Kickas.org Forums Ankylosing Spondylitis General Discussion #1 AS Web Support Group Klebsiella P. Lab Report

Kat:

I am trying to show, with my Klebsiella lab report, that there is a connection between Ankylosing Spondylitis and Klebsiella. I am HLA-B27 positive and I have a problem with Klebsiella. Prior to this lab analysis of my saliva, I had been on three different antibiotics for approximately 14 months. The association between A.S. and Klebsiella is a fact and is being ignored by a majority of the medical professionals who treat A.S.

“On the other hand, the fact that not everyone who goes NSD has the same results would indicate that not everyone's case of AS is caused by kleb.”

In the United States up until the 60’s, the Ankylosing Spondylitis as we know it today was called Rheumatoid Spondylitis. A.S. was though to be a variant of Rheumatoid Arthritis(R.A.). It was not until a publication in Rome (1961) and then one in New York (1966) that concensus was achieved and A.S. recognized as a distinct entity, quite separate from R.A. I think that there will be more splits in several existing so called auto immune diseases yet to come. The majority of individuals with A.S. are HLA-B27 positive(This is what I meant by,” if you truly have A.S.”). If you don’t respond to the no starch diet or current medications for A.S. or you are not HLA-B27 positive, then maybe you do not have A.S. Maybe you have an autoimmune disease that has yet to be named much less discovered.

“I have asked several world experts about this and their responses varied: from complete disagreement to while it may have some bearing in some patients, it is not a proved theory to this point that all people with AS live with an over abundance of KP bacteria.”

It is not an overabundance of KP that causes A.S. but the mechanism called Molecular Mimicry. This is the point that Overcomer just made. The theory of molecular mimicry, also called epitopic or antigenic mimicry was discovered in 1963 in Atlanta, Georgia by an American micro-biologist. This theory has been known for over forty-three years! This theory was put into practice while treating patients with Rheumatic Fever. As you may or may not know, Rheumatic Fever was caused by having a homology with a bacteria called Group A Streptococcus (GAS). In certain individuals, a homology existed between certain HLA antigens and GAS and heart tissue. So the immune systems of Rheumatic Fever patients started to attack their own hearts. These patients with Rheumatic Fever were given penicillin. When was the last time you ever heard of anyone with Rheumatic Fever in a developed country? A.S. is by far and away NOT the only disease being proposed by the theory of Molecular Mimicry. If you go to a medical library and look up molecular mimicry, you see a whole host of human diseases besides A.S. that are thought to be caused by the mechanism called Molecular Mimicry. These include; Type 1 Diabetes, Multiple Sclerosis, Guillain-Barre syndrome (GBS), Rheumatoid Arthritis.

“This theory, while bearing weight in some cases of AS, does not hold true in all. Dr. Enbringer's results have not been repeated in testing done outside of his pervue to the extent that he was able to achieve them.”

Dragonslayer is correct in saying that 17 countries have reported Klebsiella in A.S. patients. Some of the countries reporting Klebsiella are; England, Spain, the Netherlands, Japan and the U.S. as well as others. Please see the following link to a paper (1998) describing antibodies to Klebsiella P. in Dutch patients. (Journal Rheumatol 1998:25:743-7) This study was done eight years ago.

http://img293.imageshack.us/img293/2150/dutchkp9qo.jpg


Sincerely,

Mike

Mike,

I do the NSD/LSD and so does my son.....I'm a strong believer in it if it helps do it.

However, I get upset when we try and slam this down others throats, as the only possible cause and the treatment, and you do n't can't have AS/SpA if you do n;t respond.

However I am also a great beleiver in those that report a sustained improvement on the diet, who am I to argue against the findings that a proven patient instrument like the BASDAI is not trustworthy. If the improvement lasts over 6 months then it is not likely to be placebo effect either.

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On the causes of AS/SpA and the genetics well I've read an awful lot of the past few years and my only conclusion is that B27 is a bit of a big red herring it cannot be the only gene involved.

Some recent genetic research (I've posted the links welcome.ac.uk I think) several times says that B27 + only contributes 16% of the subsupectability to AS hence the hunt for the other genes.

