Infection

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Infection

Postby bromley » Sat Sep 18, 2004 1:43 am

Dear all,

My first attack (no previous symptoms) coincided with a chest infection - I orginally thought the loss of feeling in my left arm / hand and my painful chest was all related. When the infection cleared up (with anti-biotics) the arm / hand problem remained and that's why I was referred to a neurologist. He said the chest infection was a red herring - I find it too coincidental.

Has anyone else had a similar experience - infection coinciding with attack?

Another question: I previously gave blood twice a year - does anyone know if I can still do so now that I have been diagnosed with MS?
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Postby Felly » Sat Sep 18, 2004 3:54 am

Hi Bromely,

Viral and bacterial infections both play a role in precipitating relapse or indeed first attack in MS. Though less evidence has been found for bacterial infections playing a role than viral.

Nevertheless, studies have been done that back up much anecdotal information that bacterial infections may play a role in triggering a relapse. Predominantly though evidence relates to influenza and upper respiratory infections (i.e mainly viral).

The reason for this is that such infections trigger the immune system. It's not that they are thought to cause MS but the MS is already there (just sleeping, possibly prodomal or at a level where the symptoms are just not noticeable to you) and by triggering the immune system you spark the MS in to activity. Viral infections do this directly while bacterial infections do this in a slightly different way but still trigger the immune system.

Interestingly in light of all the discussions about bacteria, some bacterias can actually evade the immune system triggering apoptosis (cell death). There is some speculation that people who die from flu are actually dying from a bacterial super-infection that follows the viral infection.

And on the other hand, of course, antibiotics cut off the immune response and generally weaken the immune reaction over time. Which cannot be ruled out as a reason for their affect on MS. Ie. it's not because of a bacterial infection but because the immune reaction is generally weakened with long term antibiotic medication.



Giving Blood
In theory, if you are not on steroids, antibiotics or an ABCR then there should be no reason for you not to give blood. In reality it seems very dependent on the the centre - as some will exclude you because you have a serious illness. Best to contact the National Service and ask them.

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Postby SarahLonglands » Sat Sep 18, 2004 5:09 am

Hello Bromley,

I think you need to read through all the posts under" Chlamydia pneumoniae: the possible cause of MS?" and my entry in the "regimens" section to help you make up your mind about this one.

Sarah
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Postby Felly » Sat Sep 18, 2004 6:52 am

Make up your mind? No offence but don't you think this is just a bit one sided?

I am not disputing that it may be a cause for some people with MS. ie. a subset. I am all for a debate but I would like to see a more balanced debate.

There have also been plenty of studies that dispute the link between C. pneumoniae and MS. And one of the ways antibiotics may be effective is in that they also over time weaken the immune reponse.

Here are a couple of articles disputing the link - just for a bit of balance:-)

First, this one done by my neurologist who is not one of the ms is an autoimmune disease group by any means. He is very open minded before that complaint is flung to dispute his work.

<shortened url>

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.


AAN: No Causal Role Found for Chlamydia Pneumoniae in Multiple Sclerosis

HONOLULU, HI -- April 2, 2003 -- Individuals who are infected with Chlamydia pneumoniae do not appear to be at increased risk of multiple sclerosis (MS), investigators reported here April 1st at the 55th Annual Meeting of the American Academy of Neurology.


While earlier studies examined a possible causal association between MS and C. pneumoniae, their cross-sectional design did not allow researchers to determine whether infection preceded the onset of MS.


Dr. Kassandra L. Munger, with Harvard School of Public Health, Boston, Massachusetts, and colleagues elsewhere, conducted a case-control study that included 3 million U.S. military personnel and over 121,466 subscribers to the Kaiser Permanente Medical Care Program.


At least one serum sample collected before the onset of MS was available among 83 Army personnel with MS and 46 cases among Kaiser-Permanente members, and all were included in this study. Two controls were matched to each case for age and sex, and army controls were additionally matched to cases by race and date of blood collection.


The MS diagnosis was determined by medical record review. The date of MS onset was the earliest date of neurologic symptoms attributed to MS as stated in the medical records.


