Chlamydia Pneumoniae in CFS/ME & Fibromyalgia
Introduction
(Note: the original page for this became non-functional for some reason. This copy is identical except for some minor text layout details)
Chronic Fatigue Syndrome (CFS), also called Chronic Fatigue Immunodeficiency Disorder (CFIDS), or called Myalgic Encephalomyelitis (ME) in Great Britain.CFS affects 1 million Americans, with "tens of millions" more who have a fatigue condition that doesn't meet the strict criteria for Chronic Fatigue Syndrome.[2]According to the Center for Disease Control (CDC), which considers CFS an accepted medical condition,[3] there is no officially known cause or cure for CFS orfor the related, and often co-occurring, condition of Fibromyalgia Syndrome (FMS).[4]
Despite the CDC's affirmation, the syndrome and its diagnosis is still considered controversial even in this day and age. Some doctors continue to insist thatChronic Fatigue Syndrome is not a "real" disease entity. It may be rather a surprise to it's sufferers when, naively seeking medical assistance, they find that theirdoctor doesn't believe that their symptoms are from a "real disease" or merits medical treatment. That there is no known "test" for Chronic Fatigue Syndrome thatcan conclusively demonstrate its existence is one of the difficulties here.
Perhaps another difficulty is that medical practitioners are socialized to believe that feelings of their own helplessness are a sign of personal failure. A solution tothis psychological conundrum is to blame the patient by "psychologizing" the problem i.e. "It's in your head." Fortunately, acceptance of the legitimacy of thedisease has increased in recent years, even if conventional medical treatment for it continues to have little to offer of help.
As the causal factors of CFS are considered unknown, conventional medical treatment for it and for Fibromyalgia Syndrome are all palliative (symptomatic) innature: antidepressants for mood and pain associated with it, medications for sleep, stimulants for the fatigue, behavioral strategies, and so on. These can helpmake life bearable but don't fundamentally change the condition. [5]
Disease Syndromes: more common than you think -
Chronic Fatigue Syndrome is often disparaged as being a "syndrome," merely a collection of symptoms, not a disease i.e. a causal entity. Of course, a critiqueapplying to one syndrome should apply to them all, yes? A syndrome is a collection of signs and symptoms (Sign= something you can measure; Symptom=patient reports) that appear to have diagnostic consistency. A syndrome tells you nothing per se about the cause of the problem. Many different causes, andsometimes more than one cause at the same time, can result in a syndrome. Interestingly, the diagnosis of "Pneumonia," just like Chronic Fatigue Syndrome, isactually a syndrome, though it is not referred to as "Pneumonia Syndrome." The diagnosing "pneumonia" does not tell you what is causing it, which can bevariously viral, bacterial, food aspiration and so on.
Similarly, diagnosing Chronic Fatigue Syndrome doesn't tell you about possible causes until further investigation is done. There could be a variety and/orcombination of potential causes. There are examples of modern, multi-factorial and case-individualized approaches to CFS/FMS that go far beyond conventionalmedical ignorance about CFS. These combine both symptomatic treatment and search for possible causal contributors for each specific patient.[6]
The various causal factors being looked into are amply discussed elsewhere and can be found in any web search. One of the proposed causal mechanisms for atleast a sub-set of Chronic Fatigue Syndrome is that of bacterial or viral infection. Especially "occult infections" i.e. those organisms that are either typicallyoverlooked, difficult to test for, or tend to evade the immune system[7]. Within this causal possibility are infectious organisms such as Chlamydia pneumoniae.
My purpose here will be to present the information that argues for the involvement of Chlamydia pneumoniae in at least a sub-set of Chronic Fatigue Syndromeand Fibromyalgia Syndrome patients. I will outline how Chlamydia pneumoniae's known biology and impact on the body could explain some of the characteristicsymptoms and signs of Chronic Fatigue Syndrome.
At the outset it should be said that Chlamydia pneumoniae is not the only infectious agent that has implicated in Chronic Fatigue Syndrome/FibromyalgiaSyndrome. We certainly don't know if it is involved in all, a subset or merely a co-condition of such cases. But there is good reason to look further at thisparticular organism's involvement. Most of the argument discounting Cpn's involvement in CFS/FMS has been based on ignorance and poor understanding aboutthe organism itself and the difficulties of testing and treatment for it. This is an attempt at trying to correct this ignorance, and place Chlamydia pneumoniae moreclearly in the realm of possible sources for these devastating conditions.
