Looks like it pays to stay healthy if one has MS. Take immunizations, avoid infections and get treated immediately. I even took a daily VALTREX for many, many years. I think a series of viral infection caused my MS and caused some of my severe relapses.
1: Am J Phys Med Rehabil 1995 Nov-Dec;74(6):415-8
Role of bacterial infection in exacerbation of multiple sclerosis.
Rapp NS, Gilroy J, Lerner AM.
Department of Physical Medicine and Rehabilitation, William Beaumont
Hospital, Royal Oak, Michigan 48073, USA.
One hundred consecutive patients admitted to the hospital with a diagnosis
of exacerbation of multiple sclerosis were evaluated for an infectious
process. All patients received a complete blood count, urinalysis, urine
culture with susceptibility studies, blood cultures, and a chest x-ray at
the time of admission. A control group of 55 patients carrying the diagnosis
of multiple sclerosis but without symptoms of neurologic decline were also
studied. Thirty-five percent of patients experiencing exacerbation of their
disease were identified as having a significant bacterial infection compared
with 11% in the control group with quiescent disease.
These results were
significant with a P value of < 0.001. When presumptive viral and bacterial
infections diagnosed before admission were included, almost 50% of patients
could have had an exacerbation of their disease in response to an infectious
process. Bacterial infection might well play a role in precipitating relapse
in multiple sclerosis as well as influencing treatment.
PMID: 8534384 [PubMed - indexed for MEDLINE]
1: Neurology 2002 Dec 24;59(12):1837-43
Immunization and MS: a summary of published evidence and recommendations.
Rutschmann OT, McCrory DC, Matchar DB; Immunization Panel of the Multiple
Sclerosis Council for Clinical Practice Guidelines.
Duke Center for Clinical Health Policy Research, Duke University Medical
Center, Durham, NC, USA.
OBJECTIVE: To review the risk of MS exacerbations after infectious episodes
potentially preventable by vaccination, and the risks and benefits of
immunizing patients with MS. METHODS: The authors searched MEDLINE (1966 to
U.S. National Library of Medicine, Bethesda, MD), HealthSTAR, and Cumulative
Index to Nursing and Allied Health Literature (CINAHL) database (Cinahl
Information Systems, Glendale, CA) for English-language articles. Each study
was summarized and rated for quality of evidence. Then feasible data were
pooled and analyzed in meta-analysis. RESULTS: The risk of contracting
common infectious diseases in patients with MS is not well established.
There is strong evidence for an increased risk of MS exacerbations during
weeks around an infectious episode. There is strong evidence against an
increased risk of MS exacerbation after influenza immunization. There is no
evidence that hepatitis B, varicella, tetanus, or Bacille Calmette-Guerin
vaccines increase the risk of MS exacerbations. Insufficient evidence was
found for other vaccines. CONCLUSIONS:
Evidence supports 1) strategies to minimize the risk of acquiring infectious
diseases that may trigger exacerbations of MS; and 2) the safety of using
influenza, hepatitis B, varicella, tetanus, and Bacille Calmette-Guerin
(BCG) vaccines in patients with MS.
PMID: 12499473 [PubMed - indexed for MEDLINE]
1: J Periodontol 2002 May;73(5):511-6
Effects of Porphyromonas gingivalis on the central nervous system:
activation of glial cells and exacerbation of experimental autoimmune
Shapira L, Ayalon S, Brenner T.
Department of Periodontology, Faculty of Dental Medicine, Hadassah
University Hospital and Hebrew University Medical Center, Jerusalem, Israel.
BACKGROUND: Several studies have suggested that peripheral inflammation may
be involved in the etiology of multiple sclerosis (MS), a demyelinating
disease of the central nervous system (CNS). T-cells activated in the
periphery enter the CNS, leading to demyelination and axonal loss. We
hypothesized that peripheral infection by Porphyromonas gingivalis can
affect pathological processes in the CNS and aggravate MS. METHODS: Glial
cells derived from rat brains were cultured and stimulated with P.
gingivalis or P. gingivalis lipopolysaccharide (LPS). Secretion of nitric
oxide (NO) and prostaglandin E2 (PGE2) was determined. In addition, we
examined the proliferation of lymphocytes harvested from P.
gingivalis-immunized mice in response to stimulation by echephalitogenic
proteins. The effect of peripheral inflammation induced by P. gingivalis on
the clinical course of the disease was tested in experimental autoimmune
encephalomyelitis (EAE), a mouse model used for the study of MS. RESULTS: P.