Serum C. pneumoniae specific immunoglobulin G (IgG) antibody titer levels were measured using microimmunofluorescence.


Results showed no association between seropositivity for C. pneumoniae and an increased risk of MS. Overall, 69% of military personnel and 63% of Kaiser-Permanente subscribers were IgG seropositive compared with 66% and 53% of controls, respectively.


Geometric mean C. pneumoniae IgG titer levels among seropositive military personnel did not differ significantly between cases and controls, relapsing-remitting cases and controls, or primary progressive cases and controls. On the other hand, in the Kaiser Permanente group, geometric mean C. pneumoniae IgG titer levels were significantly higher in the seropositive cases than in controls (146 versus 64, P=0.009).


This difference was more dramatic for both primary and secondary progressive cases than for relapsing-remitting cases.


While their data did not identify a role for C. pneumonia infection in the etiology of MS, the possibility that infection with C. pneumonia before the onset of MS might trigger progressive disease cannot be eliminated, the investigators emphasized.

The study was supported by National Institutes of Health and the National Multiple Sclerosis Study.'



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Postby carolsue » Sat Sep 18, 2004 9:42 am

Thank you Felly, and Sarah, for sharing information from your two apparently different perspectives. I have benefited from both of you. It's so critical that we keep open minds and encourage healthy debate. I hope you two will keep it up.

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Postby bromley » Sat Sep 18, 2004 12:07 pm

Thanks for your responses.

As I'm from a non medical / science background (history / accountancy) I'm trying to get a layman's understanding of the possible causes / theories relating to ms - there appears to be many.

The response to the Crohns disease article seemed incredibly upbeat but I'm always unsure as to what really is a step forward in this area.

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Postby Daunted » Sat Sep 18, 2004 12:37 pm

Felly,

I agree that ALL MS research and related theories are quite tentative at this point. However, in the spirit of debate (the only way we really ever learn anything, in my opinion), here are couple of counter-points to your post.

1. Siriam and the Vanderbilt group have hypothesized that one problem with other researchers finding cPN is the variability in laboratory procedures from center to center. There hasn't been enough research to render this idea implausible yet. In the long-term, we'll find out- in the short-term, if Vanderbilt were to tell me I had cPN in my CSF, I personally would believe them. Others can and should make their own decisions.

2. Perhaps antibiotics are neuroprotective and that's the reason they work- but I don't buy the idea that the lower immunse response over time. Some of the case examples (out of Vanderbilt, for example) show relatively quick response- that subset can't be explained that way, anyway.

3. In any case, since MS is tremendously complicated to diagnosis and treat (as is Lyme), one wonders why all these doctors are so reluctant to at least TRY this treatment. It shows how gutless they are, in my opinion.

(Because it seems quite possible to me that there are a sub-set of those diagnosed with MS who would have terrific response to antibiotics, yet they are unlikely to ever have them prescribed. As has been pointed out, if any other part of the body showed such a constellation of symptoms with unknown etiology, a bacterium would be suspected and treated in search of response...yet in terms of MS, this does not happen).

Yes, the research has a long way to go. But, frankly, I think there's enough out for this to be a reasonable intervention to TRY. There's also enough research for doctors to stop being gutless and try to help the desperate patients suffering from these symptoms, rather than simply covering their own asses, which is what I observe here in the U.S.
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Postby Felly » Sat Sep 18, 2004 2:09 pm

I agree that ALL MS research and related theories are quite tentative at this point. However, in the spirit of debate (the only way we really ever learn anything, in my opinion), here are couple of counter-points to your post.



First of all, I am not disputing the theory per se. I just like to see all sides of the argument and so far there has not been the case on this forum.

I hope people will make up their minds about treatment but one needs as much information as possible to do this. I mean also the negative aspects so that there is a real informed choice.

I have a real problem with believing anything I read without putting some research in to it myself, hence getting myself an MSc in biochemistry and probably starting my phd next year.

There are lots of counter arguments out there to the Siriam study and I don't like the implication made here that they are all wrong. Only bad science stands on the defence that only it can be right.

