posted
The LDA and ILADS conferences 2008- Summary of scientific and medical presentations with commentary.
Dr. David C Owen BSc MB BCh LLM
The LDA and ILADS conferences were held in the Cathedral Hill Hotel, San Francisco 17-19 October 2008.
Following a welcome address by Pat Smith, president of the LDA, Steven Barthold DVM PhD gave the keynote address concerning persistence of B burgdorferi using a mouse model of infection. That persistence of infection occurs is proven but the mechanism or mechanisms of persistence are not clear. It was hypothesised that sequestration of non replicating forms of Borrelia in collagen occurs and these dormant forms begin replication when conditions are appropriate for example when the host's antibody response has subsided. Much collagen is found in the dermis, the target area of a feeding tick, and Barthold has demonstrated that transmission of Borrelia to ticks can occur even after antibiotic treatment of the host.
Mariio Phillipp PhD has been trying to shed light on how cognitive dysfunction occurs in Lyme Borreliosis. Using monkeys he has demonstrated that in the laboratory when monkey brains are exposed to Borrelia numerous cytokines are released which result in neuronal apoptosis in the presence of microglia. The relevance for chronic Lyme in humans is unclear but if damage is cytokine mediated then interventions which reduce this may be expected to help. Phillipp noted that Doxycycline reduces the immune mediator IL 6 in his experiments and he suggested that this may be relevant to the therapeutic benefit observed when this agent is used in chronic Lyme patients.
Steven Schutzer MD reported on a technique to identify the microbial population in ticks. It is becoming clear that ticks harbour a complex array of microorganisms just as many Lyme disease patients appear to be multiply infected. The technique referred to as Ibis T5000 uses non specific DNA primers enabling simultaneous identification of an array of microbes. It is hoped that the technique will result in enhanced mapping of tick borne pathogens and there is a possibility that new infective agents will be identified.
Patricia Conrad DVM PhD is a Parasitologist with an interest in Babesiosis. Conrad reported that Babesia microti is endemic in the mid west USA and in humans it may be present without causing symptoms or in some cases it may cause a flu-like illness. Anemia and thrombocytopenia may be a clue to its presence. The more recently described Babesia ducani (formerly WA1) is phylogenetically quite distinct from B. Microti but it was stated that this too may be carried asymptomatically. It was stated that there is currently no evidence that B. ducani is a Lyme co-infection and Conrad questioned the validity of some tests used to infer Babesiosis in humans. Conrad suggested that some cases of Babesia may be falsely reported as Malaria but careful examination of blood films may lead to the detection of ``Maltese Cross'' forms of erythrocytic inclusions typical of Babesia infection. There are few reports of Babesiosis in Europe and most of these are due to B divergens which typically appears to cause a fulminant illness. It is clear further work is needed worldwide to enhance our understanding of the pathology and ecology of this elusive protozoan.
Diego Cadavid MD is another worker who has been attempting to shed light on neuroborreliosis. He reported on the results of experiments using Borrelia turicatae, the relapsing fever spirochete, in mice. Mice deficient in IL 10 and antibody production were rapidly killed by the spirochtete unlike wild mice which were relatively unaffected. Mice only deficient in IL 10 production had higher cerebro-vascular vascular complications despite a low spirochete load and this lead Cadavid to conclude that IL10 plays a critical role in protecting the brain and other organs from vascular complications during borrelial infection. Comment: Lyme disease has been associated many different neurological events central and peripheral, reversible and irreversible. There is no ``neuroborreliosis syndrome'' and the causes of neurologic disturbance in Lyme disease in humans appear to be multi-factorial and complex.
