Topic: Steere's manipulation of importance of band 41?
TerryK
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Totally weird that a control group would have any known infections, let alone a spirochetal infection. Does this make sense to anyone? Does anyone know or have proof that this is true?
http://en.wikipedia.org/wiki/Allen_Steere Most troubling, Steere chose to make 20% of his control - 25 serum samples - serum derived from syphilis patients. While this group formed 20% of the control, the disease's annual incidence in the United States is about 3 cases per 100,000 - an incidence of far less, by a multiple of 300, than 1%. This statistical manipulation dramatically impacted the importance of the 41 KdA band on blotting, because syphilis cross reacts with Lyme blots at 41 Kda due to their both possessing a key flagellar potein structure. It has since enabled Steere and his cronies to confabulate that seroreactivity to the 41 kDa antigen is 'normal', when in fact it is largely only seen in advanced spirochetal infection - usually only in gingival infections when visible pus-filled pockets are present.
Terry
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-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
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TerryK
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hahaha!!! Thanks for pointing out that thread tutu! I just happen to stumble across the wiki entry while looking for something else. Hadn't seen Bruce's info yet but it is very interesting.
It seems like it would be very good to have all of the Steere studies that resulted in some damaging action by our government and the IDSA in one place. For all I know, they could already be listed somewhere. I wonder if the CT attorney general knows about this?
TreePatrol - thanks for the link. I wonder how many studies were done with patients as controls who may actually have had lyme disease? How can this be valid??? How can they get away with it???? Where is the integrity of the science behind their recommendations when something as clearly flawed as this is used to come up with test standards?? Why don't we hear ILADS bring this up when talking about flawed CDC test standards?
Terry
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Wow, great post. It explains A LOT-- I'm thinking back to my old ID duck who told me that "practically everyone" tests positive for band 41.
Posts: 390 | From Oakland, CA | Registered: May 2007
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After a year here, I have read of so many with ONLY band 41 positive, including myself...
Been wondering how could it NOT be significant? Personally can attest to rash, swollen knee, & doxy herx - but absolutely NOT
quote:Originally posted by TerryK: gingival infections when visible pus-filled pockets are present.
Terry [/QB]
Sounds like you are on the right track-just a hint of fabrication/manipulation of data! Grrrrrr....
Posts: 249 | From finger lakes, ny | Registered: Jul 2006
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Monkeying with the data to produce the right results is a Steere specialty. Look at what he did with the retrospective study on the Lyme, CT patients. He used a small control group consisting of friends and neighbors of the patients. More than one subsequently tested CDC positive in the control group. How phoney is this?
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david1097
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I have not looked at the the thread that you mentioned but you need to be aware that an early polish study found that a very high percentage of the HEALTHY population in poland (on a pro rates basis) had the 41 dKa antibody light up on the WB's with no other lyme related bands. This was found some years back and may have had some influence on Steere's approach.
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AliG
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I keep getting "topic does not exist for TuTu's thread & I come up blank for Treepatrol's.
I feel so left out.
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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AliG
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I can get the thread before & after, TuTu.
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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AliG
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WHY??????!!!!!!!!!!!!
THAT'S SOOOOOOOOOOO NOT FAIR!!!!!!
What did Oligando Bruce say????!!!!
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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quote:Originally posted by AliG: WHY??????!!!!!!!!!!!!
I have no clue!
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TerryK
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Either the originator of the post or the moderators deleted it or it was deleted due to a bug. I have no idea why it was deleted.
I've written to Bruce to ask him if he would be so kind as to post the info. It is such great info and I don't feel that I could possibly explain it or even remember all the info that he posted. I was planning on re-reading it and saving it.
AliG - Do you have the latest version of adobe acrobat installed? If not, you need to install it in order to see Tree's link because it is a pdf file. If you still can't access the info PM me and I'll see if I can help.
Terry
Posts: 6286 | From Oregon | Registered: Jan 2006
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quote:Originally posted by david1097: I have not looked at the the thread that you mentioned but you need to be aware that an early polish study found that a very high percentage of the HEALTHY population in poland (on a pro rates basis) had the 41 dKa antibody light up on the WB's with no other lyme related bands. This was found some years back and may have had some influence on Steere's approach.
there have been several european studies which examined reactivity to blots and compared to clinical status. However, most of these studies dealt with B. azfeli and/or B.garinii exposure. There are some indications that american strains are more pathogenic than european strains, and there are certainly signficant differences.
Not much is known about the serologic response to late CNS disease, because in america this has never been studied. Almost from inception, the medical establishment has regarded lyme disease as an acute phenomenon...including CNS disease, where typically only early meningitis or facial nerve study are mentioned. The steere criteria were formulated largely using sera from acute patients and arthritic patients.
Lyme encephalopathy has barely been studied. This is important, because the CNS immune response is different. But one thing we do know is that flagellin is absolutely necessary for borrelia survival, and this is NOT the case for many of the other proteins sampled by blot: they are differentially expressed surface proteins.
As such, the presence of a band at 41Kda should be interpreted as indicating exposure and possible latent or even active CNS infection. It's NOT normal to have a band to Bb at 41 KdA...in Israel, the percentage of the population reactive to this band on blot is about 8%. They don't have Bb.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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Greatcod
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From the Wikipedia article on The Allen- "A high percentage of "Steere" camp Lyme experts are former EIS officers."
Yes they are. It is my belief that for 30 years, Steere has attempted to minimize the incidence and severity of Lyme Disease, and has been very successful in that work. This just adds another chapter to the lie.
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david1097
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What is not entirely clear is if the 41 dKa band is specific to only the flagellin proteins of spirocetes, Lyme bacteria,(regardless of strain) or all flagelated bacteria. There are conflicting accounts from various publications.
I would assume that since the iGg 41 seems to be a persistent band that appears in non lyme infected people (polland and isreal have been quoted in this thread), that it is not lyme specific, but rather it is related to long life antibody to a variety of bacteria. IF this is true then that would tend to support the idea that it is in fact also related to any number of non spirocetes.
Since there are lots of flagelated bacteria out there this woudl also account for a lot of people having the antibody due to exposures to these pathogens. Even an infected scratch with some of these bacteria would then cause the 41 band to light up.
A note on testing in general.....
A point that many seem to miss is that the term "LYME Disease" has morphed into a general term to describe "unknown Lyme like bacterial infection". If one talks to some of the leading Lyme clinicians or even just listens to some of their presentations, it immediately becomes clear that of the "Lyme" patients that they see, only a fraction of them are actually infected with clinically apparent Lyme. Many of the ones that are not, are certainly infected with something and do respond to therapy but it is not Lyme. Some also have Lyme plus something else.
A quick search will show that there are LOTS of flagellated bacteria (and unflagellated ones too) that cause Lyme LIKE symptoms. Things like migrating joint pain, neurological problems, joint swelling, muscle pain etc, etc. are common with many many slowly reproducing , hard to treat or inter cellular bacteria. Some of these infections are "classically" thought to be "self limiting" and indeed they are for a while but what happens when one gets older and more of the different infections accumulate or the bodies inmmune response weakens due to age?.... In many instances, these previously hidden symptoms appear in a confusing array of seemingly unrelated observations that no one can figure out.
With lyme, also being a systematic infection with so many possible symptoms, the so called great IMMITATOR becomed the great IMMITATED, due to its ever increasingly public awareness.
