons not to like the C6, but I cannot recall them right at the moment.
Posts: 228 | From Unitied States | Registered: Jul 2015
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posted
I was told by Fallon and read other studies plus in dogs, the C6 (if positive) typically decines significantly once the infection is cleared. Since Marques is a co-inventor of the C6, its a bit embarassing that PTLDS remains positive after treatment. That suggests people with PTLDS have an ongoing infection (i.e. chronic lyme). Marques has crawled under a rock with respect to what studies show with her C6.
Studies by Idexx which makes point of care dog Lyme tests, show the other surface antigens decline like OspC but as the Vlse protein changes as an immune evasion trick, the C6 remains ( being on the Vlse protein) until the infection is truely cleared.
"The quantitative C6 antibody test can be used to measure changes in C6 antibody levels following treatment of antibody-positive nonclinical dogs."
The research with dogs is more advanced than humans because the researchers care while many human researchers are trying to maintain the status quo.
The C6 id used to detect the IR6 invariable region on the Vlse surface protein ( not one usd in US testing but is in Europe???).
It really sucks that the US testing choice of antigens for both the ELISA and WB have been frozen in time since Dearborn which was in 1994 or 21 years agao.
I guess the Europeans and other countries are more progressive about evolving their testing protocol as new knowledge rolls in. Dearborn has become like an old freezer taped shut so nobody can get in and everything is dead inside.
Since the Vlse is the major surface antigen seen by the immune system late in the infection and is a moving target, it would make sense thje C6 ( if appropriate for a set of strains and species) would be a good late marker and one that would see a decline once the spirochete is dead and the Vlse changes are no longer happening or its hiding or its become a persister.
Posts: 51 | From California | Registered: Aug 2013
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posted
The C6 value, after treatment, should decline by a factor of four, or decline to sub-positive levels (less than 1.10). One or the other.
I use to think Marques had a hand in the development of the C6, but I could not confirm that. Maybe she was the NIH interface?
Regardless, she and other C6 proponents appear to have gone MIA when it comes to explaining values in late stage and post treatment patients.
Here is an additional oddity: I spoke to an IDSA clinician who I respect, and he told me that sometimes, even when the C6 declines to normal levels, patients remain symptomatic. I wonder, in cases like that, if something like miyamotoi might be at play, overlaying the original Lyme. Of course, his observations may simply speak to the limitations of the C6. I KNOW I was against it for a while, but I cannot remember why. I also know that the about-face by all those IDSA types who trumpeted its usefullness in late stage and post treatment cases, raises red flags for me.
Where are the studies, the data, that explains away those supposed aberrant C6 values post-treatment?
Posts: 228 | From Unitied States | Registered: Jul 2015
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WPinVA
Frequent Contributor (1K+ posts)
Member # 33581
posted
I personally felt so much better when I read that:
"What is CDC Doing? CDC is working to better define the public health importance of this infection and is reviewing options for tracking the disease with our partners in state and local health departments."
Sorry... this is a serious and enlightening discussion. I just couldn't resist.
Posts: 1737 | From Virginia | Registered: Aug 2011
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surprise
Frequent Contributor (1K+ posts)
Member # 34987
posted
This is brilliant: (copied from above)
'It really sucks that the US testing choice of antigens for both the ELISA and WB have been frozen in time since Dearborn which was in 1994 or 21 years ago.
I guess the Europeans and other countries are more progressive about evolving their testing protocol as new knowledge rolls in. Dearborn has become like an old freezer taped shut so nobody can get in and everything is dead inside.'
-------------------- Lyme positive PCR blood, and positive Bartonella henselae Igenex, 2011. low positive Fry biofilm test, 2012. Update 7/16- After extensive treatments, doing okay! Posts: 2518 | From USA | Registered: Nov 2011
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posted
Forgive me for such a rushed reply - have not had time to read all th emessages here, but: Duncan wrote:
" I wonder, in cases like that, if something like miyamotoi might be at play, overlaying the original Lyme."
"Overlaying" may be more significant a word than you think. It's now obsolete to consider Bb and B. Miyamotoi exclusively as if they are two distinct microbiological entities, ever since Dr. MacDonald found a ** chimeric ** Borrelia containing the DNA of BOTH species in one spirochaete.
User "Miyamotoi", care to share your background? Are you a microbiologist? My background is in nursing. I'm based in London.
