Infectious cause

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Infectious cause

Postby bromley » Fri Dec 16, 2005 1:49 pm

Dear all,

As many of you are aware (I've bored you to death), I'm a big believer
that MS is caused / or triggered by a virus (or other infectious agent). EVB is my prime suspect, mainly because I had Glandular Fever quite badly at 15 (the only teenage / adult illness I had). My first MS attack came out of the blue at 39.

The so called outbreaks of MS also point to an infectious agent - the problem is that MS may differ in how quickly it surfaces in each individual following an infection. One can imagine an infection working its way through a town, school, housing estate etc. Those with the genetic susceptibility who caught the infection would then come down with MS - one, five, ten years later.

In some families there can be more than one case of MS. I have seen that in one Canadian family 14 members came down with MS. I also note that some users of this site with MS have parents / siblings / children with MS. The genetic susceptibility angle no doubt plays a role, but so must infections - a virus such as EBV would probably infect most of the family members.

From 2000-2002, I shared an office with two other colleagues - one male, one female. I had my first MS attack in March 2004 and was diagnosed in May 2004. I heard today from the male whom I shared an office with that he has just been diagnosed with MS. I find this quite incredible and, to me, reinforces my belief that an infectious agent is the cause / trigger of MS. As two straight men, the infection could not have passed by kissing / sexual contact, and I can say for sure that we never shared a mug etc.

I know this fact is of limited value by itself, but given that the chance of a UK male getting the disease is 1:1000, the chances of two males in the same small office being diagnosed within a relatively short timescale must be very rare (but not if an infectious agent played a part). The other interesting fact is that I asked him if he had had Glandular Fever (EBV). He is 29, but told me that he had a bad bout about six years ago (before I shared an office with him).

Does anyone else have a similar story which seems to defy probability and points to MS as having an infectious basis?


Ian
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Postby faithful » Fri Dec 16, 2005 5:05 pm

I just found out that my next door neighbor when I was a teenager (1972-1978) was diagnosed in 2000. I was diagnosed in 1997. We were neighbors in Denver, Colorado. I understand that Colorado has one of the highest rates of MS in the U.S. I had a bad case of mononucleosis in 1979. I think mono is the same thing as what you refer to as glandular fever?
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Postby LisaBee » Fri Dec 16, 2005 6:20 pm

Ian,

Here is the abstract of the Swedish study I remember seeing on PubMed and mentioned in another post. It lends support to your infectious triggering theory....I'd like to get the whole paper. It should be interesting.

^^^^^^^

Acta Neurol Scand. 2005 April 111(4):238-46
Further considerations on the distribution of multiple sclerosis in Sweden.

Landtblom AM, Riise T, Kurtzke JF.

Division of Neurology, University Hospital, Linkoping, Sweden. anne-marie.landtblom@lio.se

OBJECTIVES: The geographic distribution of multiple sclerosis (MS) in Sweden over time was compared in order to analyze homogeneity. METHODS: The distribution of MS was compared among three nationwide resources: 1301 hospital cases 1925-1934; 5425 deaths 1952-1992; and 11,371 disability pension recipients 1971-1994. RESULTS: Distributions by county (lan) were markedly non-homogenous, with greatest variations in the early prevalence series (16-232% of the national mean), less within the death data (75-170%), and least for the disability series (87-128%). Maximal rates for MS in the early prevalence series were found for the cluster of seven counties surrounding the two major lakes of south central Sweden, as well as for one region on the northern shore of the Bay of Bothnia, and another also off the Bay north of Stockholm. CONCLUSION: Though the epidemiologic sources are quite different, they are internally consistent and thus provide three consecutive cross-sectional views of the distribution over time. When considered together the data may be compatible with a thesis of the origin and spread of MS within Sweden from the south-central inland lake regions of the country. Such spread within a half century is too rapid for a genetic cause, including HLA patterns.

PMID: 15740575 [PubMed - indexed for MEDLINE]
^^^^^^^^^
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Postby bromley » Sat Dec 17, 2005 2:58 am

Faithful,

In the UK we call it Glandular Fever (or the kissing disease). I think in the US they call it mononucleosis. It disturbs me somewhat that an innocent kiss with a pretty girl in the late 1970s has had such a detrimental effect on my life.

I saw an article a few months ago that said Colorado had a rate of 1 in 500 (also New England was high). If I was in the US I'd be packing my camper van and heading off to New Mexico.