Given the ultra lethargic state of the infectious disease medical communutiy, they are illequipped and obviously ill prepared to deal with this situation. As a result thay are resistant and hostile to the concept that these infections exist in the developed world... No one wants to bring the bad news... As an example it took well over 20 years for H.Pylori to be acknowledged as an infectious disease!. This even with a sea of clinical proof.
So how does this relate to testing? If there are no bands other than 41 dKa and there are lyme like symptoms AND the other bands do not light up after antibiotic treatment I'll bet good money that the person does NOT have Lyme. I'll also bet that there is a good chance that given the symptoms they DO have some other bacterial infection.
This being said, there is a lesser but still finite chance that they have some other things that can look like lyme. These include a number of viruses AND beleive it or not Genetic diseases.
In particvual there are a families of relaping remitting geneticaly differentiated diseases that have some Lyme like symptoms.... are these in fact generationally transmitted infections (ie. Brucella), I have no idea, but they do exist.
So why am I rambling on like this? I guess its because there seems to be a overiding focus on Lyme and ONLY Lyme with some peoples interpretation of the various tests where in reality , the situation can be much more complicated.
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AliG
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quote:Originally posted by TerryK:
AliG - Do you have the latest version of adobe acrobat installed? If not, you need to install it in order to see Tree's link because it is a pdf file. If you still can't access the info PM me and I'll see if I can help.
I'm alright....I'm OK......
Thanks Terry, I rebooted and it seems to have resolved the problem.
That was freaky! It felt like something was trying to keep me from knowing what was going on here. I HATE to feel like I'm out of the loop.
This is some really interesting info.
I do believe that "Big Brother" must be aware of what's going on. I know I'm not the only one who's complained to them about it. They monitor everything, internet, e-mail, wire taps, etc.
There likely is a coverup going on. Whether it's to buy time because they don't know what to do to help yet or because they actually somehow caused the problem remains to be seen.
I have thought that, as syphilis is known to leave a genetic imprint, there might even be some hereditary transfer in other spirochetal diseases. There maybe Babesias & other protozoans passed down through the generations.
Other cultures have dietary habits and folk medicines that would deal with things like "the flu", aches & pains and other ailments. There are cultures that are known for heavy use of alcohol or flaring, raging tempers.
I think it is possible that while young, the immune system may still be strong enough to take these critters down to an unnoticeable level or beat them into hiding, with the help of some "good old-fashioned chicken soup", herbal tea, garlic & onions, etc.
Then when the immune system becomes fatigued after many years of fighting these battles, it becomes weak & is no longer able to keep up the fight.
They found Borrelia because children became severely ill, in a close proximity to each other, at the same time. Maybe there are other types of bacterial infection that exist that have similarities to Borrelia.
Then again, why do negative tests for Borrelia become more positive & show more bands after years of Tx?
It gets to be too much to think about sometimes. There are SO MANY possibilities! I can't wait until all these scientists catch up.
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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Well, people with a known tickbite and other well documented coinfections that continue to have symptoms but improve on treatment (late catches) probably do still have lyme, even if no bands but 41 show up in tests. There may also be reactivated virus or bacteria that were suppressed by the immune system before the additional burden of lyme+ was added.
It is complicated, and the ID docs apparently are only onto simple things, perhaps this is all they are capable of.
But I don't think it is accurate to suggest that all of chronic lyme cases are really something else. Please look at the animal studies which can still find spirochetes after longterm treatment. This has also been found in autopsy material of brains, etc in humans. I think I am correct in saying these tissues were PCR positive for Bb.
Posts: 8430 | From Not available | Registered: Oct 2000
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quote:Originally posted by david1097: What is not entirely clear is if the 41 dKa band is specific to only the flagellin proteins of spirocetes, Lyme bacteria,(regardless of strain) or all flagelated bacteria. There are conflicting accounts from various publications.
I would assume that since the iGg 41 seems to be a persistent band that appears in non lyme infected people (polland and isreal have been quoted in this thread), that it is not lyme specific, but rather it is related to long life antibody to a variety of bacteria. IF this is true then that would tend to support the idea that it is in fact also related to any number of non spirocetes.
Since there are lots of flagelated bacteria out there this woudl also account for a lot of people having the antibody due to exposures to these pathogens. Even an infected scratch with some of these bacteria would then cause the 41 band to light up.
A note on testing in general.....
A point that many seem to miss is that the term "LYME Disease" has morphed into a general term to describe "unknown Lyme like bacterial infection". If one talks to some of the leading Lyme clinicians or even just listens to some of their presentations, it immediately becomes clear that of the "Lyme" patients that they see, only a fraction of them are actually infected with clinically apparent Lyme. Many of the ones that are not, are certainly infected with something and do respond to therapy but it is not Lyme. Some also have Lyme plus something else.
A quick search will show that there are LOTS of flagellated bacteria (and unflagellated ones too) that cause Lyme LIKE symptoms. Things like migrating joint pain, neurological problems, joint swelling, muscle pain etc, etc. are common with many many slowly reproducing , hard to treat or inter cellular bacteria. Some of these infections are "classically" thought to be "self limiting" and indeed they are for a while but what happens when one gets older and more of the different infections accumulate or the bodies inmmune response weakens due to age?.... In many instances, these previously hidden symptoms appear in a confusing array of seemingly unrelated observations that no one can figure out.
With lyme, also being a systematic infection with so many possible symptoms, the so called great IMMITATOR becomed the great IMMITATED, due to its ever increasingly public awareness.
Given the ultra lethargic state of the infectious disease medical communutiy, they are illequipped and obviously ill prepared to deal with this situation. As a result thay are resistant and hostile to the concept that these infections exist in the developed world... No one wants to bring the bad news... As an example it took well over 20 years for H.Pylori to be acknowledged as an infectious disease!. This even with a sea of clinical proof.
So how does this relate to testing? If there are no bands other than 41 dKa and there are lyme like symptoms AND the other bands do not light up after antibiotic treatment I'll bet good money that the person does NOT have Lyme. I'll also bet that there is a good chance that given the symptoms they DO have some other bacterial infection.
This being said, there is a lesser but still finite chance that they have some other things that can look like lyme. These include a number of viruses AND beleive it or not Genetic diseases.
In particvual there are a families of relaping remitting geneticaly differentiated diseases that have some Lyme like symptoms.... are these in fact generationally transmitted infections (ie. Brucella), I have no idea, but they do exist.
So why am I rambling on like this? I guess its because there seems to be a overiding focus on Lyme and ONLY Lyme with some peoples interpretation of the various tests where in reality , the situation can be much more complicated.
what steere etc. have distorted is the relative importance of the 41 kDa band. I pointed out the israeli frequency because the same studies in america demonstrate that about 40% of the pop carry positivity to the 41 Kda band {in endemic areas}. In israel, it is something like 8 %. Israel doesn't have Bb, but does have related relapsing fever borrelia. what I am saying is that due to its constitutive expression, the flagellin band is probably the Best indicator of exposure/ possible latent infection, and is probably the mainstay of the ab response no matter stage of infection.
Bb differentially regulates protein expression of surface proteins, such as osp a, b, and c. They are regulated according to stage of infection, tissue type, and microenvironment. VlsE, another surface protein, is also regulated in this manner. However, flagellin is not differentially expressed.