If I was told that I had cPN in my CSF I would be more than willing to try this regime. As I said in my above posts I am absolutely willing to believe that cPN could provide the causal link in a sub set of patients. But I don't think it will prove to be 100% the causal link in all patients. And perhaps because its pills it doesn't seem as bad as the CRABs but there is still many risks involved. Long term use can cause neuropathy, liver damage etc etc. Not every person taking it but how it does mean monitoring is essential.


2. Perhaps antibiotics are neuroprotective and that's the reason they work- but I don't buy the idea that the lower immunse response over time. Some of the case examples (out of Vanderbilt, for example) show relatively quick response- that subset can't be explained that way, anyway.


Not all antibiotics are neuroprotective, but minocyline certainly is. Again I am not suggesting that it is the immune lowering effect in all cases but perhaps in some case this is what is happening.

As far lowered immune response - have a look at the various articles on pub med and you will see that the antibiotics in this regime are the most potent immune suppressor, furthermore there have been very mixed results in the use of them in the treatment of cPN. Some such as roxithromycin (as in this regime) increase immune reaction within the first 14 days of use and then radically lower it.



(Because it seems quite possible to me that there are a sub-set of those diagnosed with MS who would have terrific response to antibiotics, yet they are unlikely to ever have them prescribed. As has been pointed out, if any other part of the body showed such a constellation of symptoms with unknown etiology, a bacterium would be suspected and treated in search of response...yet in terms of MS, this does not happen).


I completely agree about the sub set. I think it a little unfair to say that baterium has never been suspected in MS, research such as that by Siriam has been going on for years, in to both baterial and viral causes of MS. It just hasn't up to now shown a profound causal link. Even Siriam is being cautious about making too emphatic statements.

Yes, the research has a long way to go. But, frankly, I think there's enough out for this to be a reasonable intervention to TRY. There's also enough research for doctors to stop being gutless and try to help the desperate patients suffering from these symptoms, rather than simply covering their own asses, which is what I observe here in the U.S


Sure, as long as people are aware the risks. Some antibiotics are more potent than others. I intend to take minocyline from next week (because of the neuroprotective link), compared to some of antibiotics it is a walk in the park and there is substantially more evidence that minocyline is a neuroprotective agent than that cPN is the cause of MS.

Anyway folks this is my last post on the subject or any for the matter. Maybe I will pop back sometime but for now it's goodbye.

ciao,
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Postby Xenova » Sat Sep 18, 2004 3:01 pm

I too had an excacerbation that coincided with what I believe was a chest infection. For the past few years I have dealt with a constant cold/flu-like illness. It got worse while at the same time that I was sent to a neurologist who diagnosed me with MS.

Both of the GPs I visited could not tell me exactly what I had. At the peak, I had bronchitis which produced thick phlegm. I also had hot flashes, sinusitis, and other related symptoms.

I tend to think that the origins of MS could be based on several factors, one of which is related to a bacteria.
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Postby finn » Sat Sep 18, 2004 3:10 pm

Sorry, time to leave the board.

-finn
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Postby Arron » Sat Sep 18, 2004 3:50 pm

For many years, the pendulum swung against the idea of an infectious agent being the source of MS, and the autoimmunity idea-- that "something" was going wrong with the immune system causing it to attack components of the CNS, predominated. Lately, the pendulum has swung back to the original thought that MS was caused by an infection and much research is occurring.

The fact is, no one (yet) knows. The infectious idea is attractive to many, particularly because it is far more manageable. Anti-viral and bacterial drugs exist TODAY, and under this code of thought, the average MS'er can take some control over their treatment that does not involve injections. Adding fuel to this fire are research studies such as the one about Crohn's and bacteria, the research on minocycline and MS, and the personal anecdotes and microbiologist's opinion shared by Anecdote, Byron, and others.

Countering the last sentence is the fact that these antibiotics are also neuroprotective. So the fact that they show benefit for MS might not be because they kill off an infectious agent responsible for MS (or progression), but due to their neuroprotective properties.

