Fibromyalgia and Intestinal Infection: The Bacteriophages Connection
March 15, 2002
By Theophil Hey, M.D.
Based on the scientific results of twelve years of continuous investigation we now regard as proven that a connection exists between Primary Fibromyalgia Syndrome (PFS) and evidence of bacteriophages (specific E. coli phages) found in the stool of patients.
The virology department of the Medical College in Hanover (MHH) used electron-
microscopes to detect bacteriophages (viruses) in the stool of more than 80% of patients examined. By comparison, they were detected in only 12 - 13% of the control group. Scientifically speaking, this result is deemed to be of great scientific significance.
Bacteriophages (viruses) infect their specific host cell (in this case the E. coli bacteria) and cause the E. coli bacteria to produce new viruses via the viral genes.
Up to 400 new viruses develop in this way inside the E. coli bacteria.
After the E. coli bacteria has practically surrendered its cell contents for the production of the virus it then dies (lytic virus reproduction) and bursts. A virus “brood” results. A number of the released viruses find new, not yet infected E. coli bacteria, infects them and the whole process begins anew. Medically significant and the cause of the patients symptoms are the particles of the sheaths released during the process of E-coli lysis (the death of the bacteria) - the lipopolysaccharides with their active component Lipid A - which represent highly potent endotoxins.
This means that primary fibromyalgic syndrome (often found in combination with chronic fatigue syndrome and irritable colon) is to be assessed primarily as an infection of the intestine - specific bateriophages infect their specific host cells (in this case E coli) - secondly, through the release of endotoxins, as intoxication locally (reaction of the bowels) and in the blood circulation after absorption through the intestinal walls.
If no significant change in the bacterial colonisation of the bowels comes about, this process can result in the patient experiencing an alternating course of the disease lasting months and years. To minimise or even eliminate the symptoms we must attempt to keep the virus away from its host cell (E. coli), or, at least, to minimise it permanently.
1. Cleansing of the bowels:
Day 1: e.g., salinic purgatives
Day 2 - 6: colistin sulphate ( - Diarönt mono 4x2.000.000 I.U.) together with Nystatin (4x1.000.000 I.U.)
2. Symbiosis management: -Saccharomyces boulardii (possibly permanently), 250mg 2x1 before meals, e.g., Perocur forte -Lactobacillus acid. (e.g. Paidoflor 2x1 after meals) -Lactulose ( e.g. Bifiteral 1 measure mornings)
3. Prevention of new infection: no raw meat (everything boiled or well-done; boiled salamis, boiled ham; no fast-food) no fresh milk (not been pasteurized), no cheese made from fresh milk, no raw vegetables or salad which have been grown in natural or liquid manure.
A low E-coli count means: the viruses can only infect a small number of E. coli and so cause very few to die. Consequently low amounts of endotoxins (poisons) are released.
On the other hand: mass colonisation of the bowels by E-coli bacteria at the same time as their specific bateriophages (viruses) are present can result in a massive release of poisons and exceedingly unpleasant symptoms.
We are ready at all times to help if you have further questions, but must point out that an immediate reply is not always possible.
The pathogenesis of the primary fibromyalgic syndrome
Association of primary fibromyalgic syndrome (PFS) with evidence of bacteriophages in the stool. T. Hey, General Practitioner; A. Breull; G.C.Fischer, Dept. of General Medicine; W. Verhagen, Dept. of Virology; Med. Hochschule Hannover
The symptoms of PFS have been the subject of studies by numerous authors in the past ten years; they have repeatedly been described in detail, questions have been asked as to possible causes, many possible associations discussed and more or less effective therapy methods recommended.
PFS represents a daily new challenge for us doctors - everyday we are faced with patients suffering from the unpleasant symptoms. They come hoping for an explanation - and for relief from their complaint.
This was the reason for me to make use of all possibilities available to me in an investigation into the pathogenesis of the symptoms.
It is well known that PFS is a follow-up diagnosis. BSG, blood count, RF, CRP, CK as well as internal, orthopaedic and x-ray diagnosis show no evidence of a pathological substrate. It is merely the tender-points (ACR model) which can be clinically confirmed by the examiner as being typically symptomatic.
No more was known about the complaint up to this time. There was no known cause for this illness. All attempted treatments were treatment of the symptoms using analgesics, anti-rheumatic agents, tri-cyclic anti-depressives and exhaustive clarification of the course of the illness involving a great amount of patient-time.