The Early Vanderbilt Work: Chlamydia pneumoniae in Chronic Fatigue Syndrome-
The Incomplete Research-
There is some published work linking Chlamydia pneumoniae to Chronic Fatigue Syndrome/Fibromyalgia Syndrome in medical research journals.[8] But perhapsthe most important research in this regard never reached publication. This article is the first thorough description in a public information setting.
The original initial work at Vanderbilt by Dr. Charles Stratton and his lab on Chlamydia pneumoniae in human disease was actually not first directed at MultipleSclerosis, as is more commonly believed, but looked Chlamydia pneumoniae in Chronic Fatigue Syndrome. The first grant monies received by Dr. Stratton forChlamydia pneumoniae research, using the highly sensitive tests they had developed, was from Massachusetts Chronic Fatigue Foundation in the mid to late1990's.
Dr. Stratton was asked to test blood samples submitted by the well-known Chronic Fatigue Syndrome physicians Cheney, Peterson & Bell to explore the possibleinvolvement of Chlamydia pneumoniae in their Chronic Fatigue Syndrome patients. As I understand it, the grant was given to these doctors, and the determinationof patients was by their own diagnostic selection. This research was never published, for reasons that will be explained later. The lack of publication and follow
15.09.21, 20:27 The Chlamydia Pneumoniae Handbook
cpnhelp.org/book/export/html/408 16/140
through of this work may be one of the great tragedies in a long line of them in the history of Chronic Fatigue Syndrome. Many patients may have sufferedneedlessly from this disease because the strong link between CFS and Cpn has remained largely unknown.
A remarkable finding:
In this research Dr.'s Cheney, Peterson & Bell sent blood samples from their own Chronic Fatigue Syndrome patients to Dr. Stratton's Vanderbilt Chlamydiapneumoniae lab for testing. According to Dr. Stratton, they tested 100's if not 1000's of such blood samples. These were tested using both ELISA-based serologicmethods and PCR testing using the tests developed by Stratton, et al. at the Vanderbilt Chlamydia Research Laboratory. Dr. Stratton's lab found that the majority(almost 100%) of Chronic Fatigue Syndrome patients were PCR positive for Chlamydia pneumoniae in blood samples.
That the selected patient group of Chronic Fatigue Syndrome patients had almost 100% positive PCR tests for Chlamydia pneumoniae (actual proteins, whichmeans actual presence of the bacterial particles not only an antigen response which could be remnant from prior infection) is an extraordinary finding. Further, themajority also had either elevated IgM or IgG antibodies to Chlamydia pneumoniae major outer membrane protein cross-confirming the PCR based findings.
Of course this in-of-itself does not mean Cpn is the cause of CFS. The presence of Chlamydia pneumoniae could be due to some third factor that is part ofChronic Fatigue Syndrome (such as immuno-suppression, etc). But such high of a correlation with one specific organism outweighs every other or biologicalfinding to date in CFS research. No other single variable in the CFS literature even comes close to being found in near 100% of CFS patients. Now, there are someunknowns here, especially the criterian used to select those patient samples sent to Vanderbilt. This remains unknown as of this writing.
The first research problem:
They also discovered that many of the randomly selected "healthy controls" were also Cpn PCR positive. This would tend to call into question the teststhemselves, i.e. suggesting that the tests are generating false positives. So, they tested a random sample of blood donors to have a larger pool of healthy controlsfrom which to get a baseline comparison for the study's original control group. They found that, of "healthy blood donors" about 20% were Chlamydiapneumoniae positive! This percentage was higher than expected at the time, as it was not yet understood how ubiquitous Cpn is.
However, it turns out that this matches the figures of Cpn found in recent research with healthy, young blood donors.[9] That these earlier Vanderbilt studies foundthe percentage of Chlamydia pneumoniae occurring in healthy donors replicating the current accepted findings (which range from 18-25%) lends credence to theaccuracy and sensitivity of the tests used to study this original Chronic Fatigue Syndrome sample. In other words, post hoc data suggests that their finding of anincidence of Cpn in healthy "controls" was an accurate one, not an artifact from an inaccurate test.
The next problem- treatment:
The obvious next step was to try courses of antibiotics known to be antichlamydial and see if reduction of PCR signal for Cpn correlated with reduction in CFSsymptoms. This was done by the by Dr.'s Cheney, Peterson & Bell with a sample of their patients. It turned out that no single antibiotic agent eradicated theChlamydia pneumoniae PCR signal. So, Dr. Stratton's lab, having laboriously developed the PCR susceptibility tests (described quite elegantly in the patentmaterials which can be found linked elsewhere in this website) now had to use them to discover which agents or combinations of agents were required to eradicateCpn completely, such that no PCR signal was evident in blood samples. This is called "sensitivity testing."
