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Posted: Mon Aug 29th, 2005 05:40 |
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LYME/BORRELIOSISlink
Bacteria change to L-forms whenever their environment gets very harsh.
The Brorson's found that the immune system environment in spinal fluid, which is very hard on bacteria, causes them to change to L-forms.
Brorson O, Brorson SH: In vitro conversion of Borrelia burgdorferi to cystic forms in spinal fluid, and transformation to mobile spirochetes by incubation in BSK-H medium. Infection. 1998 May-Jun;26(3)144-50
http://tinyurl.com/7ccdw
..Trevor..
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Posted: Wed Sep 7th, 2005 04:05 |
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LYME/BORRELIOSISlink
Lyme Inc.
David Whelan 03.12.07 Health
Ticks aren't the only parasites living off patients in borreliosis-prone areas.
Three years ago Heather Jenkins, a 30-year-old mom in Huntersville, N.C., was constantly fatigued and prone to colds. Her internist referred her to Dr. Joseph Jemsek, a self-described "Lyme Literate" doctor. During the initial consultation he asked if she had been bitten by a tick or gotten a rash. No, she replied, but she had gone camping once in Tennessee. He suggested she may have picked up Lyme disease there and sent her blood to a California lab that specializes in tests for tick diseases. A week later the test results came back: She had been infected by Borrelia burgdorferi, the spirochete that causes Lyme disease.
Jemsek installed a tube in Jenkins' arm and every two weeks for a year and a half sold Jenkins a $3,000 course of Rocephin, a powerful antibiotic, to infuse on her own at home. When she developed infections around the catheter in her arm the nurse would switch it. When her arms wore out she got a port implanted in her chest. As she waited for Jemsek to treat her latest infection, she collapsed on the floor, vomiting. Drug-resistant bacteria had overtaken her entire body. Jenkins landed in a hospital intensive care unit for four weeks, barely surviving. A doctor at Carolina Medical Center, where she recovered, told her that their labs could find no evidence in her blood that she'd ever had Lyme. "I was outraged," she says, and is now suing Jemsek. The near-death odyssey cost her insurance company $400,000. The action is pending, and Jemsek has made no comment.
Lyme disease, with 20,000 cases reported annually, ranks low on the list of the most prevalent infectious diseases. But it ranks first in rancor generated in the medical community. The disease is caused by bacteria related to syphilis that enter the body through a tick bite. The typical Lyme infection responds to simple antibiotics, although symptoms like arthritis and fatigue may linger in a subset of patients. Researchers at academic medical centers who study the disease say that so-called chronic Lyme, or post-Lyme, is very rare, hard to detect and not treatable with any further doses of antibiotics. The mainstream doctors warn about an epidemic of bunk diagnoses and dangerous treatments. Insurers often refuse to cover the cost of treating chronic Lyme.
Arrayed against the establishment is a fraternity of Lyme specialists, many of whom have built large practices treating ostensible Lyme patients with expensive courses of antibiotics.
Last year the North Carolina state medical board brought Jemsek in for a disciplinary hearing. Ten patients testified to nightmarish experiences. A widower said his wife had died from a morphine overdose related to Jemsek's Lyme treatments. Jemsek disputed all the charges vigorously. He also had 200 supporters show up, many of whom believe he cured them of a terrible disease. The Lyme Disease Association, a group that supports Jemsek, says that 30 chronic Lyme doctors have been similarly targeted by medical boards. Jemsek ultimately received a "suspension with stay" that allows him to keep practicing.
The light penalty may reflect the power of Lyme support groups, which blast politicians with mail and phone calls to ensure their access to expensive care. Standing with them now is Connecticut Attorney General Richard Blumenthal, who has received awards from Lyme groups and late last year announced that he was investigating the Infectious Diseases Society of America, an 8,000-member organization of doctors trained to understand diseases like AIDS, malaria and tuberculosis. Their crime? Issuing Lyme treatment guidelines to doctors that warned against using long-term infused or oral antibiotics.
Blumenthal, who hasn't yet issued any lawsuits in the case, says that the IDSA's guidelines may be in violation of antitrust laws. "Lyme disease is an extraordinarily insidious and widespread problem in Connecticut. We want to make sure that patients and physicians have unfettered choices," he declares. Insurance companies, he goes on, may be colluding with the IDSA to deny care. It's an odd charge, since a 1996 policy statement from the Federal Trade Commission and the Department of Justice says that treatment guidelines issued by medical societies do not limit competition. "You want medicine to advance by debate, not hampered by lawsuits," says Robert Buchanan, a medical-antitrust attorney in Boston.
Despite intimidation from elected officials like Blumenthal, the establishment has scored some hits against Lyme specialists. In 1993 Vithaldis Shah, a New Jersey doctor, had his license yanked for five years for sickening Lyme patients with long-term antibiotic treatments and receiving a payment from the infusion company. In 1996 a doctor in Michigan was suspended after conspiring with a home infusion company and misdiagnosing Lyme patients. In 2000 a study described the death of an anonymous woman from complications arising from treating unsubstantiated Lyme with antibiotics.
In Connecticut Dr. Charles Jones, a pediatrician, is under investigation by the state medical board for prescribing, over the phone, antibiotics for chronic Lyme to two children in Nevada, a desert state with few ticks. Jones, who pulled up to a June hearing in a stretch limo to the cheers of fans, has testified that he did not finalize a Lyme diagnosis until he saw the children in person. Since the hearings began, more upset patients have joined the action against Jones. Blumenthal, however, has criticized the medical board for its investigation.
Mainstream doctors say their guidelines are based on scientific evidence. An early study identified 25 patients with gallstones or bile blockage resulting from antibiotic treatment of unsubstantiated chronic Lyme. A more recent study of infused antibiotics published in the New England Journal of Medicine was cut short after Lyme sufferers with persistent symptoms did not respond to a course of antibiotics any better than they did to a placebo. One patient getting antibiotics had a pulmonary embolism; another had gastrointestinal bleeding.