Brian Fallon MD gave an overview of the clinical profile of chronic Lyme disease with an emphasis on biomarkers. He noted that C6 Elisa is one of the best markers of Borreliosis and has a specificity of close to 100%. As with other tests sensitivity is lacking and the search for a reliable bio-marker continues. Fallon's studies have shown that clinical features (symptoms) are the best predictors of response to treatment in Lyme disease. Fallon suggested that chronic Lyme disease should be defined in a way which is aetiologically neutral. Comment: Fallon wishes to define chronic Lyme disease to incorporate both ``Post Lyme syndrome'' and persistent infection. The problem with this approach is that there are many patients who have never received treatment for Lyme disease despite clinical features of the condition and this category of patient would be left with no diagnostic label. This author suggests that chronic Lyme disease should imply persistent infection even though this fact may remain unproven in an individual case. Such a label is not inconsistent with a concomitant pathological process which is independent of infection.
Christopher Contag PhD described a technique of Bio-Luminescence Imaging which enables localisation of bacteria in the living host. So far the technique has been used with Listeria in mice and the results have contradicted existing dogma about the condition such as the belief that the organisms are obligate intra-cellular parasites. One problem if the technique is used for Borrelia may be the need for a threshold of 100-1000 organisms for detection but if sensitivity can be improved the technique appears to have potential to increase our understanding of the pathogenesis of Borreliosis.
George Chaconas PhD has also been imaging bacterial infection in the living host. Chaconas pointed out the advantages of studies involving real time parasite-host interactions over a reductionist scientific approach which will inevitably lead to caveats. Chaconas has produced remarkable real time 2D and 3D videos of Borrelia in a laboratory host which include actual penetration of blood vessels by the organism. We were told that the images are available for viewing on the World Wide Web.
Armin Alaedinin PhD spoke about Immunologic abnormalities in post Lyme syndrome. Numerous immunologic changes are known to occur following Borrelia and other infections and auto-immunity is frequently invoked to explain some symptoms of Lyme disease when infection is no longer thought to be present. The example of Guillain Barre syndrome, which has been associated with prior Campylobacter jejuni infection, was cited as a specific example of a neurologic auto-immune pathologic process. Borrelia being a complex microbe has the capacity to stimulate the production of many different antibodies and Alaedinin's work has demonstrated that Post Lyme Syndrome patients have increased IL10 levels when compared to Lyme patients who have symptomatically recovered. The increase was comparable to those found in some other auto-immune disorders such as SLE. The hope is that a better understanding of the disturbed immunologic reactions will lead to targeted immune modulating therapies in the future. In response to a very good question from the audience Alaedini agreed that it was possible that raised the raised IL10 levels could be masking symptoms in his control group of patients and these could in fact have latent infection.
John Keilp PhD has worked closely with Brian Fallon at Columbia University. Keilp has been addressing the difficult question of whether depression in Lyme patients is secondary to the illness or independent of it. By comparing two groups of depressed patients one with a Lyme diagnosis and one without Keilp concluded that Lyme patients with mild depression have greater impairment of memory and verbal fluency than is the case in depressed patients who do not have Lyme disease.
Fabio Tavora MD is a pathologist who presented a case of fatal Lyme carditis. Evidence for Lyme in the case included EM type rash, positive blots and positive cardiac PCR. In the case in question it appears an opportunity to treat Lyme disease at an early stage was missed but whether this would have affected the outcome is, of course, unknown. Comment: The case raises the question of how often Lyme might be an underlying infection in cases of myocarditis which are commonly attributed to viral infections or hypersensitivity reactions.
Suzanne Vernon PhD gave a talk on Chronic Fatigue Syndrome (CFS) which she has studied extensively. It was stated that there are many parallels between CFS and Lyme including the lack of a bio-marker. Vernon noted that CFS is a diverse group of conditions. She has developed a model of the condition in which disturbance of the HPA axis is central. Comment: CFS affects around 4 million Americans and the severity of the illness is such that many are incapable of work. How many CFS patients have symptoms attributable to tick borne illness is not known. Even if the proportion is small the Public Health implications would be significant.
Benjamin J Luft PhD gave the final LDA talk. He spoke about studies which have investigated gene expression in B. Burgdorferi. He told the audience that under laboratory conditions around half of the potential 1400 Borrelia proteins are expressed. Conditions such as pH and temperature can be varied and the effects on gene expression can be studied. Comment: It may be rewarding to study the effects on gene expression in Borrelia under hypoxic conditions since Borrelia appears to favour areas of the host which are relatively low in oxygen saturation.