Here is an extract from Professor Kurtzke, a leading US MS expert:

'The geographic distribution of MS has been changing markedly, with a spread or diffusion from an apparent origin in Sweden. Migrants from high MS areas to low keep the risk of their birthplace only if they move beyond age 15. Those moving from low to high acquire an even higher risk than the natives, for moves between birth and age 40 or so. MS occurred in the Faroe Islands as successive epidemics following their occupation by British troops in World War II. The migration and epidemic findings are compatible with the view that clinical MS is the rare late result of a unique, but unknown, widespread, persistent infection, which is transmissible only between age 13 to 26 or so, and which is mostly acquired at earliest exposure between age 11 and 45, followed by a long latent or incubation period between acquisition and clinical onset'.


My recent posting about Canadian research and childhood MS showed that children with MS had mostly been infected with EBV. Healthy children only had a small number of EBV cases in the sample.

So in a few years time, when an MS researcher claims the Nobel prize for medicine, for identifying EBV as a trigger cause of MS, some of the prize money should find its way to Arron and those that operate the site.

What can we do if EBV is to blame? I'm not sure but it looks as if the Swedes are to blame, so I will not be buying any more ABBA records or Volvo cars. I'd forgiven the Vikings for raping and pillaging my country in the 6-8th centuries, but leaving behind such a vile disease is going too far.

Ian

PS It seems to me that either the infection e.g. EBV, stays in our CNS and the immune sytem does its best to rid us of it (causing lots of collateral damage) or that having the infection leads to the immune system going wrong which then attack our CNS cells etc. My recent post on MRI scans shows that attacks are on-going constantly - not just when we have an exacerbation. This again, points to an infectious agent throughout our CNS. Dampening down the immune system through immuno-suppressants or heavy duty therapies may not be enough if the infection persists and continues to do damage. The theory that a bacteria could be the infectious agent is a much more attractive given the anti-biotics available. However,a virus seems more likely but is more difficult to deal with. But there is hope. When HIV was identified as the cause of AIDs, very effective treatments were identified - hopefully this will happen with MS.
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Postby SarahLonglands » Sat Dec 17, 2005 4:12 am

Yes, but you must remember the fact that EBV is a fellow traveller of CPn, but just easier to isolate. I still have EBV in my system but have cleared the CPn. I have largely cleared the MS as well.

Sarah 8)
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
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Postby bromley » Sat Dec 17, 2005 5:28 am

Sarah,

Thanks - I don't have the medical background to really comment on this. I'm just basing it on my own experience with EBV.

Perhaps you were the 17 year old girl I kissed in Trafalgar Square in 1979?

No, you're too posh to have been a Punk Rocker!"

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Postby SarahLonglands » Sat Dec 17, 2005 6:21 am

You kissed a punk rocker did you? No, it wasn't me, I was nineteen or twenty!

No, David says EBV can't be the culprit as anyone with even a smattering of neuropathology would know. Early MS even before the symptoms show, cause a vasculitis which EBV never does. CPn does, though.

Have a look at these page.:

The first is a physicians page:

http://www.CPn Help.org/?q=node/70

The second is a treatment page:

http://www.CPn Help.org/?q=treatment

This is the story of a Chicago physician:

http://www.CPn Help.org/?q=icestory

And this is me, complete with evidence that I am a real person

http://www.CPn Help.org/?q=blog&from=18

You can also find out about more from other people who write here, such as Katman, a physician's wife and former concert violinist, Mrhodes40 (Marie) who is a nurse, and many others.

Going now to get some more freshly ground coffee from the Aga! :wink:

Sarah
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
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Re: Infectious cause

Postby NHE » Sat Dec 17, 2005 6:42 am

Bromley wrote:I'm a big believer
that MS is caused / or triggered by a virus (or other infectious agent).

I think the viral link might be tied to molecular mimicry. In effect, a protein associated with the virus triggers an immune response. This immune response is remembered. At some later point in time the immune system starts recognizing proteins in myelin which appear similar in structure to the viral protein. This process could be enhanced by epitope spreading. That is, once the immune system recognizes a target antigen, it will subsequently also start to recognize antigens which are similar but not 100% identical.

I've also recently started reading about a potential link with endogenous retroviruses (ERV). To the best of my current understanding, these are bits of viral like DNA sequences that exist within our own DNA (perhaps they're actual viral genes that have snuck into the human genome). The product of the ERVs is a viral like protein which then triggers an immune response. I have read that it's believed that an external stimulus, such as burn trauma, can activate the ERV sequences and that this could explain why some burn trauma patients fair much better than others even though the extent of tissue damage is similar. I apologize for the lack of links at this time due to the preliminary status of my research into this subject area, however a search on PubMed should yield several papers on ERVs.

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Siblings also have MS

Postby wilson » Sat Dec 17, 2005 8:44 am

Bromley,

I was diagnosed with MS almost 2 years ago. My MRI showed 9 lesions in T2 area. My brother was diagnosed 5 years ago with MS and my sister was diagnosed with fibromyalgia 11 years ago.