What happens in very late CNS disease? No one really knows, BECAUSE IT HAS NEVER BEEN ADEQUATELY STUDIED. THE STEERE CRITERIA were designed for early, acute disease. As far as I know, VlsE is not transcribed in the CNS, and flagellin is one of the only proteins I know of that IS transcribed.
Steere intentionally 'swift-boated' the relative meaning of the flagellin ab response. Sure, you see a cross-reaction in people who don't have exposure to Bb, BUT IT IS MUCH LOWER incidence than we are lead to believe. Typically, wrt oral spirochetes, a response is only seen when the gums are visibly infected.
As far as the poles go, and other europeans, I'm fairly certain that the 41 band they demonstrate is reflecting exposure to Bb. However, it is NOT the same strain of bacteria we see in the US. And did you know that in Europe, only 3 bands are necessary on WB to be regarded as positive? Did you know that DOGS in america require only 3 bands to rate a positive?
That's right folks...under the steere criteria, we are treated worse than DOGS.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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Lyme in the US can cause latent infection which later emerges as a full blown encephalopathy.
People need to know if they have been exposed and are running this risk. That is the main reason I harp on the flagellin band. If you have it, it probably doesn't mean much, but it COULD indicate latent infection.
Many european and non medical US scientists have published on this exact point, referring to serologically active versus inactive or latent infection as reflected by seropositivity to only flagellin or flagellin plus one other band.
Steere shouldn't have distorted the results like he did using syphilis serum. It's a pollution of science. use a normal healthy control.
Since NONE of this has been studied, that's about as much as I can say. I know what my own experiences were.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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Now, let me tell you about the real DARK SIDE of the steere/dressler criteria.
These criteria were designed to enable one thing: a vaccine trial for the OspA vaccine. That's why the band to OspA at 31 KdA was left out of the criteria for positivity, even though it is very specific to Bb.
Why then was it necessary to distort the importance of the flagellin response? I'll tell you why. It's because they had to test the vaccine in an endemic area. And a significant percentage of vaccinees were ALREADY SHOWING seropositivity to Bb exposure and possible latent/asymptomatic infection as manifested by the 41 band and maybe a few others, but not enough to be 'positive' by CDC standards. {remember, in europe 3 bands = I have lyme disease, in the US, 3 bands = normal}.
In other words, they had to run a vaccine trial on a group of people who had already been exposed or infected by Bb. If you utilize scientifically honest criteria, then YOU CAN'T DO THE TRIAL, BECAUSE A LARGE NUMBER OF YOUR VACCINEES ARE ALREADY INFECTED OR EXPOSED BEFORE THEY EVER GET THE VACCINE.
So by using less restrictive criteria, you create a situation in which there is no way to distinguish whether or not the vaccine is effective. Basically, a lot of people got a worthless vaccine.
this paradigm...which plunged thousands of vaccinees from infected areas into an unknown realm {what happens when you vaccinate someone who has already been exposed, or is manifesting late stage latency} and MAY have been the reason we saw so many reports of adverse reactions.
Individuals who were carrying latent infection, as manifested serologically by a limited ab response, these people were CUT OUT of the medical community, and they had to pretend nothing was wrong with them. And wrt lyme encephalopathy, Bb protein expression primarily in brain years after initial exposure, that has never been studied adequately to know what is signficant and what is not. All we really know is that flagellin is constitutively expressed even in brain infection.
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david1097
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Hi, I am in no way suggesting that chronic or persistent cases of lyme are not lyme. (I knwon this FIRST HAND FIRST PERSON.) What I am saying is that 41 with no other band would be highly suspicious especially after antibiotics had been given to such a patient.
Similalry what I was trying to say was that if someone is sick and ONLY 41 (as per above. ie, after anotibiotics) is lit up then if the antibody is common with flagellin of other bacteria then there would be a good chance that it is one of the other lyme like bacterial infections(assuming that there was an antibiotic response.)
Should 41 be included in the criteria.... My vote is that it is not very useful at all. I have seen people with 41 persistently lit up with no other bands and display no symptoms what so ever. This was before and after antibiotics.
I also find it hard to believe that the 75% of polish people have a lyme infection (regardless of strain).
Does anyone know of the flagellin antibody is generated as a result of other flagellated bacteria? I had for a long time assumed that it was NOT, but after some research that original conclusion is by no means clear.
I would think that is would be an easy thing to do. Just make some anitgen from various flagellated bacteria, use a lyme patients blood and do a WB.
If no ones here knows for sure I can try to give Nick harris a call to see what he says.
On the Steere issue, Steere was one of the ones that was to have made it big in seeing lymerix get to market. I am quite sure that this strongly influenced what he said about testing since for people who are confirmed as already having bb then the vacine would be useless. This means smaller market. Smaller...how much smaller??? as an example, smaller might even much significantly smaller as in the case of Poland if 41 happens to be definative (which I personally doubt) 75% smaller.....
Posts: 1184 | From north america | Registered: Feb 2003
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quote: What I am saying is that 41 with no other band would be highly suspicious especially after antibiotics had been given to such a patient.
I am living proof this statement is just not true. The only positive band I had on the WB test was 41. But at the same time as taking the WB I was positive on the LUAT and PCR.
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RoadRunner
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quote:Originally posted by duke77:
quote: What I am saying is that 41 with no other band would be highly suspicious especially after antibiotics had been given to such a patient.
I am living proof this statement is just not true. The only positive band I had on the WB test was 41. But at the same time as taking the WB I was positive on the LUAT and PCR.
I know many people that had one band and had lyme disease.
nice post duke
RR
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TerryK
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Some excellent posts here. Thanks Bruce and David for weighing in with your detailed posts.
From what I've read in the info provided by some of the LLMD's regarding WB bands, it seems like band 41 alone is not considered specific enough to state for certain that a person has been exposed to Bb.
That said, it is clear that there are an unknown number of people who are infected with Borrelia Burdorferi but are sero-negative. As Lou pointed out, there are animal studies that prove sero-negative infection. There are autopsy reports of humans that show infection despite sero-negative test results.
In the study that Tree posted, not only was it a very small study but the controls were potential lyme infected patients and they only used one strain of Bb. How can any concrete testing assumptions be made from studies like these?
I am not a doctor and I am not an expert in test design but it doesn't take one to see that many of the studies that are used by the IDSA and CDC to define testing and diagnostic criteria are far from accurate or complete.
Lyme or lyme like - I don't care if a single lyme specific band shows up on the flawed WB - I want treatment if my LLMD and I decide it is reasonable.
Terry
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david1097
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Duke, I certainly are not argueing the issue here but I am interested if you had WB's done before and after treatment? If so did both show only 41? I fully realize that 41 prior to treatment of late stage lyme might be the only one the is lit up. But I have never heard of only a 41 after start of succesful treatment.
The reason I ask this is that after abx treatment when some of the bacteria has been lysed in the body then one would expect (and indeed in many many cases) the other bands will show up at least as IgM as the body detects these foreign protein fragments.
Also how soon was the test done and how long did you have lyme before the test(s)?
Why do I ask these questios?
Before and after abx treatment-
The before and after antibiotics is an important point for if there were no other antibodies at the diffrent weights after treatment then the lyme you have might be quite different than the b31 strain that they use for making the antigen. Either that our your immunity is somehow compromized such that you could not make those antibodies??? As far as I know, even the european strains react with the the antibodies that show up in the other bands.