Willy Burdorfer PhD gave the first ILADS talk. He enthralled the audience by relating the story of his discovery of the Lyme disease spirochete. Although many scientific discoveries have an element of fortuity it was clear that Burgdorfer's discovery was the result of many years of dedication and hard work in the study of the biology of ticks. In early work Burgdorfer had focussed on Relapsing fever the infectious agent of which could be readily identified in the arthropod's haemolymph. Much later in his career Burgdorfer found a Nematode worm in one of the American ticks he was studying. This was unusual and led him to investigate specific tissues of the tick. In the mid gut he found spirochetes and, as the saying goes, the rest is history.
Stephen Phillips MD considered in detail available published evidence pertaining to chronic Lyme disease. He presented numerous citations which establish sero-negative Lyme disease and persistence of Borrelia infection as facts.
Robert C Bransfield MD is a psychiatrist who specialises in Lyme disease. Patients with Lyme disease are invariably polysymptomatic and complaints such as sleep disturbance and neuropathic pain may be severe enough to warrant symptomatic treatment. Bransfield noted that sleep disturbances occur in many chronic inflammatory disorders and he suggested a number of therapeutic approaches which may help the distressing symptoms of a patient with Lyme disease.
Judith G Llevanthal PhD has been analysing data from physicians who have been treating Lyme disease. In common with findings in adults it was reported that in children neurocognitive symptoms were among those most commonly reported by patients with Lyme disease.
Deborah A Metzger PhD MD specialises in Chronic Pelvic Pain (CPP) which is an intractable and incapacitating symptom for some women. CPP is known to be associated with various inflammatory conditions and infections and Metzger considers that Lyme disease is a very important association. Her experience in treating this difficult group of patients with various types of therapy was discussed.
Richard Horowitz MD gave a talk on his holistic approach to patients with Lyme disease. Horowitz emphasised the need to consider many other factors in Lyme patients in addition to infection. These include consideration of the need for heavy metal detoxification and correction of minor endocrine disturbances. In addition Horowitz reminded us that psychological factors may be an impediment to improvement in some cases. Horowitz noted that the symptoms of chronic Lyme disease are similar to those reported in other conditions and there was a need for continuous vigilance to ensure coexisting conditions are not missed. Comment: There is clearly a need for studies to address the efficacy of many of the therapeutic interventions in Lyme disease. One problem in doing this is patient selection since Lyme disease patients are a diverse group and in many cases the diagnosis of Lyme disease cannot be made with certainty. In the absence of such data patients are the arbiters. Judged by the numbers of patients Horowitz has treated his approach is a successful one.
Ann F Corson MD gave a talk on her experience in using German Biological medicine in the treatment of tick borne disease. These treatments are often combined by Corson with allopathic antibiotics to treat her Lyme disease patients. The methods are strongly linked to the traditional Chinese medicine theory Shan Han Lun. Comment: It is clear that for many patients antibiotics are not a complete answer to their symptoms and alternative approaches should be welcomed. Medicine is not science and physicians cannot wait for all treatments to be thoroughly proven before offering them to patients.
Garth L Nicolson PhD gave a talk on the relationship between neurodegenerative disorders and tick borne pathogens. Nicolson has intensively studied veterans of the Gulf War many of whom developed medical problems commonly known as ``Gulf War Syndrome''. Veterans additionally had a much higher than average incidence of ALS. Nicolson considers that tick borne pathogens (especially Mycoplasma and Borrelia) were an important cause of the disease burden in the veterans. Additional factors such as multiple vaccination and toxic exposure were also likely to have played an important role due to immunosuppression. Nicolson has noted that children of Gulf War Veterans have a higher than average incidence of Autism Spectrum disorders and it was suggested that this may be due to Mycoplasma transmission. Comment: Lyme disease patients often report Lyme like illness in family members. While common exposure to ticks is one possible explanation an alternative explanation of non tick associated transmission of co-infections is an interesting hypothesis.
