CFS: Suspected New Species Chronic Roundworm Parasite,Cryptostrongylus pulmoni,

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On Cryptostrongylus pulmoni and multisystemic illness

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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_ (klapow123)

 

 

Suspected New Species of Chronic Roundworm Parasite, Cryptostrongylus

pulmoni, Associated with CFS in Blinded Trials

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Lawrence A. Klapow PhD, Journal of Chronic Fatigue Syndrome, 1999 5(3/4):

247-248

 

OBJECTIVES: 1) Describe the roundworm and how to find it. 2) Determine its

occurrence in CFS and non-CFS controls in blinded trials.

METHODS: Coded three-day sputum collections, preserved in 50 % ethanol, from

24 patients and 16 controls were examined microscopically. Patients were

drawn from the CFS clinic at Brigham and Women's Hospital (Harvard Medical

School), and from three primary care practices. Identification required

screening

of numerous candidate specimens, clearing in glycerin, 1200X magnification (a

12X video mounted to the 10X ocular of a microscope set at the 10X

objective), and the use of two polarizers (one in the light source the other in

the

image path over the ocular lens). Careful examination of photo-micrographs of

both sides of the specimens, at multiple focal-depths, was required for

reliable identification. Male reproductive organs (item 5-9 below), and female

mouth parts (3,4,5,and 9-11), proved most useful for identification.

MALE (200 to 350 microns long): 1. Red in formalin, colorless in ethanol. 2.

Nerve ring is visible in most glycerin cleared specimens surrounding a

bulbless esophagus, using polarize/analyzed light. 3. A cervical flange, an

exterior membrane, winds around the anterior (lost or fragmented in most

specimens). 4. A pair of lateral ridges with triangulate crests extends the

length of

the body. 5. Spicules are very large (visible anatomy, other than terminal

bifurcation, is indistinct). 6. Dorsal genital structures consist of a pair of

projections spanned by a membrane, resembling a sail. 7. Ventral genital

structures consist of a pair of long pointed projections, twisted like a

corkscrew at their distal termini. 8. The dorsal lobe of the copulatory bursa

is very

large, supported by a bifurcated Ray 8, giving rise to four long raylettes.

9. Lateral lobes of the bursa are symmetrical: Ray 7 is very short and

indistinct; Ray 6 is long and twists under the edge of the membrane, emerging

beyond the border as a distinct point; Ray 5 is short and sigmoid; Ray 4 is

long,

straight, and robust, with its tip much closer to ray 3 than to ray 5; Rays 3

and 2 are long, straight, slender, and closely spaced.

FEMALE (550 to 950 microns long): 1. Only the front half is usually

recovered (275 to 475 microns). 2. Vulva is mid-body. 3. Bulbless esophagus. 4.

Nerve

ring is visible in most glycerin cleared, specimens under polarized/analyzed

lighting. 5. A cervical flange, an exterior membrane, winds around the

anterior and is usually fragmented or absent in recovered specimens. 6.

Cephalic

vesicle is absent. 7. Oblique cuticle ridges forming chevrons are minimal,

faint, and rarely seen in a few specimens. 8. Caudal area has paired papillae,

and terminal cones. 9. Buccal capsule is asymmetrical. 10. Single amphid

gland tubule. 11. The mouth has six prehensile lips. Numbered in a clockwise

direction: lips 1 and 2 are short, followed by 3 which is long, followed by the

amphid tubule, the asymmetrical buccal capsule, and three long lips, 4,5 and

6. 12. Cuticle striations are visible with a polarized light source and

eyepiece optical analyzer.

RESULTS: Decayed specimens of C. pulmoni were found in 50 percent of

three-day sputum samples from CFS patients (12 in 24), but not in 16 controls

(chi-square association, P<0.003). The infection rate, corrected for test

sensitivity, is conservatively estimated at 66 percent (95% CL, > 44% to >

84%). Two

positive patients re-tested two years later were both still positive. Late

larval stages were also found in sputum. Approximately 50 to 100 hours were

needed to isolate and identify each specimen.

CONCLUSION: Cryptostrongylus pulmoni infects a large percentage of CFS

patients, estimated at 66 percent in the current study, and is significantly

associated with the syndrome (chi-square P<0.003) in blinded analyses. It

appears

to have chronic properties. Microscopic identification is difficult and time

consuming due to the decayed state of most specimens, their small size, and

extreme rarity.

Specialized, though inexpensive and simple, imaging techniques are needed

for positive identification. Research to develop a DNA marker is in progress.

_Contact Dr. Klapow_ (klapow123)

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