How long infected before test-
If the test was done soon after infection then it is known that antibodies will no be produced yet, but are the bacteria in the blood? PCR would tell. Same thing for the urine, maybe they are released in the urine prior to the bodies immune responce.
If any of these apply to your case (or anyone's case) this might be an important avenue to follow because many people are in a catch 22 sitation. You can't test for a few weeks, so you have to treat empirically before the infection has time to become entrenched BUT if you treat empirically you will mute the immune reposnse and the tests will come back negative in the future. So what are you supposed to do??????
P.S. i strongly suspect that this is the fault with the single capsule cure concept. It is a self fulfilling arguement, treat only enougth to kill the positive test results and deal with the bad stuff a few years down the road when it looks like something else.........
Posts: 1184 | From north america | Registered: Feb 2003
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quote:Originally posted by david1097: Hi, I am in no way suggesting that chronic or persistent cases of lyme are not lyme. (I knwon this FIRST HAND FIRST PERSON.) What I am saying is that 41 with no other band would be highly suspicious especially after antibiotics had been given to such a patient.
Similalry what I was trying to say was that if someone is sick and ONLY 41 (as per above. ie, after anotibiotics) is lit up then if the antibody is common with flagellin of other bacteria then there would be a good chance that it is one of the other lyme like bacterial infections(assuming that there was an antibiotic response.)
Should 41 be included in the criteria.... My vote is that it is not very useful at all. I have seen people with 41 persistently lit up with no other bands and display no symptoms what so ever. This was before and after antibiotics.
I also find it hard to believe that the 75% of polish people have a lyme infection (regardless of strain).
Does anyone know of the flagellin antibody is generated as a result of other flagellated bacteria? I had for a long time assumed that it was NOT, but after some research that original conclusion is by no means clear.
I would think that is would be an easy thing to do. Just make some anitgen from various flagellated bacteria, use a lyme patients blood and do a WB.
If no ones here knows for sure I can try to give Nick harris a call to see what he says.
On the Steere issue, Steere was one of the ones that was to have made it big in seeing lymerix get to market. I am quite sure that this strongly influenced what he said about testing since for people who are confirmed as already having bb then the vacine would be useless. This means smaller market. Smaller...how much smaller??? as an example, smaller might even much significantly smaller as in the case of Poland if 41 happens to be definative (which I personally doubt) 75% smaller.....
You're ignoring some crucial points. First of all, there is not much out there which demonstrates that there is equivalence between the pathogenicity and antibody response in american strains versus european strains. You're making a dangerous assumption. In fact, the estimate has been made by at least one author that the ratio of asymptomatic: symptomatic lyme in europe is 1:8, but in the US is closer to 1:1.
The studies in poland...and in germany involved a population that lives/works in the woods, or involved occupations/hobbies which tend to lead to a high frequency of tick bites. These aren't general population studies.
The 41 band appearing on these blots is representing exposure to Bb. As stated previously, it is a constitutively expressed gene {flagellin} which is absolutely necessary for Bb survival, and as such is the earliest and most consistent antibody response regardless of stage of infection. None of the osps can be considered as comparative..they are differentially regulated.
I've read the studies...cross reactivity to flagellin only occurs among spirochetes...relapsing fever, leptospirosis, syphilis. actually the syph cross reaction occurs at 40 KdA. the use of recombinant antigens avoids this.
My point is this: reactivity to 41 KdA doesn't equate to active infection, but it IS a marker of exposure. whether it is important in latency or late disease confined to CNS, NO ONE HAS PUBLISHED ON THIS. NO ONE HAS PUBLISHED ON Bb PROtEIN EXPRESSION IN LYME ENCEPHALOPATHY.
Your comments on 41 not being important after abx treatment are dangerous. Steere himself has published on 'seronegative' disease, ie, that as in syphilis incomplete or ineffective treatment can abrogate the serum antibody response. IN this context, any remaining antibody responses might be important.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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here's an example of one of the polish studies...note that nowhere are '75%' of the population identified as carriers...the carrier rate IS much higher in high risk group...and also notice how the polish scientists discriminate between asymptomatic and symptomatic infection...something we DO NOT see in US studies.... ...............................................
Risk of tick-borne bacterial diseases among workers of Roztocze National Park .Cisak E, Chmielewska-Badora J, Zwoliński J, W�jcik-Fatla A, Polak J, Dutkiewicz J. Department of Occupational Biohazards, Institute of Agricultural Medicine, Lublin, Poland. [email protected]
The objective of the present study was to assess the risk of borreliosis and anaplasmosis {ehrlichiosis} among the forestry workers of the Roztocze National Park {south-eastern Poland} by examination of Ixodes ricinus ticks living in park area with PCR method, and by the serological and clinical examination of the workers. In 406 examined ticks, the prevalence of infection with Borrelia burgdorferi sensu lato was 11.5 %. The nested PCR reaction for determining the genospecies showed that the most common was Borrelia burgdorferi sensu stricto {55.3 % of total positive} followed by Borrelia afzelii {38.3 %}. As many as 6.1 % out of 115 examined ticks showed the presence of Anaplasma phagocytophilum DNA. The infection rate was high in males and females {14.3 % and 11.1 % respectively} and low in nymphs {1.5 %}. In 46 out 113 examined forestry workers {40.7 %} the presence of specific IgG and/or IgM antibodies against Borrelia burgdorferi sensu lato was found in ELISA test, while only 4 out of 56 urban blood donors showed a positive response {p<0.0001}.The prevalence of IgG antibodies against Anaplasma phagocytophilum determined with the use of indirect immunofluorescence test {IFA} was 17.7 % in forestry workers compared to 5.4 % in reference group of blood donor}s {p<0.0}. No correlation was found between the presence of antibodies to A. phagocytophilum and to B. burgdorferi s. l.
Clinical investigations of 113 forestry workers showed 3 cases of borreliosis {2.7 %} and no cases of anaplasmosis. In conclusion, forestry workers of the Roztocze National Park in south-eastern Poland are often exposed to Ixodes ricinus ticks infected with Borrelia burgdorferi and Anaplasma phagocytophilum, and show a high proportion of asymptomatic borreliosis and anaplasmosis manifested by a positive serologic response, while the number of clinical cases is relatively low.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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Here's a more damning study, on polish dogs. Note the disturbing lack of correlation between PCR results and seroreactivity. such studies point in dogs to a very high rate of seronegative disease. also, realize that in dogs there is no evaluation of neuropsychiatric disease, b/c it is impossible to assess the behavior...
.................................................
