Infections and Multiple Sclerosis Relapses

Researchers at the Universities of Glasgow and Strathclyde will try to understand why auto immune diseases like rheumatoid arthritis and multiple sclerosis are so rare in countries where parasitic worm infections are common and whether this may lead to new effective arthritis treatments.

Yes, that’s right. Parasitic worms living inside the bodies of populations from tropical regions without causing them any trouble at all. And perhaps, strangely, providing some benefit. Which leaves you to wonder if Mother Nature doesn’t know just exactly what she’s doing after all…

The scientific community is well aware of an inverse relationship between worm infections and diseases like rheumatoid arthritis, inflammatory bowel disease, type-1 diabetes and multiple sclerosis. Countries where people are naturally infected with this particular parasite seem to have lower rates of these conditions than those countries where this type of infection doesn’t occur or has been eradicated.

Luckily for the squeamish among us, it’s not the actual parasitic filarial nematode worm that the Scots scientists are wanting to put into our bodies, it’s a large molecule they secrete known as ES-62. This substance is found in the bloodstream of parasite infected people in the tropics, and seems to provide some protective benefit against the inflammation the worms should be causing in their human hosts. The good news is that ES-62 has no known adverse effects, leaving the body perfectly able to fight off other infections.

“ES-62 appears to act like a ‘thermostat’ to effectively turn down disease-causing inflammation while leaving essential defense mechanisms intact to fight infection and cancer,” according to Iain McInnes, a member of the research team and Professor of Experimental Medicine at the University of Glasgow. “This property also makes ES-62 a unique tool for scientists to identifying how such disease-causing inflammation occurs.”

The team is going to try and produce a synthetic version of the ES-62 molecule from the worms in an effort to come up with an anti inflammatory therapy that works effectively for auto immune diseases like rheumatoid arthritis, inflammatory bowel disease, type-1 diabetes and multiple sclerosis. The three-year study is being funded by the UK's Arthritis Research Campaign.

Earlier work has also shown ES-62 to have real potential as a therapy for allergies too.

Source: Artwoo ©2006-2008 ClknGo Software Corporation. (24/11/08)

OBJECTIVE: Recent studies in peripheral blood mononuclear cells (PBMCs) have indicated that exacerbations of multiple sclerosis (MS) could be associated with the reactivation of latent varicella-zoster virus (VZV).

METHODS: Ultrastructural observations for viral particles were made by electron microscopy in cerebrospinal fluid (CSF) from 15 MS patients during relapse, 19 MS patients during remission, and 28 control subjects. Initial findings were reproduced in a confirmation cohort. In addition, DNA from VZV was quantified by real-time polymerase chain reaction in PBMCs and CSF from a large number of MS patients (n = 78).

RESULTS: We found by electron microscopy the presence of abundant viral particles identical to VZV in CSF obtained from MS patients within the first few days of an acute relapse. In contrast, viral particles were not seen in CSF samples from MS patients in remission or from neurological control subjects. Also, DNA from VZV was present in CSF and in PBMCs during relapse, disappearing in most patients during remission. The mean viral load was 542 times greater in CSF at relapse than in CSF at remission and 328 times greater in CSF at relapse than in PBMCs at relapse.

INTERPRETATION: The ultrastructural finding of viral particles identical to VZV, together with the simultaneous presence of large quantities of DNA from VZV in the subarachnoid space, almost restricted to the periods of exacerbation, as well as its steady diminution and eventual disappearance from clinical relapse to clinical remission are surprising and constitute the strongest evidence to support the participation of VZV in the pathogenesis of MS.

Source: Ann Neurol 2008.(12/03/08)

The finding suggests that when the body's immune system is occupied with an external threat, it might be less likely to misfire, which happens in conditions known as autoimmune disorders. Multiple sclerosis is an autoimmune disorder that attacks the myelin sheath that protects nerve fibres.

The study tracked 12 multiple sclerosis patients who were found to have an intestinal parasite and compared them with 12 other patients. Over four years, there were stark differences. There were three relapses among the patients who had the intestinal infection and 56 relapses in the other group.

Patients with the parasitic infection also had minimal changes in disability scores compared with the other group, according to a study in this month's Annals of Neurology by Jorge Correale and Mauricio Farez of the Raul Carrea Institute for Neurological Research in Buenos Aires.

The study suggests that one reason for the apparent increase in autoimmune disorders in recent years could be the decline of infectious diseases in certain countries. Because parasites often cause long-lasting infections, the researchers hypothesised that such infections could make persistent demands on the body and thereby reduce the likelihood that the immune system will attack healthy tissue.

Source: SouthCoastToday.com © 1995-2007 The Standard-Times.(16/01/07)

Investigators, in a report in the journal Neurology, note that published epidemiologic environmental observations point to infection as a possible causative factor or trigger in the onset of MS.

"Microorganisms induce strong immune responses specific for their own antigens, but microbial infections can also trigger responses against self-antigens, promoting inflammatory responses," they point out.

"Since no single microorganism has been identified as a clear etiologic agent in MS, a more likely explanation for the epidemiologic environmental observations is that infections introduce a proinflammatory bias in immune responsiveness in MS patients that is capable of triggering disease activity and exacerbations."

Dr. Jorge Correale from Raul Carrea Institute for Neurological Research in Buenos Aires, Argentina, and colleagues say their study supports this line of thinking.

The researchers followed 60 MS patients who were instructed to report as soon as they experienced symptoms of an infection.

The team found a threefold increase in the rate of MS exacerbations during the "at-risk period" ranging from 2 weeks prior to 5 weeks after the onset of symptoms of infection, compared with time periods outside this window.

Any MS attack during the at-risk period was considered temporally related to the infection.

When a narrower "at-risk" time window was considered around infection (2 weeks prior to 2 weeks after symptom onset), the risk of MS exacerbation was elevated fourfold.

"Viral and bacterial infections were equally associated with exacerbations," Dr. Correale and colleagues note.

The researchers also observed a significant increase in disease activity on magnetic resonance imaging among 20 patients who underwent serial imaging studies, as well as increased T cell activation and proinflammatory cytokine concentrations during infection-related MS exacerbations.

Relapses temporally linked to systemic infection caused more severe and sustained deficit than exacerbations with onset outside the at risk window, the researchers also report.

Source: Neurology, August 22, 2006. (09/09/06)

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