Another paper in the Annals of Internal Medicine calls chronic Lyme a "functional somatic syndrome," similar to other nebulous ailments like Gulf War Syndrome, chronic fatigue and fibromyalgia. Another study in the same journal found that 60% of Lyme disease patients lacked any evidence of previous or active Lyme infections. Some of these patients suffered from depression, arthritis or other diseases. "There are lot of people who have fatigue or musculoskeletal pain. We want to help them but not with long-term antibiotics," says Dr. Gary Wormser, an infectious disease expert at New York Medical College who helped write the guidelines that prompted Blumenthal's attack. After the latest idsa guidelines came out in November, Wormser and his Valhalla, N.Y. lab were the target of a protest attended by hundreds of chronic Lyme patients and supporters; one sign said "Wormser Lies … Patients Die."
Many of the chronic Lyme patients are upset that their insurance companies won't cover unlimited treatments. WellPoint (nyse: WLP - news - people ) will pay for only four weeks of IV antibiotics, citing published peer-reviewed studies. But science is no match for the Internet, where Lyme patients swarm chat boards to bemoan the persecution of their doctors and egg on politicians. Some celebrities have joined in the fray, such as novelist Amy Tan and Daryl Hall of rock duo Hall and Oates, both of whom say they suffer from chronic Lyme.
Tan's doctor is Raphael Stricker, president of the International Lyme & Associated Diseases Society, which represents chronic Lyme doctors and patients. Stricker's San Francisco clinic also advertises its ability to treat obesity, infertility, erectile dysfunction and AIDS. In 1990 Stricker was forced out of UC, San Francisco after the school claimed he falsified data in what had been a seminal AIDS study. Before he discovered Lyme he spent two years as associate medical director at a penis enlargement clinic.
Stricker and many of his chronic Lyme allies send their blood tests to a California lab called Igenex, which was once investigated by Medicare and the state of California for pumping out too many positive tests. Nick S. Harris, chief executive of Igenex, says he passed both investigations easily, but in 2001 the federal Office of the Inspector General put Igenex on a list of noncompliant labs. It paid fines totaling $48,000. Harris says his firm has had no recent brushes with regulators. Harris says that his tests are more sensitive than ones given by lab giants Quest Diagnostics (nyse: DGX - news - people ) and LabCorp, yielding positive results 25% of the time. The big national labs typically return positive results 8% of the time. He acknowledges that his results are more open to interpretation, which could facilitate more positive diagnoses. "Patients, because of the Internet, have become my best salesmen," Harris says.
Jemsek, who in 2005 collected $6 million from Blue Cross Blue Shield of North Carolina, is still practicing, having declared his earlier practice bankrupt. He opened a new cash-only practice, spending $8 million on a building with a waterfall and grand piano. On the Internet patients exchange tips about how to keep seeing him. In his statement to the medical board after the stayed suspension of his license, Jemsek, who declines to be interviewed, said: "I've got 400 letters of support here, many single-spaced and several pages long."
David Whelan is with the Silicon Valley Bureau, Forbes.
=============================================================
Why are conventional antibiotics effective for some Lyme patients but not others?
We Lyme sufferers hear all the time about other people who had Lyme as bad as we do that recovered from conventional antibiotic regimens. How come some of us recover from, say, Rocephin, while others don't? Is it because those who recover are not genetically predispositioned to having their vitamin D metabolisms de-regulated by the infections?
(I'm currently trying to get my doctor to do vitamin D tests for all her Lyme patients. If only some of us have de-regulated vitamin D ratios, then it would explain why some of us recover from conventional antibiotics and some of us don't and hence require the MP.)
Mike
..............................
Mike,
No, it is because your definition of 'recovery,' and the definitions of others, are probably very different.
At the Chicago Conference Belinda defined recovery as basically getting to feel 20 years younger - as getting your life back. There has never been any recovery to this point before the MP. In the past patients were happy if they could just get to see it through another day...
Rocephin is palliative in Th1 disease. It suppresses the Th1 symptoms, but they come back when you stop, as the bacterial load is multiplying while Rocephin inhibits your immune system from killing the Th1 pathogens.
Lab workers have used Beta-lactam antibiotics for decades to induce bacteria to turn into the L-forms which cause the Th1 diseases. The beta-lactams (penicillins and cephalosporins) actually protect the L-forms as they are being created from the dying blood-borne infection. The overuse of beta-lactams may well be responsible for much of the proliferation of autoimmune disease over the last 20 years, IMO.
..Trevor..
Why doesn't the MP use some of the other antibiotics?
What degree of healing is possible with the MP?
Last edited on Mon Feb 26th, 2007 23:22 by Foundation Staff
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Posted: Sat Sep 10th, 2005 21:28 |
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(filename)
Why the MP cures chronic borreliosis when other treatments fail
Taken from an article written by J.C. Waterhouse, Ph.D., in her Issue 8, 2005 Update, found in CISRA's Synergy Health Newsletter which may be obtained for free from http://SynergyHN.com.
"I have learned a number of additional things since I wrote it (Ed.-an earlier article) that may prove useful to others. Although many patients do report improvement with extended use of antibiotics for chronic Lyme Disease, for many, the improvement is inadequate, or relapse occurs, even with long term intravenous antibiotics. In my own case, I used various oral antibiotics in several combinations at high doses for 2 years and did not improve significantly. I also used Mepron for 3 weeks for Babesia and did not improve (in fact, the Mepron had a negative impact, in that I developed a sensitivity to it and it took a very long time to excrete the Mepron after I finished taking it).
"However, the good news is that there is a newer treatment approach that is showing great promise in Lyme Disease. I have used this approach, called the Marshall Protocol, for the last 8 months and have been having much greater success than previously. The approach uses a specific type of immune modulation, together with low doses of certain antibiotics, to more effectively kill the cyst forms of bacteria hiding inside cells. Some believe the cyst or cell wall deficient (CWD) forms of the bacteria are the true source of the chronic symptoms of Lyme Disease, as well as a variety of autoimmune and other unexplained inflammatory syndromes. The Marshall Protocol (MP) was developed by Trevor Marshall, Ph.D., for sarcoidosis, but has recently been showing promise in other diseases thought to be caused by these CWD forms of bacteria (for more details and references on this approach, see Issue 7 on web site).