Daniel J Cameron MD (current ILADS President) spoke about strategies to prevent chronic Lyme disease. He noted that the number of cases of Lyme disease reported to the CDC continues to rise. Furthermore the CDC acknowledges that reported cases may represent less than 10% of the true incidence. Additionally other tick borne illnesses are not considered in the figures. Cameron believes that it is only through consideration of neglected facts about Lyme disease that public bodies such as the CDC could develop more effective prevention strategies.
Dr. David C Owen
Cardiff, Wales, UK October 2008-10-20
This article has been donated to the UK charity Lyme Disease Action for free distribution. The opinions expressed herein are solely those of the author, Dr. David C Owen
-------------------- My biofilm film: www.whyamistillsick.com 2004 Mycoplasma Pneumonia 2006 Positive after 2 years of hell 2006-08 Marshall Protocol. Killed many bug species 2009 - Beating candida, doing better Lahey Clinic in Mass: what a racquet! Posts: 830 | From Mass. | Registered: Aug 2006
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bettyg
Unregistered
posted
up; buried on page 2; everyone has missed this or were like me and had to sob, scroll on by since paragraphs are too long to comprehend/read by neuros like me.
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mojo
Frequent Contributor (1K+ posts)
Member # 9309
posted
Thank you, Dr. Metzger for covering Chronic Pelvic Pain!!!!!!!
My Dr. attended that session.
Posts: 1761 | From USA | Registered: May 2006
| IP: Logged |
posted
Good summary. Funny reading this as Dr Owen was my first LLMD before I switched to Horowitz in June. Good to see he is keeping up his education. I think he needs it.
-------------------- Pos BB and Bart(Q & H IGG pos) Began treat 1 year after start of illness. Diagnosed Feb 2007. Posts: 648 | From Ireland | Registered: Jan 2007
| IP: Logged |
lymednva
Frequent Contributor (1K+ posts)
Member # 9098
posted
Broken up for easier reading.
The LDA and ILADS conferences 2008- Summary of scientific and medical presentations with commentary.
Dr. David C Owen BSc MB BCh LLM The LDA and ILADS conferences were held in the Cathedral Hill Hotel, San Francisco 17-19 October 2008.
Following a welcome address by Pat Smith, president of the LDA, Steven Barthold DVM PhD gave the keynote address concerning persistence of B burgdorferi using a mouse model of infection.
That persistence of infection occurs is proven but the mechanism or mechanisms of persistence are not clear.
It was hypothesised that sequestration of non replicating forms of Borrelia in collagen occurs and these dormant forms begin replication when conditions are appropriate for example when the host's antibody response has subsided.
Much collagen is found in the dermis, the target area of a feeding tick, and Barthold has demonstrated that transmission of Borrelia to ticks can occur even after antibiotic treatment of the host.
Mariio Phillipp PhD has been trying to shed light on how cognitive dysfunction occurs in Lyme Borreliosis.
Using monkeys he has demonstrated that in the laboratory when monkey brains are exposed to Borrelia numerous cytokines are released which result in neuronal apoptosis in the presence of microglia.
The relevance for chronic Lyme in humans is unclear but if damage is cytokine mediated then interventions which reduce this may be expected to help.
Phillipp noted that Doxycycline reduces the immune mediator IL 6 in his experiments and he suggested that this may be relevant to the therapeutic benefit observed when this agent is used in chronic Lyme patients.
Steven Schutzer MD reported on a technique to identify the microbial population in ticks.
It is becoming clear that ticks harbour a complex array of microorganisms just as many Lyme disease patients appear to be multiply infected.
The technique referred to as Ibis T5000 uses non specific DNA primers enabling simultaneous identification of an array of microbes.
It is hoped that the technique will result in enhanced mapping of tick borne pathogens and there is a possibility that new infective agents will be identified.
Patricia Conrad DVM PhD is a Parasitologist with an interest in Babesiosis.