The key questions are:

1) Do bacteria or viruses cause MS?
1a) Do bacteria or viruses cause MS only in a particular subtype of the disease?
2) If they don't cause it, do bacteria or viruses make someone's MS worse?
3) Do MS'ers generally respond well to antibiotic treatment?
4) If they do, does treating an MS'er with antibiotics cause improvement via the antibiotic action of the drug, or the neuroprotective one?

Again, we don't know... yet. The holes are being filled in, though... very rapidly.
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Postby Byron » Sat Sep 18, 2004 4:15 pm

The explanation that Minocycline is useful for MS because in the long-term it reduces the strength of the immune system seems to be a total red herring to me.

Anecdotally, when an MS patient takes antibiotics, nothing of note happens for about two days. Then, there is a significant flareup of many, if not all symptoms already reported. Four to five days later, these symptoms go away. Along with that, the fatigue that is so common to MS sufferers also vanishes. Completely. Sleep patterns are normal. The word "cured" is not inappropriate to describe the results. In my personal experience, for one data point, the patient goes from spending weekends sleeping (or trying to), to spending weekends working in the backyard.

Now, if you do not accept the infection-model for MS, how is all of this dramatic, sudden improvement explained? Why would a patient get worse before getting better? I can see an easy explanation for getting worse: if MS is an autoimmune disease, then something that helps the immune system will make things worse. Most of the symptoms reported in the past few years re-appear. But then, why so dramatically better? The response is immediate - it takes 48 hours from the peak of the flareup to a total absence of symptoms.

This can all be explained very easily if one accepts the germ theory of disease for MS: for one, the fatigue that patients suffer is caused by the body fighting a long term infection. It takes about two days for the antibiotics to start killing off the bacteria. The bacteria, when they die, release toxins which cause flareups. In five days or so (depending on the bacterial load), all of these toxins have been flushed out and so the patient is cured. The fatigue vanishes because the body is no longer fighting the infection.

Please note that I have been careful to not mention Chlamydia pneumoniae so far. It might or might not be responsible for MS. But the improvements that are caused by teteracycline-class antibiotics are difficult to deny, and the course of the disease, both ups and downs while taking these antibiotics can be acceptably explained by saying that they are cleaning up an infection.
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Postby SarahLonglands » Sun Sep 19, 2004 6:28 am

Gosh, I was only away for a day and all this awaited me on my return!

I only started my posts because of the results of my MRI scan 6 months after starting treatment. No misdiagnosis possible here, having seen the original scans. Nobody on that thread seemed inclined to raise a debate: was I supposed to start one myself? I could argue with myself all day, but there sees very little point. I was talking solely from my own experience, which I thought some people might like to share.


Once one has been diagnosed with progressive MS in the UK as Felly will no doubt know, none of the ABCRs are available. The only possible treatment as and when needed is intravenous steroids. Other than that, it is an appointment with the MS nurse, then go away and get on with whatever the disease throws at you. When my husband started me on antibiotics it was not with any expectation of success. However, we became more hopeful when I started a Herxheimer reaction very soon afterwards, showing that there was a chronic infection somewhere.

No-one ever claimed that Cpn was responsible for all MS; MS could well be polymicrobial. Cpn makes holes in small blood vessels (you can see this in retinal vasculitis where a fluorescein dye test is used) and makes holes in the BB barrier (that is what causes the white spots in a Gd enhanced MRI scan) and other blood-borne organisms could get into the brain through these holes. Even dormant viruses.

1. The Furrows et al paper. Negative PCR for Cpn in patients with MS. Laboratory technique is all-important. This is only one of many negative studies, which is not in any way to criticize the people involved, since Cpn is notoriously difficult to work with. Where the much more sensitive techniques used at Vanderbilt have been duplicated (round the world) positive results have been obtained. Cpn becomes strictly intracellular in chronic disease, so you would expect only tiny quantities of bacterial DNA. More importantly, Cpn RNA has been found in the CNS of MS patients and others with inflammatory CNS disease, actively synthesizing hsp60*. This is a protein thought to lie at the root of many chronic diseases which have an autoimmune component.
<shortened url>
*heat shock protein 60