"In this update, I also want to provide my current perspective on some other topics mentioned in the 2002 article. With regard to testing methods, although Igenex Laboratory probably still provides the most sensitive tests for Lyme Disease likely to be covered by insurance, I think the Bowen test is probably actually more sensitive in detecting Borrelia infection (http://www.bowen.org). It may be true that some people who consider themselves fairly healthy may still test positive on the Bowen test, however they will typically have low titers (and it is possible they may have some mild symptoms, or develop symptoms later). It appears that you can use the titers (or concentrations of bacteria) found with the Bowen test to monitor the level of bacteria in your body.
"However, if you want to use your financial resources most efficiently, another strategy might be to skip individual tests for bacteria and instead test for vitamin D metabolites. The two vitamin D metabolites that need to be measured are 1,25D and 25D, and for the most accurate results for 1,25D, you must use a lab that freezes the samples for transport (for more information, see Issue 7 or http://www.marshallprotocol.com). The ratio of 1,25D to 25D are used in the Marshall Protocol (MP) to indicate the level of inflammation occurring due to infection by CWD bacteria, which include Borrelia burgdorferi, as well as many other species of bacteria.
"Unfortunately, many studies are reporting low vitamin D levels and recommending vitamin D supplements, as a result of measuring only the inactive precursor form of vitamin D (25D). As occurred in my own case, this practice of measuring the wrong type of vitamin D can lead to problems in people with certain inflammatory conditions. My level of inactive precursor 25D was low, while my active, 1,25 vitamin D hormone was elevated, and contributing to my symptoms. The 1,25 vitamin D hormone may be elevated in patients with low 25D because infected macrophages are causing an excessive, unregulated conversion of 25D to 1,25D. The high 1,25D can directly cause many symptoms, as well as help the bacteria to increase and can actually lead to bone loss.
"As for testing for other coinfections, Dr. Marshall believes that early evidence suggests that various coinfections will be eliminated by the immune system as you recover using the MP. Thus, if you do the MP, you may also choose to forego individual tests and treatments for tick-borne coinfections."
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Posted: Sun Sep 25th, 2005 00:24 |
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Why might a person have many serious symptoms yet have a low Bowen RIBb test dilution ratio?
The Bowen test looks for borrelia burgdorferi bacteria. I have read somewhere that they use commercially available borrelia burgdorferi antibodies produced from animals for their q-RIBb test. The Bb part of the name stands for borrelia burgdorferi.
There is also STARI Disease now recognized by the CDC, which stands for Southern Tick-Associated Rash Illness. The CDC says that the illness has Lyme-like symptoms, but cannot be detected with the current Lyme-borreliosis lab tests, and is caused by the borrelia lonestari bacteria, and distributed by the Lone Star tick. This disease is recognized by CDC for less than two years, or, about that length of time. The CDC says that STARI is found in the Southeast section of the U.S. There may be other borrelia that are loose in the U.S. and not even thought of, much less found and proven by the CDC.
Perhaps, a person had contracted STARI (borrelia lonestari bacteria) first, which may have given them time to multiply to be the greater in numbers. Then, contracted an infection of borrelia burgdorferi bacteria at a later time, which gave one the low dilution ratio on the Bowen test, since their numbers have not yet increased tremendously. Or, even some other borrelia is involved other than borrelia lonestari? Or, some other CWD bacteria other than borrelia?
The symptoms of both infections are supposed to be the same. And since both are CWD (cell wall deficient) bacteria, they are combining their efforts on your immune system in a Th1 inflammatory response, to make one's symptoms so severe, yet give one the low dilution ratio on a Bowen RIBb test.
Perhaps, what is needed is a rapid indentification test that will incorporate both borrelia lonestari antibodies as well as borrelia borrelia antibodies, which will then give one a dilution ratio for each bacteria. And solve this mystery! Perhaps, even a more complete gnenome study of all borrelia bacteria is needed, but with the ability to "mate", and share genetic material to the new "offspring" as proven by researchers at the NJ Medical School, this could lead to a very interesting piece of work.
This is another good reason why I believe that the Dept.of Healths should require doctors to report any case that show borrelia bacteria in symptomatic peoples' bodies even if it does not pass the CDC criteria for Lyme disease. The data is needed!
Thankfully, the Marshall Protocol should be able to "cure" all brands of borrelia infection, without knowing which one it is fighting.
George Howell
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Posted: Sun Oct 2nd, 2005 22:24 |
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Why do some Lymies say the MP doesn't work?
(filelink)
Q: I have received messages that some lymies don't think that the protocol works for them... any evidence of lymies getting full recovery from this??? I am reading a lot about lymies having difficulty with the MP (me included).. Does that mean that we are completely different then the sarcies and thus don't get the same good results? Or are they all similar stealth pathogens that get wiped out by this protocol?
~Flyer
Reply: What it means, I think, is that there are some people out there who seem to be happy if Lymies remain sick. Every Lymie who has reported their progress to me has moved forward to recovery while on the MP. Their titres drop month by month. For example, Susan, one of the delegation that was with us in Bethesda, now has a zero Borrelia titre, and is starting to put her life back together. Yet some of the Lyme 'experts,' and some of their sycophants, seem intent on slowing our inertia. As a member of that community you need to ask yourself - why?
We had a similar phenomenon in sarcoidosis, but over the last year the voices raised against truth and reason gradually fell silent. I suspect it will be the same in the CFS and Lyme communities, once folks stop trying to convince themselves that the MP doesn't work - and realize that it is their only hope 
Flyer, thanks for being one of the 'pioneers.' It isn't easy to pluck those arrows from your back...
..Trevor..
____________________
Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Posted: Fri Oct 7th, 2005 05:11 |
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Can borrelia change from spirochete to coccoid to L-forms?
The problem is actually a lot more complex than it seems. The genome of Borrelia has about 40% of its genes on mobile plasmids, and not on the primary chromosome. So (arguably) there could be hundreds of different versions of B.burgdorferi out there.