Conrad reported that Babesia microti is endemic in the mid west USA and in humans it may be present without causing symptoms or in some cases it may cause a flu-like illness.
Anemia and thrombocytopenia may be a clue to its presence.
The more recently described Babesia ducani (formerly WA1) is phylogenetically quite distinct from B. Microti but it was stated that this too may be carried asymptomatically.
It was stated that there is currently no evidence that B. ducani is a Lyme co-infection and Conrad questioned the validity of some tests used to infer Babesiosis in humans.
Conrad suggested that some cases of Babesia may be falsely reported as Malaria but careful examination of blood films may lead to the detection of ``Maltese Cross'' forms of erythrocytic inclusions typical of Babesia infection.
There are few reports of Babesiosis in Europe and most of these are due to B divergens which typically appears to cause a fulminant illness.
It is clear further work is needed worldwide to enhance our understanding of the pathology and ecology of this elusive protozoan.
Diego Cadavid MD is another worker who has been attempting to shed light on neuroborreliosis.
He reported on the results of experiments using Borrelia turicatae, the relapsing fever spirochete, in mice.
Mice deficient in IL 10 and antibody production were rapidly killed by the spirochtete unlike wild mice which were relatively unaffected.
Mice only deficient in IL 10 production had higher cerebro-vascular vascular complications despite a low spirochete load and this lead Cadavid to conclude that IL10 plays a critical role in protecting the brain and other organs from vascular complications during borrelial infection.
Comment: Lyme disease has been associated many different neurological events central and peripheral, reversible and irreversible.
There is no ``neuroborreliosis syndrome'' and the causes of neurologic disturbance in Lyme disease in humans appear to be multi-factorial and complex.
Brian Fallon MD gave an overview of the clinical profile of chronic Lyme disease with an emphasis on biomarkers.
He noted that C6 Elisa is one of the best markers of Borreliosis and has a specificity of close to 100%.
As with other tests sensitivity is lacking and the search for a reliable bio-marker continues.
Fallon's studies have shown that clinical features (symptoms) are the best predictors of response to treatment in Lyme disease.
Fallon suggested that chronic Lyme disease should be defined in a way which is aetiologically neutral.
Comment: Fallon wishes to define chronic Lyme disease to incorporate both ``Post Lyme syndrome'' and persistent infection.
The problem with this approach is that there are many patients who have never received treatment for Lyme disease despite clinical features of the condition and this category of patient would be left with no diagnostic label.
This author suggests that chronic Lyme disease should imply persistent infection even though this fact may remain unproven in an individual case.
Such a label is not inconsistent with a concomitant pathological process which is independent of infection.
Christopher Contag PhD described a technique of Bio-Luminescence Imaging which enables localisation of bacteria in the living host.
So far the technique has been used with Listeria in mice and the results have contradicted existing dogma about the condition such as the belief that the organisms are obligate intra-cellular parasites.
One problem if the technique is used for Borrelia may be the need for a threshold of 100-1000 organisms for detection but if sensitivity can be improved the technique appears to have potential to increase our understanding of the pathogenesis of Borreliosis.
George Chaconas PhD has also been imaging bacterial infection in the living host.
Chaconas pointed out the advantages of studies involving real time parasite-host interactions over a reductionist scientific approach which will inevitably lead to caveats.
Chaconas has produced remarkable real time 2D and 3D videos of Borrelia in a laboratory host which include actual penetration of blood vessels by the organism.
We were told that the images are available for viewing on the World Wide Web.
Armin Alaedinin PhD spoke about Immunologic abnormalities in post Lyme syndrome.
Numerous immunologic changes are known to occur following Borrelia and other infections and auto-immunity is frequently invoked to explain some symptoms of Lyme disease when infection is no longer thought to be present.
The example of Guillain Barre syndrome, which has been associated with prior Campylobacter jejuni infection, was cited as a specific example of a neurologic auto-immune pathologic process.