Whilst some papers/books etc say B27 -ve variant may be a different disease or less severe the the +ve, the ASIF commisioned research acouple of years ago (Dr MA KHAN and some leading AS Dr.s search I've posted this as well) the differences were age of diagnosis and onset may be latter although some had disease for many years. The earlier thoughts were put down to studies not including enough of the negs to get a clear picture. Some ethic groups never have B27 and yet they still suffer from AS!

If you read the lengthy reports from studies Kleb does n't seem to be the only bug in over aboundance in some of the study groups, but were there is an overabundnance they seem to be Gram Negatives. (Reactive Arthritis springs to mind there). Maybe this is due to different background genetics as if I remember some of the none Kleb studies were in Germany, and France. From researching IBD I know that some of the HLA genes linked for possible IBD, varied beteeen different nationalities.

The NOD2 gene in IBD has been linked to SI'itis,

Other candidate genes which have been examined include B60/61 HLA-DR0103 and interesting one was MANK, which lead to the production of a genetically modelled mouse with similar features to AS. It differed from the B27 mouse in that it's toes were not affected by arthritis like the B27 mouse but had flat feet bone spurs and seversal other hallamrks of AS.

Research indicates that a calcium reabsorbtion process after injury (PPI?)etc is effected by this gene......

if goes on and on in frankness just as someone finds a possible explanantion it does n't explain enough.

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So I guess we have to wait for answers in the mean time do what is best for ourselves with our own variation of the disease and offer out what helped what did n't.

David

Hi, David:

While I know that you don't mean to distort things you have found while researching the issues, your statements are more than mere oversimplifications:

Quote:

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On the causes of AS/SpA and the genetics well I've read an awful lot of the past few years and my only conclusion is that B27 is a bit of a big red herring it cannot be the only gene involved.

Some recent genetic research (I've posted the links welcome.ac.uk I think) several times says that B27 + only contributes 16% of the subsupectability to AS hence the hunt for the other genes.

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In the first place, the MHC HLA B27 is not a gene; it is just one of many results of genetics and just a very tiny portion of the whole genetic story and a small part of the total Osp compliment. This portion of the Osp, or similar sequences in non-B27 AS, is DIRECTLY INVOLVED in the disease; it is not just a "marker."

16% is a reasonable number, but NOT for total GENETIC contribution; in fact it has nothing at all to do with genetics but IMPLIES that 84% of the potentiation of AS is due to non-genetic factors--like environment. We both know that the most obvious and pertinent part of our 'environment' is that which we present to our alimentary tracts, but physicians--who have not yet healed themselves--have for years selectively ignored the obvious.

Now, if you have misstated this work to such an extent, how many other people are so confused that they cannot recognize outright fraud in the studies, or separate competent science from fabrication (and nobody can do this just by reading the abstracts). In fact this problem is even more evident amongst doctors; they can read two papers with totally opposite conclusions (results) and cannot decide which one is based upon a false premise. DO NOTHING AT ALL is the end result--aka 'benign neglect.'

Thus, we are stuck by not having an 'officially recognized' CAUSE of AS. We get hand-me-down drugs from RA research, instead of the really useful drugs that could be designed for AS, based upon acceptance of Ebringer's (and others) work.

I have no problem proving the NSD using Bayesian analysis; enough history has elapsed that the statistics can overcome the lies and [**BLEEP**] lies, but even when the NSD is accepted by everyone in possession of even moderate logical prowess, this will still not prove any connection with our favorite pathogen. I'm just going to have to start raising the gnotobiotic mice we can later introduce to the Kp germ, but I'm sure that a pharmaceutical company will bribe some 'Dr. Nick' to introduce yet another fake 'theory' in opposition. It is all politics and marketing spin--nothing gets reduced to useful practice when everyone has a voice; the ultimate democracy is a bureaucracy of infinite mass.

For every doctor and every scientist and academician who does not have AS, it is just fine to debate the issues and then do absolutely nothing, but I am glad that at least one scientist has done the work to nail down WHICH of the over 200 enterobacteriaceae causes AS! I have used this information to great personal advantage, and even indirectly supported those specific findings. Additionally, I have never found even one single related question that could not better be answered using the pathogenesis model and specific germ than any other proposed 'theory.'