If you look at the master Genome list at URL
http://www.ncbi.nlm.nih.gov/genomes/lproks.cgi
you will find only two Borrelia species fully sequenced. One was sequenced by TIGR and one from Germany. Look at the sizes - 1.52 vs 0.99
This is because the Germans are only reporting the Chromosome and 2 plasmids, while TIGR is reporting chromosome and 21 plasmids.
Unfortunately the Borrelia genome has proven too complex for many of our institutions to fully assimilate, and this is an excellent example. Both groups are correct, but they are looking at the species in different ways.
A similar situation exists within the Mycoplasma species. Look for example, at this species comparison:
http://www.zmbh.uni-heidelberg.de/M_pneumoniae/genome/MP_MG_Comp.GIF
The rapid pace of advance in science's knowledge of the genome has left 99.9% of our Infectius Diseases specialists behind. It will take a new generation to come along who can understand the new genomic tools.
..Trevor..
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Posted: Fri Oct 7th, 2005 05:15 |
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(filelink)
Why does the MP appear to be taking longer to resolve Lyme/borreliosis and CFS than sarcoidosis?
I think that, in general, CFS and Lyme patients have had more long-term intervention from supplements and pharmaceuticals than many of the sarcies. Additionally, their disease is not as apparent as, for example, lupus or sarcoidosis, and this means that they generally are more ill before they get help. A sarcoidosis patient, for example, may die of pulmonary insufficiency or cardiac arrest before their overall systemic organ status degenerates to that of some of the CFS and Lyme patients.
I don't think there is any fundamental difference in the species, however. I myself suffered from debilitating fatigue for almost a decade, and had to work my life around my unusual sleep and rest patterns. It was seeing that fatigue in the diabetes patients (whom I was researching) that first made me realize the common threads through all the Th1 diseases.
It takes time to kill the intracellular bacteria and neurological inflammation is especially resistant because nervous tissue is poorly perfused by blood. The folks who are the sickest will need to be very patient because their inflammation is so extensive and it isn't possible to kill the bacteria rapidly without intolerable immunopathology.
I do think it is important that CFS and Lyme patients do face up to the extent of their illness, however. Think about this - it takes 2 years or more for the bacteria to be killed, at the fastest rate your body can kill them. It is absolutely amazing what that quantity of bacteria must have been doing while they were living in your tissues
..Trevor..
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Posted: Fri Oct 14th, 2005 06:47 |
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Info published about Lyme disease is not up-to-date
This article discusses variations of Bb-spirochetes and how researchers react to it:
http://tinyurl.com/77npx
=====================
While I understand that the material in this release may sound earth-shattering to folks who have come in contact with only the traditional view of Lyme disease, the material here is still not up-to-date, and is very limited in its outlook.
I do understand pretty well what the issues are here, and I have tried several times to communicate them to the MP membership.
The problem is that the Lyme genome is not homogenous, despite what the 'experts' would have you believe. There is a chromosome with about 500,000 bp and 21 linear and circular plasmids with nearly as many genes on them as are on the chromosome. Each plasmid is mobile and self-replicating. So it is in fact stupid (IMO) to keep talking about Borrelia as one species. It is not one species. It is not even close to being one species. It is not even clear how much of the genome is necessary to create a viable spirochete, let alone viable L-forms. So to talk about variations in sub-species is missing the point. Please, first define the species itself, then talk about sub-species variation. The same goes (to a lesser degree) for Treponema and Rickettsia.
Some sarcoidosis and CFS patients have no borrelia-specific markers. Clearly, borrelia is not the only organism involved in Th1 disease.
But those who understand these pathogens (at the detailed level of their genome) cannot yet communicate with the clinicians who are out in the field, and who get to speak to the press. We speak a different language.
How many of the sources quoted in this article would even know what a plasmid is? That is the problem that patients face. The genome has brought a revolution in knowledge about pathogenic species that only a fraction of the medical community (less than 1%) are equipped to understand. In general, patients will have to wait at least a decade for any of the concepts about these diseases to change - wait until either 'Continuing Medical Education' gets given teeth, or a new generation of clinicians comes into the workforce.
Thanks for posting this article anyway, I guess it gives us the chance to discuss the real issues.
.Trevor..
ps: maybe we need a conference just on this one issue. The next problem is how we get the agenda CME certified (by folks who don't have a clue)
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Posted: Fri Oct 14th, 2005 07:33 |
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(filelink)
HLA tests for Lyme disease
The HLA axis haplotype is almost certainly caused by the bacteria which have infected the patient, rather than by any genetic defect in the patient. You will find HLA haplotypes showing up in all the Th1 diseases. They are of no prognostic or diagnostic value at this point in time. For example, one of the strongest in Lyme, HLA-DRB1*1501, is also aberrent in Sarcoidosis, MS and Lupus (SLE).
The paragraph reflecting the commonality of HLA axis haplotypes throughout the Th1 diseases can be found at
http://yarcrip.com/sarcoidosissuccumbs-preprint.htm
..Trevor..
=================================
A case-control study to examine HLA haplotype associations in patients with posttreatment chronic Lyme disease.
Source: Journal of Infectious Diseases, Sept 15, 2005 v192 i6 p1010(4)
Author: Mark S. Klempner, Gary H. Wormser, Karen Wade, Richard P. Trevino, Jianming Tang, Richard A. Kaslow and Christopher Schmid
Full Text COPYRIGHT 2005 Published by University of Chicago Press.
Abstract:
In a comparison of 95 patients with systemic symptoms that persisted after antibiotic treatment for acute Lyme disease (posttreatment chronic Lyme disease) and 104 control subjects without such symptoms after antibiotic treatment, we sought associations between human leukocyte antigen class II (DRB1 and DQB1) markers and posttreatment chronic Lyme disease. No strong association between posttreatment chronic Lyme disease and any class II allele or genotype was found.
...............................................................
The key to understanding the results of this study are contained in the following words "Control subjects consisted of a convenience sample of patients who had been treated for early Lyme disease associated with erythema migrans during the 12 months before entry into this study."