This was a greater challenge than most of us would think. Along the way to infecting mice and cell cultures with Cpn and looking for effective combinations ofantibiotics, they discovered that the available laboratory mice and commercial cell cultures widely assumed by scientists to be "clean," and thus proper startingpoints for introducing new variables, were themselves often infected with Chlamydia pneumoniae. This could seriously skew the interpretation of their tests. SoDr. Stratton's lab had to first develop methods to clear the cell cultures of Chlamydia pneumoniae and prove such clearance using their sensitive PCR testing. Thisis a remarkable bit of science here. Their finding that common biological laboratory materials are contaminated with Cpn appears also to be relatively unknown.
From all of this they managed to find that only certain combinations of antibiotic agents (described elsewhere in this website) would completely eradicateChlamydia pneumoniae from tissue cultures and laboratory mice, as indicated by clearance of Cpn PCR signal. No single antibiotic treatment, nor any series ofantibiotics one at a time, was able to eradicate Cpn. Now that they had the combination antibiotic protocol (CAP) protocol, they could test the impact oferadicating Cpn on the resulting CFS symptoms, and then confirm whether patients were actually clear of Cpn from the blood testing.
And another thing…
As in all research, there is always another problem ahead. This time the problem was with the reactions to the clinical treatment itself being tried by Dr.'s Cheney,Peterson & Bell, as well as by Dr. Stratton with his own Chronic Fatigue Syndrome patients. The treatment was indeed working to kill Cpn, but the toxicity of theCpn kill was causing existing symptoms to worsen significantly. The dropout rate using the combination antibiotic protocol (CAP) for Chronic Fatigue Syndromewas very high. Many patients were unable to see it through to the endpoint of the whole of the treatment process—where PCR signal was absent for Cpn. As Dr.Stratton put it to me in an interview, "The cure appeared worse than the disease." It was difficult for the treating physicians to keep patients on the protocol longenough to begin to see significant symptomatic improvement. This was due to two major difficulties.
Die-off reactions- When combinations were used the die-off reactions from this potent mix could be as bad, or worse, than the Chronic Fatigue Syndrome itself.Little was yet known about how to support patients through these reactions, or what exactly their nature was.
Length of treatment- Moreover, the length of treatment of Cpn with these combination antibiotic protocols for Chronic Fatigue Syndrome was very long. It wasdifficult to get patients to "stay the course" without extraordinary support, or dedication on the part of both the patient and the physician.
It was quite a challenge for the Chronic Fatigue Syndrome physicians, including Dr. Stratton, to know how to manage these responses and how to support theirpatients to hang in with a treatment that seemed to have little short term gain.[10] Of those patients (a small number) who Dr. Stratton treated personally and whocontinued after the end of the study through the full course of protocol there was, says Dr. Stratton, "100% improvement of symptoms."
Why did the eradication of Chlamydia pneumoniae cause such reaction in CFS patients? People treated for actual pneumonia caused by Cpn (community acquiredpneumonia) don't appear to have severe reactions to their antibiotics after all.
First, the combination antibiotic protocol (CAP) was far more effective than a single antibiotic used in standard treatment of Cpn pneumonia because it attackedall of the phases of the Cpn life cycle. A single antibiotic only kills Cpn in one of it's life phases. The symptoms of CFS disease are related to Cpn's toxic andinflammatory impact on the body. The more you kill at once, the more these reactions.
Secondly, CFS patients appear to have built up a very high load of Cpn, spread through a large variety of tissues: the bone marrow, the connective tissue, the liver,the spleen, the vascular system, heart, and so on. When you have a highly toxic organism being killed in large numbers, in a wide variety of tissues, you havemore severity of reactions.
Additionally, the overall Chlamydia pneumoniae bacterial load appears to be one of the big determining factors in the length of the therapy needed. The higher theload, the longer the therapy required.
Implied in this also is...
* The longer one has had the disease,
* The more organ systems affected,
* The less resilient the patient from age, additional illnesses, etc.,
...The longer and more challenging is the treatment required.
15.09.21, 20:27 The Chlamydia Pneumoniae Handbook
cpnhelp.org/book/export/html/408 17/140
As a group, patients with Chronic Fatigue Syndrome/Fibromyalgia Syndrome appear to have higher Chlamydia pneumoniae loads in more different organs andtissues, compared to say MS patients, making treatment with the CAP more challenging, longer, and creating a significant dropout rate as it took longer to see thebeneficial results versus the immediate term die-off reactions. But further research into this very promising but challenging treatment process was halted beforequestions about how to improve the treatment process could be answered.