gingivalis LPS and heat-killed bacteria induced secretion of the
proinflammatory mediators NO and PGE2 by CNS glial cells. Lymphocytes
derived from P. gingivalis-immunized mice proliferated in the presence of
the echephalitogenic protein myelin basic protein. Injection of P.
gingivalis into subcutaneous chambers in mice, followed by EAE induction led
to aggravation of the disease. CONCLUSIONS: The present study provides
evidence that infection with a periodontal pathogen, such as P. gingivalis,
may play a role in the pathogenesis of CNS inflammatory disorders such as
PMID: 12027253 [PubMed - indexed for MEDLINE]
1: J Neurovirol 2001 Jun;7(3):220-7
Viruses can silently prime for and trigger central nervous system autoimmune
Theil DJ, Tsunoda I, Rodriguez F, Whitton JL, Fujinami RS.
Department of Neurology, University of Utah School of Medicine, Salt Lake
City, Utah 84132, USA.
Although many viruses have been isolated from patients with multiple
sclerosis (MS), as yet, no one agent has been demonstrated to cause MS. In
contrast, epidemiological data indicate that viral infections are associated
with exacerbations of MS. Here, we present data showing that virus
infections can subclinically prime animals for central nervous system (CNS)
autoimmune disease; long after the original infection has been eradicated, a
nonspecific challenge/infection can trigger an exacerbation. The priming
infectious agent must show molecular mimicry with self-CNS antigens such as
glial fibrillary acidic protein (GFAP), myelin associated glycoprotein (MAG)
or myelin proteolipid protein (PLP). The subsequent challenge, however, may
be nonspecific; complete Freund's adjuvant (CFA), or infection with a
recombinant vaccinia virus encoding an irrelevant protein, could trigger CNS
disease. In the CNS, we could detect a mononuclear cell infiltration, but no
demyelination was found. However, if the pathogenesis of MS is similar to
that of this novel animal model for CNS autoimmune disease, our findings
could help explain why exacerbations of MS are often associated with a
variety of different viral infections.
PMID: 11517396 [PubMed - indexed for MEDLINE]
1: Axone 1998 Jun;19(4):67-70
Urinary tract infections may trigger relapse in multiple sclerosis.
Metz LM, McGuinness SD, Harris C.
Multiple Sclerosis Clinic, Foothills Hospital, Calgary, AB.
Multiple Sclerosis (MS), a demyelinating disease of the central nervous
system, is the most common neurological disease affecting young adults in
North America and, in the majority of cases, is associated with accumulating
disability. Urinary tract dysfunction affects up to 90% of the MS
population, and urinary tract infections are encountered in up to 74% of the
tested population. Viral infections have previously been shown to trigger
acute exacerbation and it is our experience that urinary tract infection
also commonly precedes relapse, and, when recurrent, is associated with
neurologic progression. We present three case studies from our MS Clinic
where recurrent UTI was associated with acute exacerbation and neurologic
progression refractory to intravenous steroid treatment. Interferons,
protein signaling molecules, have recently been found to play a role in
acute exacerbation and disease progression in individuals with MS. Viral
infections induce interferon release which may activate T cells to produce
gamma-interferon. Interferon-gamma precipitates relapse and stimulates
production of tumour necrosis factor-alpha, a cytokine directly toxic to
oligodendrocytes. Bacterial infections similarly induce interferon release
and may activate immune pathways that result in MS exacerbation and
PMID: 9849133 [PubMed - indexed for MEDLINE]
1: Lancet 1985 Jun 8;1(8441):1313-5
Clinical viral infections and multiple sclerosis.
Sibley WA, Bamford CR, Clark K.
Over an 8 year period, 170 patients with multiple sclerosis (MS) and 134
healthy controls were assessed at monthly intervals in order to ascertain
environmental factors which might be important in producing exacerbation or
progression of the illness, and to compare the frequency of common viral
infections in the two groups. During cumulative periods designated "at risk"
(2 weeks before the onset of infection until 5 weeks afterwards) annual
exacerbation rates were almost 3-fold greater than those during periods not
at risk. Approximately 9% of infections were temporally related to
exacerbations, whereas 27% of exacerbations were related to infections.
Frequency of common infections was approximately 20-50% less in MS patients
than controls; it was progressively less in those with greater disability.
Even in minimally disabled patients with similar potential for infectious
contacts, the infection rate was significantly less than in controls,
suggesting that MS patients could have superior immune defences against
PMID: 2860501 [PubMed - indexed for MEDLINE]