I honed in on HLA-DRB1 allele *1501, which is commonly abberent in the Th1 diseases. It has been noted to be deviant in Sarcoidosis, Multiple Sclerosis and Lupus (SLE). Sure enough, there is the allele indicated strongly as being present in both symptomatic and asymptomatic Lyme.
However, because the 'control' sample were not really controls at all, but people who were already known to have been infected, the statistics used by the authors to analyse their data did not flag this *1501 allele (or indeed, any of the others).
But maybe that is what the authors wanted? Useless results? Or maybe they just didn't realize just how stupid it is to select an infected 'control' group?
I read this study as showing that patients with Chronic Lyme, Lupus, Sarcoidosis and Multiple Sclerosis all have aberrent alleles at HLA-DRB1*1501. Further that this study provides strong evidence that, once infected, the Lyme bacteria continue to live on in nearly all the Lyme victims, even those who are asymptomatic, and the alleles of the HLA axis provide persuasive evidence for the existence and persistence of Chronic Lyme.
..Trevor..
============================================
I don't believe that the HLA axis genetic changes are necessarily handed down in an individual's DNA, I believe that the HLA axis (HLA-DRA, HLA-DRB and HLA-DQ) are all mutations caused by the pathogens responsible for Th1 infection.
Only that hypothesis explains why so many different diagnoses end up with common HLA haplotypes, yet there is not determinate diagnostic value to be obtained by measuring them. Yes, I know, some of the HLA haplotypes are 50% greater in this, that, or the other diagnosis, but genetics should result in 100% and 0% and anything else is just statistical noise, and should be discarded, IMO.
..Trevor..
How does Th1 inflammation develop? What is successive infection?
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Posted: Thu Oct 20th, 2005 04:52 |
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Do not donate blood if you have Lyme/borreliosis
"Ms. Nguyen emphasized that "anybody who has had B microti is permanently prohibited from donating blood" and is registered in the blood bank system of the Red Cross nationwide. **However, it is important to identify those people infected with B microti prior to blood donation.** According to Ms. Nguyen, most of the transfusion-related transmission occurs through people who are infected with the tick-borne disease but who are asymptomatic".
Tick-Borne Disease Transmission by Blood Donation Prevalent in Endemic Areas
Mary Beth Nierengarten
Medscape Medical News 2005. © 2005 Medscape
Oct. 11, 2005 (San Francisco) The need to develop strategies to prevent transmission of tick-borne disease via blood transfusion is increasing as new reports continue to surface. Although not as much in the popular press as Lyme disease, Babesia microti is creating its own quieter havoc.
In a study presented here at the Infectious Diseases Society of America 43rd annual meeting, Megan Nguyen, BS, from the American Red Cross in Rockville, Maryland, presented data from a six-year study that showed the prevalence of B microti transmission via blood transfusion in areas where the tick is commonly found.
Examination of 13,573 samples from blood donors from 1999 to 2004 in endemic regions of Connecticut showed that 175 samples (1.3%) tested positive for B microti infection based on indirect fluorescent antibody testing.
Of these 175, 129 donors consented to participate in a three-year follow-up study in which they were tested by IFA for the presence of antibodies to B microti as well as receiving nested polymerase chain reaction (PCR) testing for parasitemia on a regular basis. Overall, 27 donors (21%) were found to have parasitemia as indicated by a positive PCR test, suggesting that some patients have persistent, ongoing infection.
In addition, parasitemia rates decreased from 55% in the first two years of the follow-up study to 3% in the third and final year. Ms. Nguyen said the study did not show a clear reason for this, adding that many factors could account for it.
Ms. Nguyen emphasized that "anybody who has had B microti is permanently prohibited from donating blood" and is registered in the blood bank system of the Red Cross nationwide. However, it is important to identify those people infected with B microti prior to blood donation. According to Ms. Nguyen, most of the transfusion-related transmission occurs through people who are infected with the tick-borne disease but who are asymptomatic.
Identifying infected people before they donate blood is therefore an important goal in reducing the risk of transfusion-related B microti transmission, but the best way to do this is not yet clear, she said.
Richard Whitley, MD, a professor of pediatrics at the University of Alabama in Birmingham who moderated the session, told Medscape that prospective blood donors are not currently screened routinely for tick-borne diseases, an issue that needs to be addressed by local blood banks.
However, Ms. Nguyen told Medscape she is hopeful "that there will be screening" or a U.S. Food and Drug Administration (FDA) approval for testing before donation. Unfortunately, she added, she does not know of any test under investigation for FDA approval.
IDSA 43rd Annual Meeting: Abstract LB-3. Presented Oct. 7, 2005.
http://www.medscape.com/viewarticle/514364?src=mp
Reviewed by Gary D. Vogin, MD
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Can I donate blood, organs, tissue or bone marrow if I have a Th1 inflammatory disease?
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Last edited on Wed Jan 17th, 2007 04:36 by Foundation Staff
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When To Suspect Lyme Disease
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This essay, written by John D. Bleiweiss, M.D. in April, 1994 is very long, but also very comprehensive. The reader suspecting Lyme symptoms should either identify with a number of sections of this article, or, in this absence, be fairly certain of excluding the possibility of Lyme. (Any Doctor investigating prudent treatment for Lyme Disease would do well by reading this essay.)
When to Suspect Lyme ..John D. Bleiweiss, M.D.
Traditionally, the public has been advised to suspect Lyme (LD) if a round or oval, expanding, red rash develops 3-32 days after a deer tick bite associated with or followed by a flu-like illness. This limited description will apply to only some cases. About 50% of patients do not recall one or more of tick bite, rash or flu-like illness. The rashes associated with LD can assume a variety of morphologies including vesicular, urticarial, eczematoid or atrophic (Acrodermatitis Chronicum Atrophicans). For many patients, neurologic, cardiac, arthritic, cognitive and/or psychological complications predominate. While deer ticks and LD have a well known affiliation, other potential vectors can carry the spirochete that causes LD (Borrelia burgdorferi; Bb). These include, the lone star tick, fleas, the biting flies (e.g. green-headed fly) (and mosquitoes?). A case of suspected transmission via blood transfusion has been reported by Dr. Burrascano.