Prevalence of DNA and antibodies to Borrelia burgdorferi sensu lato in dogs suspected of borreliosis.Skotarczak B, Wodecka B, Rymaszewska A, Sawczuk M, Maciejewska A, Adamska M, Hermanowska-Szpakowicz T, Swierzbińska R. Szczecin University, Faculty of Biology, Department of Genetics, Poland. [email protected]
The aim of the paper was an attempt to correlate clinical signs with the presence of DNA of Borrelia burgdorferi {sensu lato} s.l. and the antibodies against B. burgdorferi s.l. in the blood of dogs. Among the animals studied there were 62 dogs delivered to the Veterinary Clinic in Szczecin and 30 from the Municipal Animal Shelter in Szczecin with varied clinical signs of borreliosis. In all cases the owners admitted frequent contacts of their dogs with ticks, both in the past, as well as shortly before the onset of sickness. We used two methods: PCR for detecting DNA of B. burgdorferi s.l. and ELISA test for detecting antibodies against the spirochete. Lameness, the principal symptom of canine borreliosis was the most frequent symptom of the group of 31 PCR-positive animals. The other most common symptoms in PCR-positive dogs were fever, swelling of joints and loss of body weight. DNA of B. burgdorferi s.l. was most frequently detected in the blood of dogs of the group 2-5 years old {13/54.1 %}. ELISA tests specific for IgG antibodies were positive in 37 of 92 sera {40.2 %} taken from examined dogs. Lameness was observed in 15 of 37 IgG-seropositive dogs and in 25 of 55 seronegative animals. In 54 % of dogs with the antibodies, swelling of instep- and wrist joints was observed compared to only 24.4 % in seronegative dogs. An attempt to correlate the PCR results with the results of tests detecting antibodies against B. burgdorferi s.l. revealed that fewer than half {45.1 %} of the dogs with presence of DNA of the spirochete, developed an immune response. Therefore the transfer of B. burgdorferi s.l. form, the primary lesion to the target tissues, is possible in dogs which did not develop immune response or develop an insufficient response. Among 92 borreliosis-suspected dogs 54 {over 58 %} were diagnosed positively using laboratory methods. In most cases there was a correlation between clinical symptoms of borreliosis and presence of DNA B. burgdorferi, thus PCR may contribute to improving to a large extent diagnostic of canine Lyme disease.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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I've read in several places (usually with names such as Sigal, Steere, Halperin, et. al. on them) that antibodies generated against the 41 KdA band for Bb may be the genesis of autioimmune conditions that occur "after the spirochetal infection is eliminated." These antibodies seem, from their research, to attack human myelin, which can result in MS, ALS, etc.
Make what you will of that -- but a quick lit search will pull up quite a bit of writing on this topic....
-------------------- "Looks like freedom but it feels like death.. It's something in between, I guess"
Leonard Cohen, from the song "Closing Time" Posts: 822 | From California | Registered: Jan 2006
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northstar
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that antibodies generated against the 41 KdA band for Bb may be the genesis of autioimmune conditions
Yes, that is a catchy little phrase that they like to keep repeating. I'm waiting for the melody accompaniment now.
Those people are looking every where for that Holy Grail of autoimmunity.......maybe it's here, oh it could be. Wait a minute, it could be there........
It's got to be here somewhere cuz those symptoms sure ain't continuing infection. Oh no....no way!
If you make the assumption the 41 is autoimmune, then what about the effect of syphyllis on 41? It has to be autoimmune, too? Oh...I see, only in lyme is it auto immune!
And how come old 23-25 aren't on the invitation list? They may feel left out. Why just 41?
Whew!
N/
Posts: 1331 | From hither and yonder | Registered: Sep 2005
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I tested positive through Igenex with multiple bands before treatment. Only took abx for 4 months and stopped for a year. Never got better just gave up hope too early I guess. I just got tested again before restarting treatment and nothing came up but IGG 41 and 58 kda. I read the explanation of the w/b but after reading all this about 41kda and finding that 58kda is just heat surface protein or whatever, you guys are making me question things.
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david1097
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I am confused about about the issue here. The qestion (that I though this was about) was what is the real significance of the 41 dka band both IgG and IgM. Thank you for clarifuying that the 41+/- is spirochete specific.... however, there are a lot of spirochetes out there, many of which are even transmitted in water and exposure can occur orally....
So the question is still, what is the prevelence of 41 both IgG and IgM in the general population. This is the critical point. No doubt that those with lyme have 41 lit up but that is not the question, the question is how many with 41 lit up don't have lyme?
Witha non specific reposnse, I would find it hard to believe that everyone with a 41 IgG reactivity has lyme or has been exposed to it since there are a lot of spirochetal diseases that are even more prevelant than lyme in some regions of the world. There are regular reports of far off (and not so far off) outbreaks of things like pinta, leptospira etc. in the various infectious disease news groups. How many are unreported or indetected?
All of my comments are irrelavant if 41 only reacts with lyme but eveything I have read indicates that this is not the case. If there are some convincing references someone can point me to I would be glad to change my mind but until then to me,someone with 41 is of interest and might warrant further investigastion in a patient depending on symptoms but is totally non diagnostic.
On the antibody produciton after ABX. I think you are overlooking an important question. Sero negativity that is reported by steere et.al. is just that, no objective serum reponse in a person with Lyme. There might be many reasons for seronegativity but one important point is that lack of response brought about by early use of abx is (as far as I know) not totally understood(and may in fact be antibiotic family specific) and is may be short term in nature in nature.
While it is clear that there may be no humoral response in these cases, does this mean that once abx are removed and the antigen is later presented to the immune system through the lysing of the bacteria via a repeat application of an antibiotic that there would still be no response? I think the answer is that in that case a response would be generated, but this is only my guess.(there are conflicting publications on this)
In a practical test, steere should have ) treat the seronegative patients, with abx and then looked for some sort of reponse? I would really like to know if he he did this? I suspect not.
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david1097
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Improver,
Did you identify any possible co-infections? I have talked to several people that had babesia as well as lyme. The lyme treatment was not very effective, but the babesia + Lyme was (although slow).
The muting of the bands other than 41 is common in late stage lyme so what you are describing does not sound unsual, but it also might mean that the lyme was knocked out. Still with no response from initial treatment if it were me I would strongly suspect an other, co-resident problem (snce you had multiple bands to start with).
Remember that lyme looks a lot like some other things, and that some other things can look a lot like lyme. If the intial treatment knocked out the lyme all it may have done is allow the other infection to expand to take its place.
I guess the critical question is was there any change in any of the symptoms at all? This is sometimes a hard question to answer since there seems to be a lot of overlap but after time you can sort out the symptoms into different groups. Once you do this, it is easier to make an objective observation.
Posts: 1184 | From north america | Registered: Feb 2003
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You're making some good points. To respond to most of them I'm going to have to access my secret trove of documents which is not immediately handy. Give me a day.
WRT specificity of the 41 KdA response, that is really what this is all about. I read many articles by shapiro, steere, etc. in which they proclaimed the lack of specificity, that oral spirochetes caused this phenomenon too, and 41 was insignificant. But then I researched it myself and discovered that they were fudging.
Humans RARELY have an ab response to oral spirochetes, and then typically only when there is massive and visibly obvious gum infection present.
German research {I believe by wilske} showed that Bb does not cross react on blot with other flagellated bacteria, with exception of syphilis, leptospirosis, and relapsing fever.
ALL of these very rare {in US} illnesses can be ruled out through testing. Syphilis has an incidence of 3 per 100,000; lepto and RF much less than that. So within the US, there really isn't much out there that can cause a cross rxn at 41. EBV has been reported, but this has barely been studied, and only anecdotally. Certainly when one looks at the european studies, which compare workers in endemic areas to urban folk, the difference is striking.
There certainly seems to be a great deal of seroreactivity to Bb, and I can't think of any other phenomenon which would account for that under the conditions. EBV infects something like 95% of the world's adult population.
Very few studies on wholely nonendemic pops {for example, a group from new zealand} for seroreactivity have been pubbed. In most cases, another explanation can be put forth, such as endemic tropical spirochetal illnesses.
The israeli study I mentioned...that is striking...8% positive. In the US, in an endemic area, you get results similar to the polish study...>40%.