Best to You,
John

actually John, HLA B27 denotes both the "antigen"- that is the protein that sits on the surface of nucleated cells and ALSO the gene [sometimes specified as "allele"] that encodes that protein- the gene allows the specific messenger RNA (mRNA) to be made (i.e. transcribed) and thereby allows the specific protein to be made from that mRNA by the cells (i.e. translated).


http://ghr.nlm.nih.gov/condition=ankylosingspondylitis#genes

(see also: http://ghr.nlm.nih.gov/gene=hlab)

"...Researchers have determined, however, that a particular version of the HLA-B gene (called HLA-B27) increases the risk of developing this disorder.

The HLA-B gene provides instructions for making a protein that plays an important role in the immune system..."


http://www.merckmedicus.com/ppdocs/us/common/cecils/chapters/279_002.htm
"HLA-B27

The major histocompatibility complex (MHC), on the short arm of chromosome 6 in humans, is one of the most polymorphic regions of the human genome. This is particularly so for the B locus, which constitutes part of the class I MHC genes in this complex. There are probably more than 200 different alleles at this locus, of which B27 is one. As with all HLA alleles, there is codominant expression of B locus genes, so that most individuals who are "B27 positive" are heterozygous for the B locus and there appears to be little clinical or prognostic significance associated with the less common homozygous B27 state...."


http://www.rheuma21st.com/archives/report_050225_hlab27.html

http://www.ncbi.nlm.nih.gov/entrez/query...st_uids=3485286


the use of pejorative language in discussion does not really allow for thoughtful distinction between various scientific theories, it only lowers the tone of the converstaion.

Mike, I'm sorry, but I am not convinced that kleb p or molecular mimicry are the cause of AS in all cases. I do not doubt that one or both is at the root of some cases, but I definitely doubt that it is the cause in all cases.

Can I give you my reasons in med. speak? No I can't. I don't know the words or medical language well enough to do so. However, I will say that every doctor/expert I have spoken to has told me that they do not yet know the absolute cause of this disease. And I'm not just talking about general practitioners or rheumatologists who should know better - I'm talking about rheumatologists and researchers who spend time studying this and other arthritic diseases. And please don't even try to discount what they have told me by telling me that I'm not talking to the right experts. 'My' experts do not agree with 'yours'. Until they can all agree on one root cause of AS, we are going to have to agree to disagree, and I am going to continue asking people not to make blanket statements about this disease that quite simply cannot be proven 100%, or even 80%.

"Dragonslayer is correct in saying that 17 countries have reported Klebsiella in A.S. patients. Some of the countries reporting Klebsiella are; England, Spain, the Netherlands, Japan and the U.S. as well as others. Please see the following link to a paper (1998) describing antibodies to Klebsiella P. in Dutch patients. (Journal Rheumatol 1998:25:743-7) This study was done eight years ago.
"

Please note, as I stated to John earlier, some of the experts to whom I have spoken personally come from England, the Netherlands, the US, India, Ireland and Germany. You will see that the first three countries match three of the countries in your quote above. So, who do I believe? Experts from the same country don't all agree, let alone experts from every country.

I do not know the cause of AS. As I am not medically trained or educated, I would not presume to state that I do know the cause. This is one theory. It certainly applies to some people with AS. All you can state with any certainly is that it plays a part in your personal case of AS. However, you cannot with any degree of responsibility make the claim that it applies to everyone.
I am HLA-B27 positive. I have neither IBD, nor IBS, nor do I have intestinal problems in general. I have found that certain starches cause problems for me, but others most definitely do not. Does that mean I do not have AS. According to what you seem to think, it does. Sorry, but I do. Unequivocally, definitely, and undoubtedly, I have AS. They don't know why I have AS, except that I show the genetic factor, and I am the only person in my family to have developed AS in the last 100 years that we know of. I am but one anomaly in a disease full of them. Every individual case of AS is one big anomaly - some cases share characteristics/causes with others. Some don't. This is why I object to these statements that they are all caused by one thing. You do not know that. You cannot know that. To claim that you do is hubris in its finest example.

Mike, I am not trying to be argumentative or obnoxious, just trying to stand up for the people here who also disagree with this stance. And trying to ask that you and other Believers in this theory respect the fact that we don't all agree with you. We must be allowed to do our own research, which may or may not lead us to agree with you. By all means, share information with us, but please do not conclude/state that this research applies to every single one of us.

Hugs,