The demonstration of Bb by PCR in two museum mouse specimens dating from 1894 (Massachusetts) and in ticks collected during WW II, provides a mechanism for potential life long exposure and disease which predates the formal 1975 discovery of LD. An occasional patient will date their symptoms which resolved on antibiotic therapy for LD to early childhood. Before the diagnosis was made, patients would dismiss those symptoms with the statement: "I've always had those problems". That resigned characterization implies that the longevity of the symptoms rules out a reversible cause. Subsequent resolution of the long standing symptoms on antibiotic therapy for LD belies that notion. Symptoms of LD can begin within days of inoculation with Bb or appear belatedly, but usually in the first to fourth month. Mice inoculated intraperitoneally had Bb demonstrated in the brain on biopsy 12 hours later with a peak at 48 hours (Stockholm Conference, 1990). Dr. Luft has published the detection of Bb by PCR (Polymerase Chain Reaction) in the CSF (Cerebrospinal fluid) of humans 2 weeks after the appearance of non-CNS related symptoms!
If dissemination can occur early, then staging the disease according to the temporal appearance of symptoms may be irrelevant. The absence of symptoms related to a particular organ system doesn't necessarily exclude the presence of Bb from that organ. Conversely, due to the possibility of symptoms being engendered by chemical mediators and autoimmune reactions by the host (against non-viable but immunoreactive DNA blebs), organ dysfunction and attendant symptoms can appear at sites removed from the actual spirochetes. The diagnostic and therapeutic problems that these phenomenon entail should be obvious.
Rapid dispersion of Bb could lead to the prompt appearance of complications; e.g., meningitis. There is no absolutely predictable clinical sequence for LD. The flu-like syndrome may be absent from the initial presentation and may endure once established without treatment. Cardiac and neurologic complications can be observed sometime within the first 3 months after microbiologically contracting the disease. Arthritis (i.e., joint inflammation; distinct from arthralgias; i.e., joint pain) can also accompany the initial clinical course, but more often develops later on between the second and sixth month from inoculation. The onset of complaints can not only be subtle and desultory, but delayed for a year or more. One of my patients denied all LD related symptoms until her husband died, whereupon, a plethora of complaints cascaded into her life beginning that very day. Another had an annual flare of LD as part of an anniversary reaction centered on the date of his mother's death.
Moreover, the early constellation of symptoms can have a paucity of findings with unidimensional presentations: the onset of solitary problems such as vertigo, or recurrent upper respiratory tract infections. Over time, as the untreated LD percolates, symptoms accrue to the burgeoning clinical picture until a multisystem presentation is created. Other patients can have their manifold symptoms complex develop in the manner of an avalanche. These patterns represent the extremes of a clinical continuum between which there are many variations on the theme ranging from mild to severe disease. Thus, The failure of a pathognomonic (unique and specific) presentation to consistently unfold causes sufficient clinical confusion, that a punctual diagnosis is problematic. Therefore, a high index of suspicion is placed at a premium. If a clinician can't reconcile preconceived notions about how LD should announce itself with a patient's history and physical findings, it is a disservice to the patient and an abdication of professional imperatives to presumptuously conclude that the symptoms are psychosomatic or that the patient is faking!
Antecedent or concomitant factors which can cause symptoms and physical changes de novo or aggravate contemporary problems are reliably solicited on close questioning of LD patients. Females experience an exacerbation of their LD symptoms before or during their menses, while pregnant and with oral contraceptive hormones. Many patients have symptoms intensify or reappear with physical and emotional stress, if sleep deprived, after exercise, in a hot bath, after alcohol consumption, with fasting (hypoglycemia) or dehydration. Humidity, low barometric pressure, cold or rainy weather can elicit arthralgias, fatigue, encephalopathy or headache. A cold draft of air can precipitate the appearance of pain in exposed skin and the underlying bone, or even VII cranial nerve (Bell's) palsy. Patients with poor control of symptoms abhor the extremes of ambient temperature. Typically, heat intolerance is revealed as irritability, headache, excessive perspiration or sleepiness. Photophobia can enhance the somnolent propensity that can occur while driving a car. Significant head trauma has incited severe symptoms that later resolved with antibiotic therapy for LD. A sudden acceleration of encephalopathy (see below), headache and dizziness, thought of as putative post-concussion syndrome, can be evoked by head trauma. Diagnostic inaccuracy will be minimized by not indolently attributing all problems following head trauma to the most obvious cause. I routinely advise my patients with LD to abstain from cigarettes, alcohol and steroids because therapeutic inadequacy or an avoidably prolonged convalescence is frequent (Dattwyler, RJ, Lancet 1:687, 1987 - on steroid use). Patients have described clinical deterioration when steroids were used fortuitously or intentionally when hypoadrenalism was absent. Another hazard attending palliative steroid use is that some symptoms will be concealed, rendering the clinical picture less interpretable. In a private communication, a physician related that one of his LD patients succumbed to fatal cardiomyopathy after receiving steroids. One helpful caveat is to avoid the use of electric blankets or sleeping in water beds with the electric current activated, otherwise you might wake up with one or more LD symptoms. Allergic and chemical hypersensitivities can enhance or cause symptoms to emerge temporarily.
Symptoms vary stereotypically during the day. Joint stiffness and "brain fog" are often reported on rising in the AM (but not solely in the AM). Fatigue can be unrelieved by sleep, or develop between noon and 4 PM, whereupon a short nap provides refreshment. "Madman Syndrome" (explosive irritability) may appear toward the end of stressful work period or late in the evening. A "mad face" can herald imminent detonation.
Prior to proper diagnosis, patients habitually report that they were assigned the following diagnoses most often: Chronic Fatigue Syndrome, Multiple Sclerosis, Fibromyalgia, Lupus, Candidiasis, Chronic mononucleosis, Hypoglycemia, and Stress-related illness. If these appear in a differential diagnosis, then LD should be considered.
