Infection as a cause of multiple sclerosis
BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7373.1128 (Published 16 November 2002) Cite this as: BMJ 2002;325:1128All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Infection as a cause of multiple sclerosis.
I found this
editorial both fascinating and stimulating. Professor Murray
in his final paragraph states regarding aetiology 'a current popular
overarching theory postulates a genetically predisposed individual who
develops a viral infection that disrupts the vascular relations in the
blood-brain barrier and initiates an immune reaction .........' There
is one other factor capable of breaching the blood -brain barrier that
merits consideration - trauma.
The role of the blood-brain barrier in disease causation is
fundamental to other pathological processes and this may also have an
occasional relationship to trauma. It is also an impression
that the dramatic improvents in the prognosis of childhood leukaemia
has had much to do with the early administration of intrathecal
chemotherapy and the permeability of the blood brain-barrier to disease.
An essay on the pathophysiology of the blood -brain barrier - It's
permeability to disease, drugs, antibodies, infective agents, T & B
lymphocytes etc. would be welcome.
James E Parker
Competing interests:
None declared
Competing interests: No competing interests
I have never had strep, and at 18 started experiencing the joy of
primary progressive MS. I have an older sister, 10 years my senior and
she has had strep so many times it now only shows up as a rash. The older
sister is MS free. This puts a damper on strep, or is it that there is no
one answer to MS?
I did contract Lymes before the MS and as a child I was fed poorly.
My parents divorced when I was 4; father got me. Or is it the fact I was
exposed to toxins from his construction company? MS won't have an answer
to fit everyone affected by it. I'm not a doctor, but I have been living
with MS for 10 years and have talked to a lot of people. We can't afford
to be closed minded, this is what I have learned.
Thank you.
Competing interests:
I have pp MS and have never had strep.
Competing interests: No competing interests
Jock Murray speaks the same tired old mantras as does Embury.
Competing interests:
None declared
Competing interests: No competing interests
Dear Sir,
In Internal Medicine, streptococci induce vasculitis-phenomena.
I have observed some patients of post-streptococcal-cerebral
diseases.
Other post-streptococcal-reactive diseases associated are impetigo,
rheumatic fever [Sydenham's chorea].
I do hope streptococci should be on list of etiologic factors of multiple
sclerosis.
Competing interests:
None declared
Competing interests: No competing interests
The MS data base does not support the author's statement that "the
conclusion is that multiple sclerosis .. is determined by...an
environmental factor." The current evidence points to multiple
environmental factors acting in concert with multiple genes to result in
MS. One just has to look at the epidemiological evidence from Australia
where MS prevalence systematically increases 7 fold from tropical
Queensland to temperate Tasmania.(1) UVB supply and consequent vitamin D
supply can explain ~ 80% of this variance (2) but at least one more
environmental factor is required to precipitate the disease in the first
place. Progress in MS research will accelerate when the concept of
multiple environmental factors becomes a working hypothesis.
Given that the MS is regarded as an autoimmune disease by most MS
researchers, the environmental factors which should be regarded as prime
suspects are those which promote autoimmunity either by increasing the
activation of autoaggressive T cells or by decreasing suppresssion of such
pathogenic cells. A decrease in vitamin D, an CNS immune suppressant,(3)
would represent an example of the latter whereas an infectious agent which
contains epitopes which cross-react with myelin antigens(4) would be an
example of the former.
Using this line of reasoning, other potential environmetal factors which
need to be investigated include food proteins which can potentially result
in autoimmune cross-reactions (eg dairy proteins),(5) deficiencies in
omega 3 EFA which is a significant immune suppressant(6) and the lack of
childhood infections (hygiene hyothesis) which results in defective immune
suppression.(7)
One would hope that the determination of the environmental causes of MS
would once again become a focus for MS research because our best hope for
developing an effective therapy for MS is through such knowledge.
1. Hammond SR, English DR, McLeod JG.The age-range of risk of
developing multiple sclerosis: evidence from a migrant population in
Australia.Brain. 2000 May;123 ( Pt 5):968-74.
2.van der Mei IA, Ponsonby AL, Blizzard L, Dwyer T. Regional
variation in multiple sclerosis prevalence in Australia and its
association with ambient ultraviolet radiation. Neuroepidemiology. 2001
Aug;20(3):168-74.
3.Hayes CE. Vitamin D: a natural inhibitor of multiple sclerosis.
Proc Nutr Soc. 2000 Nov;59(4):531-5.
4.Wucherpfennig KW, Strominger JL. Molecular mimicry in T cell-
mediated autoimmunity: viral peptides activate human T cell clones
specific for myelin basic protein. Cell. 1995 Mar 10;80(5):695-705.
5.Winer S, Astsaturov I, Cheung RK, Schrade K, Gunaratnam L, Wood DD,
Moscarello MA, O'Connor P, McKerlie C, Becker DJ, Dosch HM. T cells of
multiple sclerosis patients target a common environmental peptide that
causes encephalitis in mice. J Immunol. 2001 Apr 1;166(7):4751-6.
6.Calder PC. n-3 polyunsaturated fatty acids and cytokine production
in health and disease.Ann Nutr Metab. 1997;41(4):203-34.
7.Sewell DL, Reinke EK, Hogan LH, Sandor M, Fabry Z.
Immunoregulation of CNS autoimmunity by helminth and mycobacterial
infections.Immunol Lett. 2002 Jun 3;82(1-2):101-10.
Competing interests:
None declared
Competing interests: No competing interests
Dear Sir,
in general medicine streptococci induce vasculitis.
I observed several cases of post-streptococcal-reactive-
cerebrovascular disease.
Other post-streptococcal-reactive diseases were associated:
Erysipelas, glomerulonephritis.
I do not understand, why streptococci are not on the list
of possible causes.
Sincerily Yours
Friedrich Flachsbart
Competing interests:
None declared
Competing interests: No competing interests
As a medical student in Cape Town in the late 1940s, we were taught
that Multiple Sclerosis was not found in the Southern Hemisphere. In the
post WW II period, with an extensive immigration from the UK and Europe,
it became part of the differential diagnosis of "unexplained" neurological
symptoms - first in new immigrants and later in South African born
patients. Could this support an infection hypothesis?
Competing interests:
None declared
Competing interests: No competing interests
Re: Re: Streptococci as a cause of multiple sclerosis
I had strep throat as a child many times. I then develped a strep
infection in my ankle requiring drainage and IV antibiotics for 2 weeks. I
also had impetago )sp) on my scalp at least twice. My point being, the
ankle strep was NOT secondary to a throat infection. It came on suddenly
with sever pain, swelling, heat, redness and a major fever over 104. There
were no breaks in the skin. Many people have strep and never know it. My
case was tracked to our family cat as the carrier. I suffered from joint
pains and swelling off and on from that point on but always tested
negative for Lyme (as many positive cases often will.) I believe MS is an
infection that is contagious to suseptible people. I think there is a link
between Type II diabetes and leukemia as well. My MS came about within
months of receiving a series of 3 rabies vaccines for my job. I think
playing around with the immune system is dangerous to those who are
genetically at risk.
Competing interests:
I have RRMS, dx'd in 1993.
Competing interests: No competing interests