Research is halted-
At about this point in the research, word was getting out in the medical community that they were testing blood samples from Chronic Fatigue Syndrome patients.There ensued a deluge of protest from medical colleagues who objected to research with Chronic Fatigue Syndrome being conducted at Vanderbilt. According toDr. Stratton, the objections were "quite heated."
Why would microbiological research, as hard-science an aspect of the medicine as one could imagine, stir such heated outrage?
At that time, the late 1990's the diagnosis of Chronic Fatigue Syndrome was hugely controversial. Even more than it is today. Despite having a CDC casedefinition, a significant number of physicians believed that Chronic Fatigue Syndrome did not exist as a real medical entity or diagnosis. They believed that it wasa false, catchall "syndrome," essentially representing psychiatric problems. Therefore it was not considered a legitimate area of serious scientific medical research.
The expressed concern was that the reputation of Vanderbilt University, and by extension the protesting physicians who were associated with Vanderbilt, would besullied by sponsoring work such a medical "non-entity" and be seen as fostering specious science. This kind of reaction was not just reflective of physicians onlyassociated with Vanderbilt of course. In general at this time, scientists or institutions associated with any kind of Chronic Fatigue Syndrome research were seen asincompetents, and were often made pariahs to conventional medicine. CFS research was often a career ender for career scientists. The reactions from potentialpublication journals at this time were similar. Please remember that this was only 10 or 12 years ago, and these attitudes still exist today in medicine.
At about this time the grant money for this study ran out. As Dr. Stratton was serving only as the testing laboratory, he did not have access to the patient datahimself to have adequate controls over patient selection and the like to make for publishable results. Vanderbilt itself did not have a CFS clinic to draw from.
As Dr. Stratton's expertise was in Chlamydia, not in CFS, he turned his research interests towards an area of research on Cpn with less diagnostic controversy, andwhere Vanderbilt did have it's own disease based clinic. Dr. Stratton and his colleagues, spearheaded by Dr. Siram in neurology, shifted the focus of their researchto Multiple Sclerosis. This was done in part to have a widely accepted, "legitimate" nosological (diagnostic) entity for research. As an accepted neurologicaldisease, no one could call MS a psychological problem. As many of us know, this research has turned out to be almost as controversial, although for differentreasons than the CFS study.
While one might wonder at Dr. Stratton's penchant for seeking controversy, the reality is that any research that cuts across accepted conventional viewpoints inmedicine is likely to face rejection and derision. Anyone who knows Dr. Stratton would know that controversy is not at all a motivator in picking his researchareas, Chlamydia is the motivator. Dr. David Wheldon, a colleague and friend of Dr. Stratton's, noted Dr. Stratton's avoidance of the limelight by saying that he"Tends to hide his considerable light under a bushel."
There are probably other factors operating here as well. Any treatment process requiring a combination of three to four antibiotics for a very long period of time isanathema to most conventionally trained MD's. Most physicians have only the rudiments of microbiology in their training, and no basis to understand thecomplexities of treating multiple life-phase infectious agents.
As well, the development of antibiotic resistant strains of bacteria has created a kind of phobia about the long term use of antibiotics amongst most practicingMD's. This attitude is even more true for the use of multiple antibiotics at the same time. It is ironic that physicians who see nothing wrong in pumping patientsfull of multiple chemotoxic agents for cancer treatment will balk at the suggestion of far less harmful multiple antibiotic agents, calling it "polypharmacy."Ironically too, it is actually the use of multiple antibiotics in the CAP for Chlamydia pneumoniae that truly minimizes the chance of developing bacterialresistance, while repeated courses of single antibiotics, the "conventional medical" approach, creates much higher risk for developing bacterial resistance.
At any rate, these very interesting findings were never pursued. We still don't know what percentage of CFS patients are PCR positive for Chlamydia pneumoniae,and exactly how much Cpn is the origin of symptoms in this disease syndrome. What we do know is that those of us who have diagnosed CFS/FMS and havepositive blood tests for Cpn have benefited, slowly, gradually, but significantly in many of our symptoms from the CAP for Cpn based on Dr. Stratton's work. Thisimprovement is true as well for a number of CFS/FMS patients who, while not testing positive for Cpn using standard tests that are not as sensitive as those usedby Dr. Stratton's lab, have evidenced typical die-off reactions to the CAP antibiotics, suggesting Cpn infection. Is it the case for all CFS/FMS? No one knows.