On cursory inspection, many patients with LD appear deceptively well but in fact feel awful Don't be fooled! The mien of a Lyme patient ranges from phlegmatic, sullen, staring off into space, to one of agitated anxiety and hyperkineticism. Their oral and written recitations similarly vary from cryptic to being overinclusive and circumstantial. Geschwind's Syndrome embraces some varieties of LD encephalopathy precisely (Textbook of Internal Medicine, Ed: Kelly, 1989, p. 2509). Stuttering was reported by several patients to coincide with the onset of their LD and often proved reversible.
Patients most frequently report fatigue that varies from mild to debilitating. Usually there is a loss of interest and initiative so that lounging around becomes habitual. This derives not from laziness, but results from lassitude. Attempts to indulge avocational or vocational pursuits is frequently interdicted by either the languor of Lyme or by encephalopathy. There is a tendency to nap, sleep that is not rejuvenating, and hypersomnolence at inopportune moments; e.g., in the classroom or during a favorite pastime. Sleeping away entire days is not unknown. Paradoxically, at usual bedtimes, patients often experience insomnia or frequent awakenings. Sleep does not always provide respite as ferocious or vivid nightmares can occur. Childhood night terrors can be due to LD or more mundane causes.
Intermittent fevers range from low grade to 104.5 degrees F. The typical context for high fevers is in the first week of antibiotic therapy especially if multiple agents and/or IV drugs are used. While fever is the hallmark of the classic Jarisch-Herxheimer (J-H) reaction, its appearance is inconstant. Compared with most causes of high fever, the patient can look and feel their best during or shortly after the fever with a relatively non-toxic demeanor. This can sometimes be diagnostically helpful. The differential diagnosis of febrile seizures in infants should include LD. Many LD patients have routinely subnormal body temperatures so that the appearance of a temperature of 98.6 degrees F may be compatible with a low grade fever analogous to diabetics.
Very often, the pinna and ear lobes are varying shades of red. Less commonly, a similar erythema can be observed on the hands or malar (upper cheeks) areas. A malar rash is not pathognomonic of Lupus, if in fact SLE is distinct from LD (Abstract 55A, V LD Symposium). Fifth Disease (slapped face) is suspected of being due to LD. Lymphocytoma of the ear lobes has been encountered more often in Europe. Cold hands and feet even in warm environments occurs and some patients have Raynaud's phenomenon. Potentially contributing to this vasoconstriction are excessive levels of vasoconstricting hormones, magnesium and potassium deficiency, limbic or hypothalamic dysfunction due to CNS infection, local inflammation of capillary sphincter or hypothyroidism. Eczema and psoriasis can appear in conjunction with LD. A female LD patient had generalized psoriasis covering 40% of her body. Antibiotics for LD gave total relief.
Alterations of cutaneous sensation are very common. Most often there is numbness and tingling (paraesthesias)of the central face, fingertips, scalp and in the extremities. Muscle twitching usually occurs in the eyelids and extremities. Tremors, myoclonic jerking of entire extremities or truncal shudders can suggest pseudoseizures but is attributed to neuritis. Patients also report electric shocks, dysesthesias (abnormal sensory responses to stimuli), painful or itchy skin and flushing. An inordinate amount of exertional or non-exertional sweating may be described in the absence of hyperthyroidism. One of my patients experience anhydrosis (inability to sweat) for 27 years until antibiotics were given for LD.
Dizziness, imbalance and clumsiness can become very frustrating as patients drop objects or knock them over, trip a lot, turn into the wall when rounding corners, and develop sloppy and slower handwriting.
Many use the phrase "a vibration in my head". Others remark that they feel "toxic". Along with the "brain fog", these colloquialisms connote LD until proven otherwise.
Eventually the majority, but not all, complain of one or more of "foggy brain", forgetfulness, anxiety, mood swings, loss of initiative, depression, impairment of concentration, inattention, easy confusion or disorientation when attempting intellectual tasks. Paper shuffling can be the end result when patients attempt to organize or assimilate even limited amounts of information. These problems, and the others described below, constitute the salient features of Lyme encephalopathy.
Short term memory impairment causes patients to forget what they were going to say, why they entered a room, where objects were placed, the previous sentence or plot content, calendar dates, their schedules, names and faces of familiar people, even family members. Cognitive neglect caused one patient to wander around the room looking for the room looking for the pencil clenched between his teeth. A mother left her infant and baby carriage in my office parking lot and went home. Others forgot how to spell even simple words, how to read or must re-read with varying degrees of comprehension. One patient drove to Philadelphia instead of the desired Princeton destination because the initial letters were identical and confused him. After shopping for groceries, another patient placed her shoes in the refrigerator and stored the food in the clothes closet. Lyme patients can lose their way home or on the way to work, bypassing otherwise familiar exits or plain forgetting where they are in time and space or how they got there. This is known as topographical disorientation or environmental agnosia. Elementary math problems may prove insurmountable. Numerical errors are common. Sequential task performance is compromised in Lyme. Lyme patients have a penchant for saying, "Wait a minute", 2-3 times rapidly when the only demand on them is to record a phone number, which also speaks of perseveration.
Inattention frequently characterizes the way patients relate to the world. Some patients participate passively, unable to initiate or engage in the usual forms of social and intellectual exchange. Verbal and written forms of expression have a typical Lyme flavor. The content demonstrates disorganization, an inability to follow a train of thought and there is a proclivity to ramble on and on in great detail which propels further confusion amongst the forest of details. Ubiquitous among the myriad cognitive flaws are the frequent errors of word selection or pronunciation and the consistent word and number reversals.
Concentration on a task can be problematic because attention span is abbreviated. As increasing amounts of information have to be processed, the Lyme patient becomes proportionally lost, disoriented, frustrated, fatigued and finally must desist from further intellectual activity. The desire to initiate projects and social interaction is often blunted if not absent altogether. Thus a deterioration in academic and vocational performance is a frequent manifestation of LD in children and adults..