You can't run a vaccine trial on that. There would be no way of discerning whether the seroreactivity occurred before or after vaccination. I am saying that what they did was write off everyone who had latent/asymptomatic borreliosis by demeaning their blot results and calling them normal. they were grouped together with the greater number of seropositives who were, for genetic and strain reasons, seroreactive but not in danger of developing late CNS disease. and suggesting that b/c of disease dynamics and what is now known to happen as infection progresses {differential expression of proteins} those with late stage encephalopathy {which is what afflicts most chronic neurocases} were written off, and continue to be written off.
They ASSUMED that this would be a minor percentage. Notice how wormser etc. deride the possibility of neuropsychiatric lyme...rarely is it mentioned, even by such luminaries as Halperin {I say that sarcastically} and the CDC HAS NEVER MENTIONED OR WARNED THE PUBLIC OF THIS LATE DISEASE MANIFESTATION.
By the way, there's no evidence that VlSE, the basis for the C6 test, is expressed in CNS tissue. What they are seeing in lyme in the US is two infections -the early acute form which affects body, skin, joints...and later CNS infection which apparently goes intracellular.
Intracellular = declining antibodies or even absent antibodies...that is what is seen in bartonella and brucellosis.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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posted
one other point...lysing the bacteria should expose new antigens to the immune system. most of the antigens Bb presents under normal conitions are OSPs. so I would expect a different response there. I don't think anyone has studied this. it seems complex.
steere, in his dressler study, failed to temperature shift his borrelia cultures. That's forgivable, I suppose, but since then we have learned that Bb differentially regulates certain immunogenic proteins according to temperature. at human body temperature, a number of important proteins are known to induce ab response in baboons. none of these proteins are tested for on his blots; no one has done a damn thing to study these proteins.
It's very likely that a number of proteins which we produce antibodies for and which are important to human infection dynamics are NOT currently being tested for on blot or otherwise.
Basically, I'm under the impression that all this crap has turned into a public health disaster and they are doing their best not to make amends, but to duck and cover and screw everyone over. There's no accountability among these stooges.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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"Basically, I'm under the impression that all this crap has turned into a public health disaster and they are doing their best not to make amends"
- Public Health Disaster
- They know it.
- The evidence exist.
- We just need influential people/politicians to join us....I think there is plenty of scientific evidence showing how this disease destroys lives in our society and is misdiagnosed.
- Even if we win on the scientific field, the final battle or last word would take place on the POLITICAL arena and nothing else.
And to end my opinion (which has nothing to do with 41 band) we should emphazise more on the link between Lyme and MS/Alzheimers ,since these conditions are the ones more reocognized.
Regular people usually won't read about borrelia itself.
Learned that Mitt Romney's wife has MS...
Posts: 983 | From The sky | Registered: Feb 2005
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quote: I certainly are not argueing the issue here but I am interested if you had WB's done before and after treatment? If so did both show only 41? I fully realize that 41 prior to treatment of late stage lyme might be the only one the is lit up. But I have never heard of only a 41 after start of succesful treatment.
I did take another WB about 15 months after the first. My LLMD asked me why because I had a positive PCR he said don't waste your money. I did take it and it was still far from a CDC positive. On the second WB I had a positive 41 and a "ind" on bands 31, 23 and 60. My LLMD said he would call it a positive though.
quote: Also how soon was the test done and how long did you have lyme before the test(s)?
I went camping in late August 03' and had the tests done in the middle of Dec 03'. I think I was reinfected. I had symptoms for years and used to pull off ticks all the time and never really knew how serious Lyme was. I grew up in Wisconsin and in the early eighties my father had a bullseye and was given two weeks of doxy. He has had problems ever since. Actually, I can trace many symptoms back to shortly after that incident with my father.
quote: The before and after antibiotics is an important point for if there were no other antibodies at the diffrent weights after treatment then the lyme you have might be quite different than the b31 strain that they use for making the antigen. Either that our your immunity is somehow compromized such that you could not make those antibodies??? As far as I know, even the european strains react with the the antibodies that show up in the other bands.
If I understand this correctly it would be the opposite of what you are saying. B31 strain is the antigen they use for the LUAT and the PCR (OSPA). According to Nick Harris band 31 is the most Lyme specific band of all. He says no other organism known has OSPA. So if I was positive on the PCR and not the WB then it would be opposite of your statement?
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david1097
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I think there is confustion on teh B31 strain and the band at 31 dKa. These are ot the same. The B31 strin is the lab grown vareity that is typically used to make the antiogens for all the bands in the various tests.... as bruce illuded, it may not be the best choice because the bacteria is likely quite different in the body and may generate different proteins that are not even tested for. An the kicker is that the longer uyou have the infection, the longer the organism has to tune its self so that no antibodies are produced. This could be why you are showing any other bands... Remember that The 41 band may be persistent because the flagelin strands are inside the bacteria and are not exposed to direct attack from the anitbodies and the antibodies are only generated in response to dead bacteria. As a result there is no incentive for the bacteria to become invisible in that regard.
On another note,
In all this testing stuff there is something that eveyone is missing. It is just common sense... here it is.
If the lyme bacteria is so difficult to find in the body and blood of a late stage infected person/animal then how in hell can the tick pick up enough bacteria in its meal to sustain the disease? Its got to be in the blood at higher concentrations, but where?
Posts: 1184 | From north america | Registered: Feb 2003
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posted
Very interesting stuff! Thank you for posting this.
Could someone explain what the criteria is that makes some "seroreactive but not in danger of developing late CNS disease?"
I ask, because I believe I went undiagnosed while pregnant with my son. He is now five. He doesn't exhibit any Lymie discomfort (has hereditary hypotonia...). Nonetheless, I had him tested during his recent regular physical.
Labs were Medical Diagnostic in NJ and Stony Brook University in NY.
His western Blot had "CDC Specific" on kDa Band 41 for both IgM and IgG. No other bands showed up.
Is this registering exposure? Or is he likely to develop Lyme later and this is the blip on the radar?
Thanks in advance for information.
wiserforit
Posts: 508 | From Banks of the Hudson | Registered: Jul 2006
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posted
Some of these questions would be answered if there were more honest research being done and published in this country. It is perfectly obvious that the science is being perverted to produce a political result. As long as the NIH throws its billions at compliant researchers (those who know what the expectations are and produce them), and those people rise in the academic hierarchy, achieve positions at journals that roadblock papers with the "wrong" point of view, then we will not have real answers to these questions.
Before lyme, I actually believed that scientists all looked for the truth and disseminated the results whatever they were, as long as they were honest. I don't think that anymore.
Posts: 8430 | From Not available | Registered: Oct 2000
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quote:Originally posted by david1097: On another note,
In all this testing stuff there is something that eveyone is missing. It is just common sense... here it is.
If the lyme bacteria is so difficult to find in the body and blood of a late stage infected person/animal then how in hell can the tick pick up enough bacteria in its meal to sustain the disease? Its got to be in the blood at higher concentrations, but where?
Cystic forms in blood?
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david1097
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wiser...
I wish I knew th answer to that. I suspect that many children of families that have someone that has lyme will show that band. But why and what does it mean??? I really don't know (and I would really like to know). All I can say is just watch for other signs.
ldfighter..
On the cystic form.... I have my doubts. here's why.