Introduction
(Note: the original page for this became non-functional for some reason. This copy is identical except for some minor text layout details)
Chronic Fatigue Syndrome (CFS), also called Chronic Fatigue Immunodeficiency Disorder (CFIDS), or called Myalgic Encephalomyelitis (ME) in Great Britain.CFS affects 1 million Americans, with "tens of millions" more who have a fatigue condition that doesn't meet the strict criteria for Chronic Fatigue Syndrome.[2]According to the Center for Disease Control (CDC), which considers CFS an accepted medical condition,[3] there is no officially known cause or cure for CFS orfor the related, and often co-occurring, condition of Fibromyalgia Syndrome (FMS).[4]
Despite the CDC's affirmation, the syndrome and its diagnosis is still considered controversial even in this day and age. Some doctors continue to insist thatChronic Fatigue Syndrome is not a "real" disease entity. It may be rather a surprise to it's sufferers when, naively seeking medical assistance, they find that theirdoctor doesn't believe that their symptoms are from a "real disease" or merits medical treatment. That there is no known "test" for Chronic Fatigue Syndrome thatcan conclusively demonstrate its existence is one of the difficulties here.
Perhaps another difficulty is that medical practitioners are socialized to believe that feelings of their own helplessness are a sign of personal failure. A solution tothis psychological conundrum is to blame the patient by "psychologizing" the problem i.e. "It's in your head." Fortunately, acceptance of the legitimacy of thedisease has increased in recent years, even if conventional medical treatment for it continues to have little to offer of help.
As the causal factors of CFS are considered unknown, conventional medical treatment for it and for Fibromyalgia Syndrome are all palliative (symptomatic) innature: antidepressants for mood and pain associated with it, medications for sleep, stimulants for the fatigue, behavioral strategies, and so on. These can helpmake life bearable but don't fundamentally change the condition. [5]
Disease Syndromes: more common than you think -
Chronic Fatigue Syndrome is often disparaged as being a "syndrome," merely a collection of symptoms, not a disease i.e. a causal entity. Of course, a critiqueapplying to one syndrome should apply to them all, yes? A syndrome is a collection of signs and symptoms (Sign= something you can measure; Symptom=patient reports) that appear to have diagnostic consistency. A syndrome tells you nothing per se about the cause of the problem. Many different causes, andsometimes more than one cause at the same time, can result in a syndrome. Interestingly, the diagnosis of "Pneumonia," just like Chronic Fatigue Syndrome, isactually a syndrome, though it is not referred to as "Pneumonia Syndrome." The diagnosing "pneumonia" does not tell you what is causing it, which can bevariously viral, bacterial, food aspiration and so on.
Similarly, diagnosing Chronic Fatigue Syndrome doesn't tell you about possible causes until further investigation is done. There could be a variety and/orcombination of potential causes. There are examples of modern, multi-factorial and case-individualized approaches to CFS/FMS that go far beyond conventionalmedical ignorance about CFS. These combine both symptomatic treatment and search for possible causal contributors for each specific patient.[6]
The various causal factors being looked into are amply discussed elsewhere and can be found in any web search. One of the proposed causal mechanisms for atleast a sub-set of Chronic Fatigue Syndrome is that of bacterial or viral infection. Especially "occult infections" i.e. those organisms that are either typicallyoverlooked, difficult to test for, or tend to evade the immune system[7]. Within this causal possibility are infectious organisms such as Chlamydia pneumoniae.
My purpose here will be to present the information that argues for the involvement of Chlamydia pneumoniae in at least a sub-set of Chronic Fatigue Syndromeand Fibromyalgia Syndrome patients. I will outline how Chlamydia pneumoniae's known biology and impact on the body could explain some of the characteristicsymptoms and signs of Chronic Fatigue Syndrome.
At the outset it should be said that Chlamydia pneumoniae is not the only infectious agent that has implicated in Chronic Fatigue Syndrome/FibromyalgiaSyndrome. We certainly don't know if it is involved in all, a subset or merely a co-condition of such cases. But there is good reason to look further at thisparticular organism's involvement. Most of the argument discounting Cpn's involvement in CFS/FMS has been based on ignorance and poor understanding aboutthe organism itself and the difficulties of testing and treatment for it. This is an attempt at trying to correct this ignorance, and place Chlamydia pneumoniae moreclearly in the realm of possible sources for these devastating conditions.