2. The Munger et al paper. The authors say that that they found no serological evidence of Cpn in MS, but if you read the paper you find that there is a statistically significant rise in titres in people with progressive as opposed to RRMS. This is especially significant because it was not remarked upon by the authors. It shows that, when Cpn becomes chronically active and immunostimulatory, the disease turns progressive. (This correlates well with another study (Hintzen, Rotterdam) which showed an association between new respiratory infection with Cpn and relapse in RRMS.) <shortened url>

As far lowered immune response - have a look at the various articles on pub med and you will see that the antibiotics in this regime are the most potent immune suppressor, furthermore there have been very mixed results in the use of them in the treatment of cPN. Some such as roxithromycin (as in this regime) increase immune reaction within the first 14 days of use and then radically lower it.

Funnily enough, my increased immune reaction occurred before roxithromycin was added to my regime, because we had to order it from France. Also the antibiotics used in the recent small Vanderbilt trial were chosen specifically for their lack of immunomodulatary properties.

But when other researchers tried to confirm Sriram's results, many of them failed. Skepticism has been running high, and in April 2001, the title of a review in Trends in Microbiology bluntly summed up the feeling of many researchers: "Chlamydia pneumoniae and multiple sclerosis; no significant association."

Sriram disputes this finding, noting that other labs used different methods than his and might have missed the bacteria. To resolve the issue, he and the other researchers agreed to conduct a blind test of cerebrospinal fluid from the same set of MS patients and controls. Sriram found Chlamydia in 73% of the people with MS and 23% of those without. The other three labs found no evidence of Chlamydia at all.

The above quote is from Finn's link, to show how some labs find it so difficult culture c pn.

And here is a link to an abstract, <shortened url> in the full article of which one can find the following quote:
PMS: 'The likelihood of remission after such an interval [1 year] is low.
At my worst just over a year ago I would have measured 6 - 6.5 on the EDSS scale, but now I am barely 2, this after being progressive for, in all honesty, about three years. This is why I say it is worth trying, never mind lumbar punctures and all that: I have never had one.

That's all for now, because Byron and Arron have already said what else I would have said so there is little point in saying more for now.

Sarah
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from a medical microbiologist (David Wheldon)

Postby dwheldon » Mon Sep 20, 2004 8:10 am

I certainly wouldn't claim that Chlamydia pneumoniae is the cause of MS in everyone with the disease, though the evidence for a connection with at least some subsets is now very strong.

A risk/benefit analysis would seem to favour a trial of antibiotics - they are fairly harmless, and the benefits are potentially very significant. But the outcome may not be certain. MS is a complex, multifactorial and many-phased illness, and it's possible that a number of different entities may be encompassed by the same diagnostic label.

Some of the patients I have treated with antibiotics are doing well; they are mostly those with RR or early PMS. Others, particularly those with late disease or with dense deficits of long standing, seem to show no benefit. But a trial - say for three to six months - of doxycycline (with or without roxithromycin) would seem reasonable.

A note about the flu-like reactions which may be seen when starting doxycycline or minocycline in those with active disease. I doubt if one would get these reactions were the antibiotics functioning only as immune modulators.

It is very important to say that a lack of a reaction does not predict a poor outcome of treatment; it may just reflect a small or local bacterial load or a quiescent infection.
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Postby CCmom » Mon Sep 20, 2004 12:54 pm

We had the "other side" of the viral/bacterial spectrum at the onset of Colby's first exacerbation. He had a really severe stomach virus one week prior to the optic neuritis setting in, then hemiparalysis followed.

His initial diagnosis was encephalomyelitis, and he was treated with i.v. steroids only.

Just thought I would throw him into the mix. The antibiotic theory is highly intriguing to me, since I believe far too many people are misdiagnosed to start with, and could benefit from antibiotic therapy, if only their docs would admit that they don't know and try it.

I have a friend on another board with an MS diagnosis, yet she also has severe acne. Everytime she uses doxycycline for her acne, her MS symptoms improve. Coincidence? I would be afraid to say that!

Have a great day!

Kim
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