Melissa Kaplan's
Chronic Neuroimmune Diseases
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Last updated January 1, 2014

On Cryptostrongylus pulmoni and multisystemic illness

Excerpted from the MMI email list

©2003 Lawrence Klapow PhD

Is the fact that no well accepted, dominant, causative infectious agent has been found to date, sufficient to give up the prospect that one might exist? I think not. Yet in the absence of an accepted positive finding, and an integrating physiological theory that connects the known facts, the infectious theory of CFS is, if not stone cold dead, then at least deeply comatose at this point.

I'd like to offer my own integrating theory of the disease in the hope that others might wish to pursue it. The main tenet is that a new species of occult roundworm parasite associated with CFS is defeating the antiparasitic immune response in a way which both suppresses IgE, and destabilizes mast cells so that they are discharged against harmless antigens, or even spontaneously, and thus can not be focused on killing the parasite.

I would suggest two main possible pathways. First, the parasite secretes a homologue of interferon-alpha which induces anti-viral 2-5A, increasing the IgE binding protein CD23 which lowers IgE in serum (can provide literature citations for this reaction chain to those who are interested). Roundworms are reported to secrete interferon-like substances. Also, there is actual evidence of an abnormal form of interferon-alpha in CFS patients (David Bell, "Doctors Guide To CFS"). I am trying to get support and collaboration for a study to look at CD23 in CFS. It shows a significant inverse correlation with IgE in chronic roundworm infections. If such a pattern exists we could then go on to look for further evidence for abnormal INF-alpha in patients. I would welcome the help of CPAR biochemists and others in this endeavor.

The second mechanism involves the well documented secretion of vasoactive intestinal polypeptide (VIP)-like substances by several parasitic roundworms. VIP has broad and varied actions. It controls mast cell stability, autonomic blood pressure reflexes, and gastric motility. It would be interesting to look for an abnormal form of VIP in CFS, presumable secreted by a roundworm parasite.

Adding the fact that roundworms secrete substances which induce autoimmunity and look like neurotoxins, would bring still other findings in CFS under a single umbrella. Since cortisone, which also lowers IgE and is known to exacerbate roundworm infections, can be increased by stress, stress itself could favor the establishment of a chronic roundworm infection.

Interestingly, after some period of time animals with chronic roundworm infections show lower than normal serum cortisone via HPA central activity, possible as a protective response to raise an otherwise suppressed IgE.

Considering the above, given the question of whether CFS is a disease of:

A. disruption of the antiviral pathway;
B. autonomic blood pressure dysregulation;
C. mast cell instability with multiple triggers (allergy symptoms, EI, MCS);
D. irritable bowel syndrome;
E. autoimmunity;
F. a hormonal disease of low serum cortisone via the HPA axis;
G. a stress reactive disease.

The answer may very well be "all of the above", due to a single causative infectious agent. Equally important we would have a "Motive". Why are all these seemingly unrelated things happening? This question seems to go largely unanswered in most of the CFS theories, except perhaps for the psychosomatic hypothesis, which I think is too broad. By seeming to explain everything it explains very little. In the infectious theory the motive is adaptive and makes evolutionary sense: a parasite has evolved the ability to secrete powerful chemicals which disrupt the hosts immune response, allowing it to become a chronic infection. Furthermore it is so successful at this strategy that it can become miniaturized and sustained at extremely low population numbers, features which make it virtually (but not entirely) undetectable.

From the viewpoint of the clinician, different patients may show varying constellation of symptoms. This too does not mean the disease must have multiple causes. In fact my own illness has gone through many changes in symptoms, some phases lasting for months or years. At times it looked primarily like a respiratory disease, at other times like a bowel disease, or allergic disease, or autoimmunity, or an attention/alertness problem or autonomic blood pressure disease, etc., all accompanied by flu-like fatigue, malaise and pain. I would suggest the possibility that these varying symptoms could be explained by an infectious agent which has evolved multiple and redundant mechanisms for responding to the status of the host's immune system. That is not to attribute intelligence to the parasite, but simply to suggest that it has evolved many mechanisms to defeat the complex and redundant immune response of its mammalian host, each if which can be brought into play at different times.

Of course, any disease category which relies heavily on exclusionary criteria, is very likely to include multiple conditions even if it has a dominant underlying pathology, infectious or otherwise.

If anyone thinks they can help explore the bio-chemical elements of my infectious theory, I welcome their interest.

Contact Dr. Klapow

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