The Early Vanderbilt Work: Chlamydia pneumoniae in Chronic Fatigue Syndrome-
The Incomplete Research-
There is some published work linking Chlamydia pneumoniae to Chronic Fatigue Syndrome/Fibromyalgia Syndrome in medical research journals.[8] But perhapsthe most important research in this regard never reached publication. This article is the first thorough description in a public information setting.
The original initial work at Vanderbilt by Dr. Charles Stratton and his lab on Chlamydia pneumoniae in human disease was actually not first directed at MultipleSclerosis, as is more commonly believed, but looked Chlamydia pneumoniae in Chronic Fatigue Syndrome. The first grant monies received by Dr. Stratton forChlamydia pneumoniae research, using the highly sensitive tests they had developed, was from Massachusetts Chronic Fatigue Foundation in the mid to late1990's.
Dr. Stratton was asked to test blood samples submitted by the well-known Chronic Fatigue Syndrome physicians Cheney, Peterson & Bell to explore the possibleinvolvement of Chlamydia pneumoniae in their Chronic Fatigue Syndrome patients. As I understand it, the grant was given to these doctors, and the determinationof patients was by their own diagnostic selection. This research was never published, for reasons that will be explained later. The lack of publication and follow
15.09.21, 20:27 The Chlamydia Pneumoniae Handbook
cpnhelp.org/book/export/html/408 16/140
through of this work may be one of the great tragedies in a long line of them in the history of Chronic Fatigue Syndrome. Many patients may have sufferedneedlessly from this disease because the strong link between CFS and Cpn has remained largely unknown.
A remarkable finding:
In this research Dr.'s Cheney, Peterson & Bell sent blood samples from their own Chronic Fatigue Syndrome patients to Dr. Stratton's Vanderbilt Chlamydiapneumoniae lab for testing. According to Dr. Stratton, they tested 100's if not 1000's of such blood samples. These were tested using both ELISA-based serologicmethods and PCR testing using the tests developed by Stratton, et al. at the Vanderbilt Chlamydia Research Laboratory. Dr. Stratton's lab found that the majority(almost 100%) of Chronic Fatigue Syndrome patients were PCR positive for Chlamydia pneumoniae in blood samples.
That the selected patient group of Chronic Fatigue Syndrome patients had almost 100% positive PCR tests for Chlamydia pneumoniae (actual proteins, whichmeans actual presence of the bacterial particles not only an antigen response which could be remnant from prior infection) is an extraordinary finding. Further, themajority also had either elevated IgM or IgG antibodies to Chlamydia pneumoniae major outer membrane protein cross-confirming the PCR based findings.
Of course this in-of-itself does not mean Cpn is the cause of CFS. The presence of Chlamydia pneumoniae could be due to some third factor that is part ofChronic Fatigue Syndrome (such as immuno-suppression, etc). But such high of a correlation with one specific organism outweighs every other or biologicalfinding to date in CFS research. No other single variable in the CFS literature even comes close to being found in near 100% of CFS patients. Now, there are someunknowns here, especially the criterian used to select those patient samples sent to Vanderbilt. This remains unknown as of this writing.
The first research problem:
They also discovered that many of the randomly selected "healthy controls" were also Cpn PCR positive. This would tend to call into question the teststhemselves, i.e. suggesting that the tests are generating false positives. So, they tested a random sample of blood donors to have a larger pool of healthy controlsfrom which to get a baseline comparison for the study's original control group. They found that, of "healthy blood donors" about 20% were Chlamydiapneumoniae positive! This percentage was higher than expected at the time, as it was not yet understood how ubiquitous Cpn is.
However, it turns out that this matches the figures of Cpn found in recent research with healthy, young blood donors.[9] That these earlier Vanderbilt studies foundthe percentage of Chlamydia pneumoniae occurring in healthy donors replicating the current accepted findings (which range from 18-25%) lends credence to theaccuracy and sensitivity of the tests used to study this original Chronic Fatigue Syndrome sample. In other words, post hoc data suggests that their finding of anincidence of Cpn in healthy "controls" was an accurate one, not an artifact from an inaccurate test.
The next problem- treatment:
The obvious next step was to try courses of antibiotics known to be antichlamydial and see if reduction of PCR signal for Cpn correlated with reduction in CFSsymptoms. This was done by the by Dr.'s Cheney, Peterson & Bell with a sample of their patients. It turned out that no single antibiotic agent eradicated theChlamydia pneumoniae PCR signal. So, Dr. Stratton's lab, having laboriously developed the PCR susceptibility tests (described quite elegantly in the patentmaterials which can be found linked elsewhere in this website) now had to use them to discover which agents or combinations of agents were required to eradicateCpn completely, such that no PCR signal was evident in blood samples. This is called "sensitivity testing."
