New data on Chlamidia presence in MS

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New data on Chlamidia presence in MS

Postby Arie » Mon Jan 24, 2005 8:56 am

Citation from
http://www.bostoncure.org:8080/article. ... ode=nested

"Three research papers recently came out, one finding a link between infection with C. Pneumoniae and another that found no link and a third study is sort of in-between, saying that Cpn seems to be present, but for a number of neurological disorders, not just MS. The debate rages on."

There are links to the abstracts, which are written in a very professional language. Can anybody here comment it please? I would especially appreciate a response from Dr. Wheldon.

Arie
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Postby SarahLonglands » Mon Jan 24, 2005 10:56 am

.
I tried to get this to open but couldn't. I noticed the date was 15th January, 2004, so we no doubt have seen them already, but unless we can be told what the papers are, it is difficult to comment.

Also you might be interested in looking at the following:

http://www.davidwheldon.co.uk/ms_treatment.html

http://www.davidwheldon.co.uk/cpn-ms.pdf

Both were updated on 26th December 2004, so are much more up to date. The pdf file includes info. on various papers from other sources.


Sarah
Last edited by SarahLonglands on Mon Jan 24, 2005 11:15 am, edited 1 time in total.
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Postby Daunted » Mon Jan 24, 2005 11:05 am

Sarah,

I was able to access it-

We have discussed these issues before if not seen these exact papers.

To bottom line all of this: There is conflicting evidence, detection methods are still evolving, major research centers such as Vanderbilt are still pursuing this treatment avenue, treatment must sometimes still be empirical.

Here are the three papers:

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Chlamydia pneumoniae and the risk for exacerbation in multiple sclerosis patients.

Buljevac D, Verkooyen RP, Jacobs BC, Hop W, van der Zwaan LA, van Doorn PA, Hintzen RQ.

Department of Neurology, Erasmus MC, 3000 CA Rotterdam, The Netherlands.

In this prospective study of 73 relapsing remitting multiple sclerosis patients followed up for a mean of 1.7 years, the relation was tested between serologically defined Chlamydia pneumoniae (CP) infection periods and exacerbation rate. Episodes of serologically defined CP infections were observed in a subgroup, and these episodes were associated with increased risk for exacerbation. CP polymerase chain reaction was positive in most of the CP seropositive patients. No correlation was found between the anti-CP antibody increase and titers of control antibodies

and

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Chlamydophila pneumoniae infection of the central nervous system in patients with multiple sclerosis.

Furrows SJ, Hartley JC, Bell J, Silver N, Losseff N, Stevenson S, Chapman M, Thompson EJ, Ridgway GL, Giovannoni G.

Microbiology Department, University College London Hospitals, London WC1E 6DB, UK. SFurrows@aol.com

BACKGROUND: Chlamydophila pneumoniae has been postulated as an aetiological agent in the pathophysiology of multiple sclerosis. Previous studies show conflicting results. OBJECTIVE: To investigate patients with multiple sclerosis and other neurological diseases for evidence of past or present infection with C pneumoniae. METHODS: 19 patients with multiple sclerosis and 29 with other neurological diseases were studied. Evidence was sought for past or present infection with C pneumoniae using polymerase chain reaction (PCR) and cell culture of cerebrospinal fluid (CSF), and enzyme linked immunosorbent assay and microimmunofluorescence of serum. RESULTS: C pneumoniae was grown from the CSF of one patient with multiple sclerosis. PCR was negative in all cases. Anti-chlamydial antibodies were detected in the same proportion in each group. CONCLUSIONS: This study does not support the theory of an association between C pneumoniae and multiple sclerosis.

and

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Intrathecal production of Chlamydia pneumoniae-specific high-affinity antibodies is significantly associated to a subset of multiple sclerosis patients with progressive forms.

Fainardi E, Castellazzi M, Casetta I, Cultrera R, Vaghi L, Granieri E, Contini C.