The sprirochete is ver long but very skinny. You casn see them under an optical microscope. You can even see the blebs, which are even smaller then the bacteria (not so good though). So I would assume (it is only an assumption) that the cystic form would also be visible under the same scope. The cysts that are created by dropping bacteria into water can be seen. So... if that is the case, why can't we see them under the scope, even if you filter and centrifuge them out.
The Bowen test used a florescent tag to try to let you see them but the floresence technique is usually only used to speed up a search for sparse objects (and they did indeed seem to be sparse), however in the case of borrela infection spriocitemia is visble under a scope without the need for a floresent stain, there are lots of them. One would think that the cysts would be in a similar abundant supply???? Something is not right in this regard.
I often wondered if the bacteria paracitises some of the blood cells. Once in there you won;t see them until you lyse the cell but then you have all sorts of other junk left over that is hard to sort through.
Posts: 1184 | From north america | Registered: Feb 2003
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posted
the larval ticks are picking up the bacteria during their feeding on small rodents and to a lesser extent on birds. these species maintain the disease reservoir in the wild. the ticks drink mightily off of these bacteremic hosts. the spirochetes are able to replicate inside the ticks. so it only takes a small amount to get into the tick.
that being said, not all nymphs carry the infection...even the most endemic areas you see maybe 40 or 50% of nymphs as carriers. what you have to understand is the total abundance of host reservoirs in the wild ie mice. and spirochetes go crazy in the mice...
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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quote:Originally posted by wiserforit: Very interesting stuff! Thank you for posting this.
Could someone explain what the criteria is that makes some "seroreactive but not in danger of developing late CNS disease?"
I ask, because I believe I went undiagnosed while pregnant with my son. He is now five. He doesn't exhibit any Lymie discomfort (has hereditary hypotonia...). Nonetheless, I had him tested during his recent regular physical.
Labs were Medical Diagnostic in NJ and Stony Brook University in NY.
His western Blot had "CDC Specific" on kDa Band 41 for both IgM and IgG. No other bands showed up.
Is this registering exposure? Or is he likely to develop Lyme later and this is the blip on the radar?
Thanks in advance for information.
wiserforit
No one knows the answer to these questions. If they do know, it hasn't been published. the truth is that it might mean something, but it might mean nothing.
syphilis can be passed from mother to child with devastating results. until they get inside the brain {ie start doing biopsies} they won't be able to answer the question. presumably such research has been performed in baboons. monkeys which have been pubbed don't have the same Ig characteristics as humans, but baboons do.
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RoadRunner
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wiserforit
I would get him treatmemt safe is better then sorry.
lyme disease you don't want to fool around.
if my kid he would be on abx for a few months.
RR
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david1097
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Duke,
Sorry for the condfusing response. I re-read your last comment and I think I now know what you mean.... Let me try to answer it again. (Note , the stuff below not withstanding the other post on the B31 vs band 31 is still valid).
Comment .... If I understand this correctly it would be the opposite of what you are saying. B31 strain is the antigen they use for the LUAT and the PCR (OSPA). According to Nick Harris band 31 is the most Lyme specific band of all. He says no other organism known has OSPA. So if I was positive on the PCR and not the WB then it would be opposite of your statement?
my response.....
Lets start with the PCR. The PCR is a method to amplify fragments of DNA that may be present. If there are bacteria in a sample, even minute quantities, PCR can be used to multiply select fragments of the bacterias DNA. To do this they use a specific primer that sort of looksl like what they are truying to magnify. The primer is enough like the fragemtn they want to multiply that it can replicate the dna synthsis process using the original organisms DNA. It does nto duplicate the entire DNA, just a fragement, but it is unique enought that it can be used to detect specific genetic material. PCR dose not use antogens for the testing.
On the LUAT issue. As far as I know (and someone please correct me if I got this wrong) the LUAT is sort of opposite the WB. The WB test looks for the antibodies that have been created in response to an antigen being presented. The outer surface protiens are the ones that WB looks for the antibodies for. If you hve no antibodies or if the antibodies are entirely consumed fighting the infection then there will not be any response....
The LUAT test is sort of the opposite, I think it uses antibodies in the test to look for the protien fragmetns (antigens) in the urine. So it is very possible that the LUAT might be positive and WB negative or weak.
Someone might say ....What! if the antibodies are entirely consumed fighting the infection then there will not be any response.... This might sound far fetched but there are some animals that can have all of their white blood cells consumed fighting an infection... I think it is entirely possible that the specific antibodies could be consumed in fighting the lyme antigens. In fact the purpose of the blebs that are shed may be to keep the antibodies busy and deplete them.
The fact that there was at least a weak WB response to ABX treatment is typical from what I have heard and seen. In addition, I think that the trend has been the longer and more successful the treatment, the stronger the WB response becomes.
Posts: 1184 | From north america | Registered: Feb 2003
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posted
Hugely informative.. Ill print, to digest bite by bite. Thanx all! waldenflo
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adamm
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I would also like to express that sentiment. Greatly helped me appreciate the magnitude of the atrocity being perpetrated upon us...a hugely illuminating thread.
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An attempt to correlate the PCR results with the results of tests detecting antibodies against B. burgdorferi s.l. revealed that fewer than half {45.1 %} of the dogs with presence of DNA of the spirochete, developed an immune response. Therefore the transfer of B. burgdorferi s.l. form, the primary lesion to the target tissues, is possible in dogs which did not develop immune response or develop an insufficient response. Among 92 borreliosis-suspected dogs 54 {over 58 %} were diagnosed positively using laboratory methods. In most cases there was a correlation between clinical symptoms of borreliosis and presence of DNA B. burgdorferi, thus PCR may contribute to improving to a large extent diagnostic of canine Lyme disease. ....................................
The above quote is from a polish study abstract. Think about this. In dogs studied, fewer than half that had PCR evidence of Bb infection showed an ab response on standard testing. As far as I know, this sort of study has not been published in humans. Why is this significant?
First, I'm not sure HOW the polish scientists tested for PCR. In humans, it's done on serum and CSF for most part, sometimes on joint fluid. The same is done on animals, BUT usually in animal studies, they obtain deep tissue ie skin punches for PCR testing. It matters because late stage Bb infection is a deep tissue infection, not a blood infection. Ear punch biopsies are commonly performed in mouse and other mammalian studies, but are not performed in human studies.
While dogs have different immune systems from humans, it certainly would be helpful to know whether similar results are obtained in humans. After all, such a study clearly demonstrates that ElISA and wb testing is useless in ruling out infection. It's safe to assume that the CDC, with its vast repository of blood and tissue samples from across the US and around the world, has performed such testing. The fact that it has NOT been published is illuminating. The CDC HAS published studies on Bb WB testing in some populations that are not from endemic areas...most notably, a study performed on a group from new guinea.
I have personally concluded that the CDC/EIS discovered that lyme serologic testing for later stages of infection was practically useless. They MAY have discovered that large numbers of individuals harbour non-pathogenic or apparently innocuous/latent infections in humans, and decided that most people do not advance to late neuroborreliosis. They MAY now be discovering that their calculations were incorrect, that the numbers are far larger and they might not have anticipated the development of SPECT/PET testing would reveal truths that they'd rather not see illuminated, ie that chronic lyme patients were in fact afflicted with a distinct neuropathological process.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
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I have read a big pile of the literature now, and have given up trying to get anything useful out of Steere, Wormser, Halperin, Shapiro, etc. It is impossible to sort out any true facts from the distortions.