This was a greater challenge than most of us would think. Along the way to infecting mice and cell cultures with Cpn and looking for effective combinations ofantibiotics, they discovered that the available laboratory mice and commercial cell cultures widely assumed by scientists to be "clean," and thus proper startingpoints for introducing new variables, were themselves often infected with Chlamydia pneumoniae. This could seriously skew the interpretation of their tests. SoDr. Stratton's lab had to first develop methods to clear the cell cultures of Chlamydia pneumoniae and prove such clearance using their sensitive PCR testing. Thisis a remarkable bit of science here. Their finding that common biological laboratory materials are contaminated with Cpn appears also to be relatively unknown.
From all of this they managed to find that only certain combinations of antibiotic agents (described elsewhere in this website) would completely eradicateChlamydia pneumoniae from tissue cultures and laboratory mice, as indicated by clearance of Cpn PCR signal. No single antibiotic treatment, nor any series ofantibiotics one at a time, was able to eradicate Cpn. Now that they had the combination antibiotic protocol (CAP) protocol, they could test the impact oferadicating Cpn on the resulting CFS symptoms, and then confirm whether patients were actually clear of Cpn from the blood testing.
And another thing…
As in all research, there is always another problem ahead. This time the problem was with the reactions to the clinical treatment itself being tried by Dr.'s Cheney,Peterson & Bell, as well as by Dr. Stratton with his own Chronic Fatigue Syndrome patients. The treatment was indeed working to kill Cpn, but the toxicity of theCpn kill was causing existing symptoms to worsen significantly. The dropout rate using the combination antibiotic protocol (CAP) for Chronic Fatigue Syndromewas very high. Many patients were unable to see it through to the endpoint of the whole of the treatment process—where PCR signal was absent for Cpn. As Dr.Stratton put it to me in an interview, "The cure appeared worse than the disease." It was difficult for the treating physicians to keep patients on the protocol longenough to begin to see significant symptomatic improvement. This was due to two major difficulties.
Die-off reactions- When combinations were used the die-off reactions from this potent mix could be as bad, or worse, than the Chronic Fatigue Syndrome itself.Little was yet known about how to support patients through these reactions, or what exactly their nature was.
Length of treatment- Moreover, the length of treatment of Cpn with these combination antibiotic protocols for Chronic Fatigue Syndrome was very long. It wasdifficult to get patients to "stay the course" without extraordinary support, or dedication on the part of both the patient and the physician.
It was quite a challenge for the Chronic Fatigue Syndrome physicians, including Dr. Stratton, to know how to manage these responses and how to support theirpatients to hang in with a treatment that seemed to have little short term gain.[10] Of those patients (a small number) who Dr. Stratton treated personally and whocontinued after the end of the study through the full course of protocol there was, says Dr. Stratton, "100% improvement of symptoms."
Why did the eradication of Chlamydia pneumoniae cause such reaction in CFS patients? People treated for actual pneumonia caused by Cpn (community acquiredpneumonia) don't appear to have severe reactions to their antibiotics after all.
First, the combination antibiotic protocol (CAP) was far more effective than a single antibiotic used in standard treatment of Cpn pneumonia because it attackedall of the phases of the Cpn life cycle. A single antibiotic only kills Cpn in one of it's life phases. The symptoms of CFS disease are related to Cpn's toxic andinflammatory impact on the body. The more you kill at once, the more these reactions.
Secondly, CFS patients appear to have built up a very high load of Cpn, spread through a large variety of tissues: the bone marrow, the connective tissue, the liver,the spleen, the vascular system, heart, and so on. When you have a highly toxic organism being killed in large numbers, in a wide variety of tissues, you havemore severity of reactions.
Additionally, the overall Chlamydia pneumoniae bacterial load appears to be one of the big determining factors in the length of the therapy needed. The higher theload, the longer the therapy required.
Implied in this also is...
* The longer one has had the disease,
* The more organ systems affected,
* The less resilient the patient from age, additional illnesses, etc.,
...The longer and more challenging is the treatment required.
15.09.21, 20:27 The Chlamydia Pneumoniae Handbook
cpnhelp.org/book/export/html/408 17/140
As a group, patients with Chronic Fatigue Syndrome/Fibromyalgia Syndrome appear to have higher Chlamydia pneumoniae loads in more different organs andtissues, compared to say MS patients, making treatment with the CAP more challenging, longer, and creating a significant dropout rate as it took longer to see thebeneficial results versus the immediate term die-off reactions. But further research into this very promising but challenging treatment process was halted beforequestions about how to improve the treatment process could be answered.