Multiple Sclerosis Center, Department of Neurology, University of Ferrara, Arcispedale S. Anna, Corso della Giovecca 203, I-44100, Ferrara, Italy. henryfai@tin.it

The purpose of this study was to provide further insight into the effective relevance of the association between Chlamydia pneumoniae and MS. We evaluated by ELISA technique cerebrospinal fluid (CSF) and serum levels of anti-C. pneumoniae IgG in 46 relapsing-remitting (RR), 14 secondary progressive (SP) and 11 primary progressive (PP) MS patients grouped according to clinical and Magnetic Resonance Imaging (MRI) evidence of disease activity. Fifty-one patients with other inflammatory neurological disorders (OIND) and 52 with non-inflammatory neurological disorders (NIND) were used as controls. A C. pneumoniae-specific intrathecal IgG synthesis as detected by the relative specific index was present in a small proportion of MS (17%), OIND (22%) and NIND (2%) patients and was significantly more frequent in MS and in OIND than in NIND (p<0.001) and in SP and PP MS than in RR MS patients (p<0.02). Among the patients with C. pneumoniae-specific intratecally produced antibodies, CSF high-affinity anti-C. pneumoniae IgG were found in the majority of SP or PP MS, occasionally in OIND, but not in RR MS and NIND patients. These findings confirm that the presence of a humoral immune response to C. pneumoniae within the central nervous system (CNS) is not selectively restricted to MS, but is shared by several inflammatory neurological conditions. In addition, our results suggest that an intrathecal production of C. pneumoniae-specific high-affinity IgG can occur in a subset of patients with MS progressive forms in which a C. pneumoniae brain chronic persistent infection may play an important pathogenetic role.
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Postby SarahLonglands » Mon Jan 24, 2005 11:41 am

Thankyou, Daunted,

Yes, we have seen them all. Briefly, some centres are able to culture the organism and some, such as University College, London, are not, because they don't have the best equipment. Therefore, it is a bit like the needle in a haystack analogy: if you can't find the needle it doesn't mean it isn't there, just that you can't see it.

My treatment was entirely empirical because I was did not have diagnostically positive titres, but it certainly worked and I have not had anything remotely resembling a relapse since.

Sarah
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IgG and IgM

Postby butterfly » Mon Mar 14, 2005 8:48 am

Please forgive me for asking a question that has no doubt already been addresses in this extensive wealth of information about antibiodics and Chl.pn.

But here's my question:

After a mild sinus infection in January which was treated first with amoxocillin and then zithromax I had an MS relapse -- mostly sensory but involved an enhancing lesion on my thoracic spine and an increased lesion in my c-spine. Shortly after the relapse began (before I had the MRIs) I asked my family doctor to do blood work looking for Ch.pn. antiboidies. He complied and screened for ch. pn and several related bugs. The test came back negative for both IgG and IgM on all counts. In your opinion, does this mean anything in terms of possible infection as a trigger in my MS?

Thanks for any insight you can provide.

Christy
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Postby SarahLonglands » Mon Mar 14, 2005 4:46 pm

Hello Christy,

I have time and time again come across various upper respiratory tract and sinus infections as being at the very least trigger in someone's MS, yet hardly any neurologists seem to have noticed it: they just scoff and say that it is a coincidence. When they retire they might like to look back and realise how many times they have said this.

Unfortunately CPn and other related cell wall deficient organisms are not the easiest things to detect. As I said a few postings back, it is a little like the needle in a haystack analogy: just because you can't see it doesn't mean it isn't there. The best method of detecting was developed by Stratton at Vanderbilt and is now used but several other centres, if you have to use some other method of detecting, like me, you must take what you get. I was shown to have antibodies, but at an undiagnostic level, this didn't stop my improvement, as my Addenbrooke's neurologist now admits, which was beyond all expectation. At the time of diagnosis I was well and truly SPMS and not expected to improve at all. So at the moment, you just have to try to find someone willing to treat you empirically, easier I think in the UK, unfortunately, but things are changing all the time.

Sarah :?
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