Borrelia being a complex microbe has the capacity to stimulate the production of many different antibodies and Alaedinin's work has demonstrated that Post Lyme Syndrome patients have increased IL10 levels when compared to Lyme patients who have symptomatically recovered.
The increase was comparable to those found in some other auto-immune disorders such as SLE.
The hope is that a better understanding of the disturbed immunologic reactions will lead to targeted immune modulating therapies in the future.
In response to a very good question from the audience Alaedini agreed that it was possible that raised the raised IL10 levels could be masking symptoms in his control group of patients and these could in fact have latent infection.
John Keilp PhD has worked closely with Brian Fallon at Columbia University.
Keilp has been addressing the difficult question of whether depression in Lyme patients is secondary to the illness or independent of it.
By comparing two groups of depressed patients one with a Lyme diagnosis and one without Keilp concluded that Lyme patients with mild depression have greater impairment of memory and verbal fluency than is the case in depressed patients who do not have Lyme disease.
Fabio Tavora MD is a pathologist who presented a case of fatal Lyme carditis.
Evidence for Lyme in the case included EM type rash, positive blots and positive cardiac PCR.
In the case in question it appears an opportunity to treat Lyme disease at an early stage was missed but whether this would have affected the outcome is, of course, unknown.
Comment: The case raises the question of how often Lyme might be an underlying infection in cases of myocarditis which are commonly attributed to viral infections or hypersensitivity reactions.
Suzanne Vernon PhD gave a talk on Chronic Fatigue Syndrome (CFS) which she has studied extensively.
It was stated that there are many parallels between CFS and Lyme including the lack of a bio-marker.
Vernon noted that CFS is a diverse group of conditions.
She has developed a model of the condition in which disturbance of the HPA axis is central.
Comment: CFS affects around 4 million Americans and the severity of the illness is such that many are incapable of work.
How many CFS patients have symptoms attributable to tick borne illness is not known.
Even if the proportion is small the Public Health implications would be significant.
Benjamin J Luft PhD gave the final LDA talk. He spoke about studies which have investigated gene expression in B. Burgdorferi.
He told the audience that under laboratory conditions around half of the potential 1400 Borrelia proteins are expressed.
Conditions such as pH and temperature can be varied and the effects on gene expression can be studied.
Comment: It may be rewarding to study the effects on gene expression in Borrelia under hypoxic conditions since Borrelia appears to favour areas of the host which are relatively low in oxygen saturation.
Willy Burdorfer PhD gave the first ILADS talk. He enthralled the audience by relating the story of his discovery of the Lyme disease spirochete.
Although many scientific discoveries have an element of fortuity it was clear that Burgdorfer's discovery was the result of many years of dedication and hard work in the study of the biology of ticks.
In early work Burgdorfer had focussed on Relapsing fever the infectious agent of which could be readily identified in the arthropod's haemolymph.
Much later in his career Burgdorfer found a Nematode worm in one of the American ticks he was studying.
This was unusual and led him to investigate specific tissues of the tick. In the mid gut he found spirochetes and, as the saying goes, the rest is history.
Stephen Phillips MD considered in detail available published evidence pertaining to chronic Lyme disease.
He presented numerous citations which establish sero-negative Lyme disease and persistence of Borrelia infection as facts.
Robert C Bransfield MD is a psychiatrist who specialises in Lyme disease.
Patients with Lyme disease are invariably polysymptomatic and complaints such as sleep disturbance and neuropathic pain may be severe enough to warrant symptomatic treatment.
Bransfield noted that sleep disturbances occur in many chronic inflammatory disorders and he suggested a number of therapeutic approaches which may help the distressing symptoms of a patient with Lyme disease.
Judith G Llevanthal PhD has been analysing data from physicians who have been treating Lyme disease.
In common with findings in adults it was reported that in children neurocognitive symptoms were among those most commonly reported by patients with Lyme disease.
Deborah A Metzger PhD MD specialises in Chronic Pelvic Pain (CPP) which is an intractable and incapacitating symptom for some women.