I believe there is two distinct possibilities with this anomaly: Due to genetics, my family is very susceptible to neurological disorders OR my MS is caused by an infectious disease.

I just start the abx treatment a month ago. Sometimes it just takes... a leap of faith?
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Postby Jaded » Sat Dec 17, 2005 9:29 am

Hi there Bromeley

I was never sick as a child - I never missed a day of school, college or Uni, and the only time I recall being really laid up by and infection was when I was about 24/25. I am not sure what it was - the emergency GP prescribed some abx and I was in bed for a week. My first MS event happened within a year of that. Coincidence?

I don't personally know anyone with MS. My partner at that time, who I am still in touch with, is still fit and well.

Does that fit your theory? :?

My parents are migrants - came from the med before I was born. And I am on the abx regime (since August this year - dx'd feb/march this year).

J. :)
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Postby Melody » Sat Dec 17, 2005 12:46 pm

John had anaphylactic shock due to a tree nut allergy in Dec 1997 and he went blind in his in eye on Feb 9 1998. I believe John's MS was triggered by allergies at this point. It took till Jan 2005 for a DX of MS. I believe his body had a hard fight on it's hands due to the 5 shots of adrenalin needed to pull him out of shock. I now believe something went wrong with his immune system at that time to bring on his MS. I also believe because of his allergies he was a ticking time bomb for something to go wrong. His immune system has always been out of sync so an auto immune disease does not seem out of right field in the circumstances. I also believe now that we are controlling John's intolerances and allergens which is totally controllable with diligence that he will continue to keep his Ms under control. Yes I'm taping on wood I'm not willing to chance a jinx. I also believe the inflammation caused by the attacks must be minimized and that is where his stuff listed below comes into play. My Opinions only
Last edited by Melody on Sun Dec 18, 2005 7:12 am, edited 1 time in total.
John was diagnosed Jan 2005. On lipitor 20mg .On Copaxone since July 4,2005. Vitamin D3 2000iu-4000iu (depending on sunshine months)June 10 2005(RX::Dr. O'Connor) Omega 3 as well Turmeric since April 2005. Q10 60mg. 1500mg liquid Glucosamine Nov 2005.
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Postby bromley » Sun Dec 18, 2005 6:03 am

Melody,

I think MS will turn out to be many different diseases with probably many different triggers / causes. I suspect that a virus such as EBV might be the trigger / cause for many, but that in other cases trauma, allergies, polution etc may be the trigger / cause. You've only got to look at the variation in the effectiveness of the current treatments (some do well on CRABs, others see no benefit, and also for abx) to see that it is unlikely to be just one disease.

I'm impressed by the regime your husband is following. I imagine in years to come this will be the approach to dealing with this disease. DOn't forget to feed him lots of Turkey at Christmas.

Wish you husband well.


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Postby Toyoterry » Mon Dec 19, 2005 1:08 am

The idea of an ifectious cause seems to apply to my case. I live in Lincoln Nebraska but my family originally comes from Alabama. They moved to Lincoln in 1959. At that time they had 5 children. In 1959 the two youngest were 5 and 11 years old. My twin brother and I were born in 1962. So at the time (1962) my parents had 4 children under the age of 14. The other children having been raised in Alabama. We have checked our family history and on both sides of the family there is no know case of MS. It seems strange to me that of the 4 of us who spent our childhood here in Nebraska, 2 of us have been diagnosed with MS and my twin brother is showing symptoms. We share the same genetics with our siblings but something, either the geographic location or an exposure to some infectious agent seems to be a logical hypothesis. If age of exposure is a factor, one might note that were the only siblings who spent our childhood in Nebraska, a cold and cloudy state for long periods during any year. Maybe the fact that our siblings were older protected them. Just a few thoughts.
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Postby bromley » Mon Dec 19, 2005 7:17 am

Toyoterry,

Sorry to hear that a number of your family have been affected by MS. One could imagine that a virus affected some of your family at the wrong age. Might also be that some other factor - such as vitamin D deficiency made you more prone.

Can I ask if all those affected have the same type of MS. I mentioned before that there are families with multiple cases of MS. However, family members can have different types of MS eg RR or PP. This points to MS being one disease!

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Postby Toyoterry » Mon Dec 19, 2005 2:42 pm

My older brother had symptoms that were very different than mine. His symptoms seemed to be more like PP than mine which seem more like RR. He was slowly going blind and had bladder problems while my major problem is stiffness. My symptoms seem to come and go and vary in intensity. He just seemed to slowly get worse with no major attacks. I speak of him in past tense because sadly he died of lung cancer at age 43. My twin brother, like my self, has had minor symptoms since he was a teenager but lately they have been gettting worse as he had his first significant attack this year at age 43. He has some neuropathy like myself but he has trouble using his hands, especially concerning his fine motor skills.
Terry
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