Research is halted-
At about this point in the research, word was getting out in the medical community that they were testing blood samples from Chronic Fatigue Syndrome patients.There ensued a deluge of protest from medical colleagues who objected to research with Chronic Fatigue Syndrome being conducted at Vanderbilt. According toDr. Stratton, the objections were "quite heated."
Why would microbiological research, as hard-science an aspect of the medicine as one could imagine, stir such heated outrage?
At that time, the late 1990's the diagnosis of Chronic Fatigue Syndrome was hugely controversial. Even more than it is today. Despite having a CDC casedefinition, a significant number of physicians believed that Chronic Fatigue Syndrome did not exist as a real medical entity or diagnosis. They believed that it wasa false, catchall "syndrome," essentially representing psychiatric problems. Therefore it was not considered a legitimate area of serious scientific medical research.
The expressed concern was that the reputation of Vanderbilt University, and by extension the protesting physicians who were associated with Vanderbilt, would besullied by sponsoring work such a medical "non-entity" and be seen as fostering specious science. This kind of reaction was not just reflective of physicians onlyassociated with Vanderbilt of course. In general at this time, scientists or institutions associated with any kind of Chronic Fatigue Syndrome research were seen asincompetents, and were often made pariahs to conventional medicine. CFS research was often a career ender for career scientists. The reactions from potentialpublication journals at this time were similar. Please remember that this was only 10 or 12 years ago, and these attitudes still exist today in medicine.
At about this time the grant money for this study ran out. As Dr. Stratton was serving only as the testing laboratory, he did not have access to the patient datahimself to have adequate controls over patient selection and the like to make for publishable results. Vanderbilt itself did not have a CFS clinic to draw from.
As Dr. Stratton's expertise was in Chlamydia, not in CFS, he turned his research interests towards an area of research on Cpn with less diagnostic controversy, andwhere Vanderbilt did have it's own disease based clinic. Dr. Stratton and his colleagues, spearheaded by Dr. Siram in neurology, shifted the focus of their researchto Multiple Sclerosis. This was done in part to have a widely accepted, "legitimate" nosological (diagnostic) entity for research. As an accepted neurologicaldisease, no one could call MS a psychological problem. As many of us know, this research has turned out to be almost as controversial, although for differentreasons than the CFS study.
While one might wonder at Dr. Stratton's penchant for seeking controversy, the reality is that any research that cuts across accepted conventional viewpoints inmedicine is likely to face rejection and derision. Anyone who knows Dr. Stratton would know that controversy is not at all a motivator in picking his researchareas, Chlamydia is the motivator. Dr. David Wheldon, a colleague and friend of Dr. Stratton's, noted Dr. Stratton's avoidance of the limelight by saying that he"Tends to hide his considerable light under a bushel."
There are probably other factors operating here as well. Any treatment process requiring a combination of three to four antibiotics for a very long period of time isanathema to most conventionally trained MD's. Most physicians have only the rudiments of microbiology in their training, and no basis to understand thecomplexities of treating multiple life-phase infectious agents.
As well, the development of antibiotic resistant strains of bacteria has created a kind of phobia about the long term use of antibiotics amongst most practicingMD's. This attitude is even more true for the use of multiple antibiotics at the same time. It is ironic that physicians who see nothing wrong in pumping patientsfull of multiple chemotoxic agents for cancer treatment will balk at the suggestion of far less harmful multiple antibiotic agents, calling it "polypharmacy."Ironically too, it is actually the use of multiple antibiotics in the CAP for Chlamydia pneumoniae that truly minimizes the chance of developing bacterialresistance, while repeated courses of single antibiotics, the "conventional medical" approach, creates much higher risk for developing bacterial resistance.
At any rate, these very interesting findings were never pursued. We still don't know what percentage of CFS patients are PCR positive for Chlamydia pneumoniae,and exactly how much Cpn is the origin of symptoms in this disease syndrome. What we do know is that those of us who have diagnosed CFS/FMS and havepositive blood tests for Cpn have benefited, slowly, gradually, but significantly in many of our symptoms from the CAP for Cpn based on Dr. Stratton's work. Thisimprovement is true as well for a number of CFS/FMS patients who, while not testing positive for Cpn using standard tests that are not as sensitive as those usedby Dr. Stratton's lab, have evidenced typical die-off reactions to the CAP antibiotics, suggesting Cpn infection. Is it the case for all CFS/FMS? No one knows.