I don't know if band 41 alone is diagnostic - I had accepted that it cross-reacts with other flagella and so is non-specific for Lyme. We need research that is not contaminated by the Steere camp literature. There are many good little papers out there, especially from the early days, and from Europe, but now the field is so contaminated that it is very hard for anyone to do good objective research. Some heros keep it up - go good guys.
Unfortunately, as we know, the official view is the opposite. Most MDs give great weight to the prestige of the institution and the number of times something gets repeated in the literature. They're not trained to analyze data critically, much less recognize when data has been seriously biased and manipulated. Don't get me wrong, some MDs can pick it up, and do good research, because they have a natural gift for critical thought, but it's not encouraged by their standard training.
The motive(s) for all this IDSA biased junk science is key, but I can't really discern it for sure. There are lots of interesting theories, but no proof. I think our biggest barrier is that the general public can't believe that so many doctors can be so wrong.
My current favorite motive for the Steere-camp researchers is that it is a consequence of post-modernism, the idea that there is no truth, no facts, only stories. When I was in college, it was hip to apply this idea not only to the humanities but to the sciences. Most of us in science in the Midwest blew this off, although we knew about the trend. If you believe in it, obviously there's no practical reason to do science - it's just another art form. But I think it affected the Ivy league much more heavily. Especially susceptible are those who were there not because they had an intellectual gift, but because their families pushed them into it. (You can provide your own public examples ;-)
Once you get a couple of prestigious guys who do their work this way, the rest of the flock follows along like sheep. For instance, my husband's PCP actually said "Allen Steere is the guru of Lyme disease!" He couldn't even conceive of questioning his opinion.
I was talking recently to a couple of MDs who work for pharmaceutical companies. One of them proudly said, "I can design a study to prove anything!" I said, "Well, sure, but it would be biased," by which I meant, scientifically meaningless and ethically wrong. And he replied "Everything is biased." The other MD nodded sagely. They obviously considered me naive to think that there was such a thing as (relatively) objective research. End of discussion.
If this is how Steere et al. think, it explains the whole thing. In that view, the best scientist is the most convincing con man, and the only criteria for success is keeping your story going as long as possible. There is no ethical problem with "the truth" or "the facts", because they truly believe there are no facts, no truth. Their professors told them so.
I realize this completely violates common sense; the same people don't jump off a tall building because they think "gravity" is just a good story. But I have come to think that common sense is not that common. Especially among the power-hungry and ego-ridden.
On the other hand, maybe the other theories are correct. Maybe it's insurance companies - although it's got to cost them more to treat symptoms than the cause, so if so, they're really dumb (see above about common sense - maybe they are). Or maybe it's bio-warfare - I read the books, the evidence is not compelling, but that doesn't rule it out. Or maybe the motives are all of the above.
The important thing is to expose the fact that the IDSA science is hopelessly flawed. It's so entrenched, though, that I don't know how long that will take. They've got control of the medical guidelines and the CDC, which controls the diagnosis and reporting of the disease. And the more they get dug in, the more embarrassing it would be for them to admit they're wrong. Think of all the suffering they've caused - they'll never back down, it would be too humiliating.
Also, obviously, it would help if we knew a real cure that works for everyone. The reason we have to keep taking antibiotics is that they don't completely get rid of the bug. But how can we get a cure without real research?
Well, sorry not to have a plan after all this. I'm just telling the ILADS view to everyone I know , and once in a while I get feedback that somebody got diagnosed and ILADS-treated. Keep the grapevine swinging!
And thanks again for this detailed and informative thread.
Lorima
Posts: 74 | From MA | Registered: May 2007
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posted
Hi folks, have not been readibng lymenet for ages due to many problems with usual pain, concentration, etc, but I should have cos it's so interesting.
About band p41, has anyone posted yet about the specific antigen that's patented for what's called "internal p41?" I believe it is so specific for the central part of the flagellin protein that no other flagellin antibodies, for eg leptospirosis, would react with it.
I can try and find the references where I'm remembering this from. It might be included in Western Blots now used in the UK, but I believe even then that it is awarded only 1 or a couple of points in some kind of points system. Forgive my vagueness, lyme brain really has slowed me to a standstill.
Also, can people here recall a publication about Lyme antibodies in monkeys, in which monkeys were monitored after being infected, and all the antibodies disappeared until only one was left, and that was our famous p41??
These "non human primates" as they are so coldly labelled in the scientific world, are our nearest relatives, and they have vaccines tested on them etc, so it seems pretty relevant to extrapolate these results to the human situation.
The whole sorry tale of the lies around Lyme disease is one day going to explode, but I always wonder how on earth all of the complications and twists in the tale will be put over to the general public?
Best wishes, Andromeda
Posts: 180 | From UK | Registered: Nov 2005
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While I'm still awake - there is definitely some kind of cover up going on at high levels in the UK.
Recent requests to the Medical Research Council asked to see what scientific research project requests for funding had been put to the MRC over the last 30 years or so, on the subject of Myalgic Encephalomyelitis, or ME or you might call it Fibromyalgia and Chronic fatigue Syndrome.
The MRC funds university research and sets up scientists for a long time, if they are any good and IF they are good at doing what the MRC (ie the government) want them to do.
Well it seems that research topics and projects from 1992 to 1998 are actually secret!! The MRC won't let people know what scientists requested grant money for with respect to ME research.
This is really Big Brother territory now, because we've had Lyme in Britain for as long as you have, just different strains.
It has caused us to have 200,000 people with Myalgic Encephalomyelitis, and god knows what else, without a single member of the public knowing, and most of them being labelled by a concerted bunch of insurance company-funded psychiatrists under the leadership of Prof. Simon Wessely.
We have had no Polly Murray or karen Forschner to ask the right questions and push for ME research in the past, but now there are many determined people getting to know that their sick children do not have ME, instead they have Lyme.
We are decades behind you, but catching up fast on the awareness front. The worst thing is that most people in the UK pay into the National Health Service directly from their salaries or pay packets, there is no choice.
We have been let down completely when we realise that no way can we get treatment, unless we pay tens of thousands of pounds.
BW, Andromeda
Posts: 180 | From UK | Registered: Nov 2005
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Can you cite that for me where Nick Harris stated the 31 kd band is the most specific for lyme and no other organism has OspA? I would like to use that statement when I go see my LLMD on Monday. I have an Igenex IGM with +30, ++31 , IND41, +58 and IGG with IND39, IND41. An Igenex IGG from a year ealier has IND31 , IND39, +41, +58. Thanks.
Posts: 31 | From USA | Registered: Mar 2007
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Greatcod
Unregistered
posted
This is an email I recieved from Randy Sykes in CT. Yale patented an Bbabd 41 test which they claim is 94% accurate, then mothballed it.
"Yale says don't pay attention to band 41 because it means nothing. Yet they have patented a test for lyme that only uses band 41. They also claim the test is over 94% accurate. These are the people who have been working to hang DR. Jones for treating lyme disease and refuse to respond to Attorney General Blumenthal's subpoena. This test has been put in moth balls.
US patent # 5,618,533
Also the second link, page 5 at the top right, one paragraph down, Dr Steere says that if you have band 41 this means that you either have gum disease, syphilis or lyme disease. He also states that you can tell the difference between these illnesses by a clinical diagnoses. All the lymies have band 41 but few people produce many other bands, Randy Sykes
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