Elena Cook
-------------------- Justice will be ours. Posts: 786 | From UK | Registered: Oct 2007
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posted
I recall reading about MacDonald's chimeric finding, but don't recall the details.
Miyamotoi is being treated unusually, including its filing as a species.
Currently, it's treated as a subset of b turcica, which is a reptilian-based kinda Bb. Odd, as that really doesn't fit in the NE United States, where all the flurry of discoveries has been taking place.
I THINK it's due to the GLPQ protein found in Miyamotoi, but I guess not in Bb?
They claim miyamotoi is relapsing remitting, but that Lyme is not. But of course, Lyme is, too - just ask anyone with late stage.
I wrote the overlay thing trying to explain why a third of chronic Lyme patients didn't test positive on the C6 back in 1999 when they were first touting the metric. It COULD be due to a blend, the chimera, or to straight up miyamotoi.
They need to cast a broader net. Start with the genus Borrelia, then drill down by species and strains. IF YOU TEST POSITIVE FOR THE GENUS, THEN THEY HAVE TO ACKNOWLEDGE THAT (I would hope). Subsequently, there would have to be digging as to what species etc.
eta, I'm not sure a genus-level test even exists.
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poppy
Frequent Contributor (1K+ posts)
Member # 5355
posted
Impressed with this thread. Got some very knowledgeable people here. Thanks miyamotoi for your input.
Posts: 2888 | From USA | Registered: Mar 2004
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posted
Duncan, here's Dr MacDonald's poster on the Borrelia chimera on F1000. It contains an error - (the probes Dr M used were not based on OspA - he wrote a comment asking them to insert a correction but as far as I can see they haven'e done that yet.):
"Chimera of microbes in the wild have been documented for enteric bacteria in sewage sludge and for spirochetes in termite intestinal tracts.
Genetic chimera differ from other chimera because the identification of genetic chimera is dependent on the identification of nucleotides (DNA or mRNA) from two different species which are now resident in s single organism.
Proof of chimeras in microbes offers involves intricate DNA or rRNA sequencing, with subsequent molecular interrogation of suspect microbes using DNA probes.
Herein, we offer FISH evidence using multicolor miyamotoi/burgdorferi molecular beacon DNA probes (Red= Cy5-Flagellin B-Borrelia) (Green= FITC-Flagellin-B-Borrelia burgdorferi) to prove the existence of chimeric ( Burgdorferi/ Miyamotoi) (YELLOW COLOR= summation of red and green) based on borrelia carriage of the open reading frame (gene equivalent) of FlaB genes for two genetically distinct groups of Borrelia microbes (Burgdorferi group sl and Relapsing fever group Miyamotoi sl).
Summation FISH with a yellow color in the chimeras is the product of simultaneous RED monochrome and GREEN monochrome excitation/emission of Cy5 /FITC fluorochromes to yield a YELLOW Emission fluorescent signal in the Chimera Borrelia.
Previous reports have focused on the 16 s rRNA region to prove chimera formation. This report utilizes the genes for major surface protein (OSP A =Outer Surface Protein A) and is the first report of the use of a Borrelia Outer Surface Protein Gene to establish existence of a Borrelia chimera.
Genetic diversity exists by virtue of multiple distinct mechanisms in Spirochetes and is particularly noteworthy in Borrelia spirochetes. Mutations, deletions, plasmid loss, recombination, bacteriophage activities,up regulation of genes, down regulation of genes are among the mechanisms for nucleotide diversities in Borrelia.
Relapsing Fever Group Borrelia are the most notorious Borrelia for genetic reshuffling of DNA to stay ahead of the host immune response. Until now, Genetic reshuffling in the Burgdorferi group has been thought to be relatively uncommon, in comparision with Relapsing Fever Borrelia.
The frequent Burgdorferi group DNA rearrangements of genes of the OSP C surface protein are a notable exception. This report now establishes a novel, heretofore unknown pathway for genetic diversity in Borrelia. Chimeric Borrelia in the wild have never been previously reported, hypothesized, or investigated."
-------------------- Justice will be ours. Posts: 786 | From UK | Registered: Oct 2007
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"I was told by Fallon and read other studies plus in dogs, the C6 (if positive) typically decines significantly once the infection is cleared."