CPP is known to be associated with various inflammatory conditions and infections and Metzger considers that Lyme disease is a very important association.
Her experience in treating this difficult group of patients with various types of therapy was discussed.
Richard Horowitz MD gave a talk on his holistic approach to patients with Lyme disease.
Horowitz emphasised the need to consider many other factors in Lyme patients in addition to infection.
These include consideration of the need for heavy metal detoxification and correction of minor endocrine disturbances.
In addition Horowitz reminded us that psychological factors may be an impediment to improvement in some cases.
Horowitz noted that the symptoms of chronic Lyme disease are similar to those reported in other conditions and there was a need for continuous vigilance to ensure coexisting conditions are not missed.
Comment: There is clearly a need for studies to address the efficacy of many of the therapeutic interventions in Lyme disease.
One problem in doing this is patient selection since Lyme disease patients are a diverse group and in many cases the diagnosis of Lyme disease cannot be made with certainty.
In the absence of such data patients are the arbiters. Judged by the numbers of patients Horowitz has treated his approach is a successful one.
Ann F Corson MD gave a talk on her experience in using German Biological medicine in the treatment of tick borne disease.
These treatments are often combined by Corson with allopathic antibiotics to treat her Lyme disease patients.
The methods are strongly linked to the traditional Chinese medicine theory Shan Han Lun.
Comment: It is clear that for many patients antibiotics are not a complete answer to their symptoms and alternative approaches should be welcomed.
Medicine is not science and physicians cannot wait for all treatments to be thoroughly proven before offering them to patients.
Garth L Nicolson PhD gave a talk on the relationship between neurodegenerative disorders and tick borne pathogens.
Nicolson has intensively studied veterans of the Gulf War many of whom developed medical problems commonly known as ``Gulf War Syndrome''.
Veterans additionally had a much higher than average incidence of ALS.
Nicolson considers that tick borne pathogens (especially Mycoplasma and Borrelia) were an important cause of the disease burden in the veterans.
Additional factors such as multiple vaccination and toxic exposure were also likely to have played an important role due to immunosuppression.
Nicolson has noted that children of Gulf War Veterans have a higher than average incidence of Autism Spectrum disorders and it was suggested that this may be due to Mycoplasma transmission.
Comment: Lyme disease patients often report Lyme like illness in family members.
While common exposure to ticks is one possible explanation an alternative explanation of non tick associated transmission of co-infections is an interesting hypothesis.
Daniel J Cameron MD (current ILADS President) spoke about strategies to prevent chronic Lyme disease.
He noted that the number of cases of Lyme disease reported to the CDC continues to rise.
Furthermore the CDC acknowledges that reported cases may represent less than 10% of the true incidence.
Additionally other tick borne illnesses are not considered in the figures.
Cameron believes that it is only through consideration of neglected facts about Lyme disease that public bodies such as the CDC could develop more effective prevention strategies.
Dr. David C Owen Cardiff, Wales, UK October 2008-10-20
This article has been donated to the UK charity Lyme Disease Action for free distribution.
The opinions expressed herein are solely those of the author, Dr. David C Owen
-------------------- Lymednva Posts: 2407 | From over the river and through the woods | Registered: Apr 2006
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Cass A
Frequent Contributor (1K+ posts)
Member # 11134
posted
Wow!!
Thanks for the great and informative report!
Best,
Cass A
Posts: 1245 | From Thousand Oaks, CA | Registered: Feb 2007
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bettyg
Unregistered
posted
cold feet,
THANK YOU for your labor of love in taking detailed notes that i was finally able to read in LYMNEDVA's broken up version !!
cold feet, could you add a note at the very top of where text starts that there is a broken up version by lymnednva towards the bottom please so other folks just don't scroll on by since they are unaware of this??
thanks for clicking on pencil, 3rd box to your right to do this for ALL lyme members who want to read the extensive post you wrote up for those of us unable to attend!
lymednva, God bless you for taking all this time to break up everything for yourself and all of us neuro folks who can't read/comprehend as it was typed!
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