Patients in my survey were first subjected to the same diagnostic steps before the question of a virus genesis was broached.
Antibody tests were carried out to search for Coxackie B viruses, Herpes simplex viruses, Varicella zoster viruses, Entero viruses, Adeno viruses as well as Epstein-Barr viruses but no evidence of an association with the complaint was to be found.
Attempts to breed the virus taken from the blood, urine, stool and pharyngeal wash on egg albumin also failed to produce any positive results.
I consulted with the department for virology in the MHH, Hanover and they recommended as a last diagnostic possibility examination of the stool under electron microscopes.
This diagnostic step brought evidence of vast numbers of bacteriophages in the stool of the first 5 patients!
This represented the first objectively demonstrable substrate above and beyond the clinical symptoms which was common to all patients.
The question now was: Is it at all theoretically possible for bacteriophages to harm human body cells? Can other mechanisms - triggered by the presence of bacteriophages - strain the human organism? The bacteriophages detected were quite definitely T-phages - i.e., specific E-coli phages. Which means that they cannot harm the human cell.
When this virus has reached its specific host cell and infected it, there follows a multiplication of the virus - (lytic phase) or lysogenesis occurs, i.e., the phage genom is attached to the E-coli DNA and passed on with every splitting of the E-coli. Through factors as yet unknown to us this passive virus phase can change back into the vegetative - i.e., lytic - form and so pass into the afore-mentioned multiplication process again. The E-coli
disintegrates during the process.
The sheath of the E-coli is made up of lipopolysaccharides - as are all gram-negative bacteria - including the pathogen Lipid-A, which can be defined as an endotoxin. This would mean that in this association the released endotoxins are directly to blame as human pathogenic.
Subsequently, 272 patients suffering from PFS were subjected to stool diagnosis within two years (group A). 4185 stool examinations taken from the virology dept of the MHH served as a control group. 63 patients (group B) were selected from the survey group A and from these at least three stool samples were taken at an acute stage of their illness; these were used to confirm a closer association of the illness with evidence of coli-phages.
Group D, consisting of 30 patients from our survey who quite clearly did not suffer from PFS symptoms, was used as our control group. The results showed that specific coli phages were evident in the 225 of the 272 patients belonging to group A (=82.7%).
In the control group from the medical school there was evidence of phage infestation in merely 520 of the 4,185 persons tested (=12.4%). This result is highly significant.
In the selected group B there was even clearer evidence of phages - 98.4% = 62 out of 63 persons. Results from the survey control group D lay by 13.3%, similar to control group C from the medical school (12.4%).
At the same time the department of immunology in the MHH analysed the endotoxins (LPS and lipid A) and the specific anti-bodies in the serum of the patients in group B for LPS and Lipid A in IGM and IGG form.
Evidence of endotoxins was found directly in the serum of only 7 of the 63 patients (=11.1%), but specific anti-bodies against LPS and Lipid A were found in significantly greater numbers than in a healthy control group of blood donors.
The cause of the illness and its typical alternating course must be a consequence of a lysis of E coli infected with phages occurring in the bowels and induced by bacteriophages; endotoxins are subsequently released in the bowels and absorbed via the bowel wall into the blood system. Evidence of specific endotoxins and their anti-bodies in the serum constitute proof of this conjecture.
This means that the course of the illness begins with alimentary intake of T-bacteriophages (directly or in E coli bacteria in the lytic or lysogenic phase), followed by their colonisation and reproduction in the bowels and finally the lysis of the E coli, the release of endotoxins and their absorption. The idea that the release of endotoxins in the bowels is induced by phages and that Lipid A is absorbed into the blood system has not yet been recognised as a pathogenic process. 10 picogramm lipid A per ml serum is regarded as highly toxic!
According to this investigation primary fibromyalgic syndrome must primarily be regarded as an infection (bacteriophage infect of E. coli) and secondly as an intoxication (endotoxin) which enables us to understand the diverse occurrences of this illness with its chronically alternating course.
Theophil Hey, M.D.
||Join the Discussion
|Posted by: wiserd
Nov 8, 2007
Interesting article. But how does this square with the finding that Fibromyalgia is triggered by stress and similar to post-traumatic stress disorder or that FM involves the body's inability to produce HGH and achieve deep sleep. Is there any evidence that chronic, excessive Lipid A exposure is capable of causing these problems?