Two points :
1. I would strongly advise you not to pay attention to ANYTHING Fallon says these days. Though he did good work long ago, for many years now he has been acting as a marionette of the Denialists, ever since he was given the prestigious and lucrative post as head of the Lyme centre at Columbia (which discovers nothing of value and treats no one).
In his recent paper he condemned Igenex in terms as offensive as anything the CDC camp have ever said about them.
2. Dr Fallon has no business to be telling you or anyone else what happens "once the infection is cleared" because there is as yet NO TEST IN EXISTENCE that can demonstrate that the infection is cleared.
I can't emphasise this enough.
As for Europeans being ahead of you, I don't think you guys know much about what's going on in Europe. Most Europeans, particularly in western Europe are faced with a blanket denial of chronic Lyme diagnosis and appropriate treatment because the governments concerned are following your CDC. Here in the UK, we have arguably the WORST detection rate in Europe - less than 2 per 100 000 official incidence despite having the same flora and fauna as our neighbour across the water Holland, which officially admits to over 100 per 100,000 incidence from EM rashes alone. Why is our detection rate so appalling? One of the main reasons -
-------------------- Justice will be ours. Posts: 786 | From UK | Registered: Oct 2007
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"I was told by Fallon and read other studies plus in dogs, the C6 (if positive) typically decines significantly once the infection is cleared."
Two points :
1. I would strongly advise you not to pay attention to ANYTHING Fallon says these days. Though he did good work long ago, for many years now he has been acting as a marionette of the Denialists, ever since he was given the prestigious and lucrative post as head of the Lyme centre at Columbia (which discovers nothing of value and treats no one).
In his recent paper he condemned Igenex in terms as offensive as anything the CDC camp have ever said about them.
2. Dr Fallon has no business to be telling you or anyone else what happens "once the infection is cleared" because there is as yet NO TEST IN EXISTENCE that can demonstrate that the infection is cleared.
I can't emphasise this enough.
As for Europeans being ahead of you, I don't think you guys know much about what's going on in Europe. Most Europeans, particularly in western Europe are faced with a blanket denial of chronic Lyme diagnosis and appropriate treatment because the governments concerned are following your CDC. Here in the UK, we have arguably the WORST detection rate in Europe - less than 2 per 100 000 official incidence despite having the same flora and fauna as our neighbour across the water Holland, which officially admits to over 100 per 100,000 incidence from EM rashes alone. Why is our detection rate so appalling? One of the main reasons - we use the c6!!!!
-------------------- Justice will be ours. Posts: 786 | From UK | Registered: Oct 2007
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Why on earth would anyone assume Bb would remain static vis-a-vis their DNA?
I think it safer to assume they are perpetually evolving. Every time DNA IS scrutinized, it's merely a snapshot...What are the odds whoever is looking will stumble upon the change - especially since there doesn't seem to be much unbiased scrutinizing going on these days.
Also, I swear this relapsing-remitting thing not pertaining to Lyme is preposterous.
You gotta love MacDonald. I wish I weren't so far from Ft. Lauderdale, or I'd head there in October just to shake his hand.
Posts: 228 | From Unitied States | Registered: Jul 2015
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posted
Eight Legs Bad, I know why the UK's TBD policy is off.
Not sure, however, why you say C6 is a big contributing factor, but then I don't look at the test much outside a US context.
What do you see as the test's weaknesses? It alleges to using an invariant region, so the theory is a good one.
What does it miss, unless it's Borrelia without the invariant region?
Sorry, brain is struggling today, so my wording may be off.
But this is an important subject.
What happens with people with enduring high C6 values? To me, this is undeniable proof of active Lyme, and I cannot find ANY studies or papers to say otherwise, yet the normal suspects now turn their backs on Late stage utility of C6.
But if the theory of the C6 is flawed, well, then it is flawed. Please explain how, though, when you've the chance. For instance, not enough of an immune response to register an antibody presence, or IgM mode locked in due to constantly varying surface proteins...These would account for the C6 failing in many instances, but what of the theory?
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They knew the participants had Lyme because they either had an EM or were cultured positive. ![[group hug]](graemlins/grouphug.gif)
and peer pressure have locked dogmas in place until some brave souls break up the group party. ![[confused]](graemlins/confused.gif)
![[Cool]](cool.gif)
![[Mad]](mad.gif)
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