Miklossy (NeuroReport 4:841-848, 1993) reported the detection of Bb spirochetes on dark-field microscopic examination of post-mortem brain biopsy specimens FROM PATIENTS WITH ALZHEIMER'S DISEASE! CSF and blood cultures grew out Bb from those cases. In my view, a child assigned a diagnosis of Attention Deficit Hyperactivity Syndrome (ADH) or PNI (Perceptual Neurologic Impairment) should be evaluated for LD. A 16 year old boy whose Tourette's Syndrome began at age 5, had Osp A antigen detected in his CSF. LD treatment resolved the Tourette manifestations. Another patient of mine with ADH had a positive IgM Lyme antibody in the serum. The manifestations of ADH were eradicated while on antibiotics. Distinguishing causality from mere exacerbation of ADH or Tourette by Lyme is moot, and therefore, I suggest an evaluation LD for these patients. Parenthetically, the boy with Tourette also had cognitive impairment, familial nephritis with early renal insufficiency and OCD (Obsessive Compulsive Disorder). These clinical features all remitted with antibiotics! A real estate agent's prominent encephalopathy resolved with LD treatment whereupon his commercial output jumped to a record zenith and became the recipient of numerous corporate awards. The benefits of arresting LD are self evident to him.
Personality changes are nearly universal in Lyme encephalopathy with emotional and expressive incontinence being typical. Usually there is a baseline irritability which fluctuates. Patients with LD encephalopathy react to even mild degrees of stress with frustration, anger or crying spells out of proportion to the situation. Emotions can reach escape velocity and rages can become volcanic with a momentum beyond volitional control. Unpleasantness is inevitable due to volatile tempers, super critical dispositions, and impatience with themselves or others. Lyme patients can be easily irritated by anyone just walking into the same room even though eye contact is never made or words exchanged. Low threshold exasperation in unexpected circumstances is not uncommon. Thus a parent responds to an infant's needs with anger and frustration. Perpetrators of "shaken baby syndrome" recapitulate an emotional response indistinguishable from that of a Lyme patient whose encephalopathy is out of control.
Many express morbid fears of occult illness, impending death and can be generally pessimistic or maudlin. Some develop intricate paranoid theories regarding imagined conspiracies against them. Lyme patients often evince a tendency for being overly sentimental. Hyperbolic thought finds expression in obstinacy, self-righteousness, being contentious, speaking in categoricals, and inappropriate and atypical vulgarity. Internalized anxiety results in the perception of being hurried even without a deadline or the inability to remain calm when there is no reason for not feeling calm. Panic attacks are the extreme of this anxious state and should arouse a suspicion of LD. I suspect that in addition to CNS infection of the limbic system, these phenomenon could also be the result of elevated adrenaline levels, Mg++ deficiency or hypoglycemia. A rare LD patient will admit to agoraphobia or claustrophobia.
Depression alternating with anxiety is very common in LD. Psychiatrists should routinely evaluate a depressed patient for LD before/when initiating psychotropic medication. A patient with LD may have a plausible reason to be depressed, but their emotional response can not only be incongruous with their usual coping style but also the depression can be ablated or ameliorated with control of the LD infection. Lyme encephalopathy typically vitiates an otherwise mature and functional emotional repertoire.
With a loss of voluntary and subconscious editorial control of emotions and expression in word or behavior, a patient with encephalopathy gives the general impression of being erratic, inappropriate, if not dysfunctional. Less frequently, mania, obsessive-compulsiveness, schizoaffective disorders and homicidal/suicidal ideation is encountered and has been reported. Fatal attractions are consistent with the LD style.
Adolescent hormonal surges and the emotional turmoil wrought by LD at once camouflage and exacerbate each other mutually. Thus, children tend to be unruly, hard to please and prone to atypical emotional reactions. A child who is misbehaving in class should not be dismissed as a "bad kid". Lyme can catalyze inappropriate behavior and commentary. Many patients retrospectively realize that they were out of control but in the event were unable to intercept their behavior. Misattribution as to the origin of behavioral perturbations is the rule. The development of aberrant personality traits can be gradual or even situational, further obscuring the medical etiology. An acute break from normal behavior can serve to highlight the abnormalities and suggest the need for evaluation. thus, dysfunctional behavior and intellectual incapacitation are bitterly recalled by LD patients when they finally realize how their interpersonal relationships, school and vocational conduct were negatively impacted.
Clinically, there is considerable overlap between LD and Chronic Fatigue Syndrome (CFS). In their masterful review of the pathophysiology of CFS, Drs. Rosenbaum and Susser (Solving the Puzzle of CFS, 1992) describe SPECT scan findings of brain perfusion (blood) in CFS patients. Hypoperfusion of the left temporal, right parietal and left frontal lobes were consistently seen. These regions control the very areas of functioning which are abnormal in both LD and CFS, namely verbal capacity, memory, emotions and higher order information processing. Dr. Jay Goldstein has proposed the term "limbic encephalopathy" to describe the disorders of memory, appetite, temperature and appetite regulation, libido and hormonal homeostasis seen in CFS. He advances the concept of an "agent X" which incites CFS and causes dysregulation of the immune system and the limbic components of the CNS. I feel "agent X" is Bb. I am encouraged in this view by anecdotal experience whereby CFS responded to antibiotics given either fortuitously or by way of Lyme treatment, due to positive serologies (antibody tests) for LD in some CFS patients and the development of a J-H reaction in CFS patients who take antibiotics. Crimson crescents, portrayed as diagnostic for CFS, I have detected in LD where the diagnosis was secure.
Limbic encephalopathy elegantly embraces the preceding observations in Lyme encephalopathy. It is a potential mechanism to explain my suggestion that LD can be responsible for anorexia nervosa/bulimia. Anorexia was documented in earlier studies on LD. Uncinate fits and are characterized by hypersexuality, rage states and vulgarity, are compatible with LD. Indeed, disinhibition, the release of the usual brakes on behavior, would be part of limbic dysfunction.
LD could cause reversible disturbances in brain physiology through cytokine mediators, direct infection; e.g., encephalitis and perivasculitis, demyelination, metabolic aberrations within the CNS such as regional hypoperfusion, altered rheologic (flow) characteristics of blood, intracellular acidosis and the depletion of ATP. Permanent changes may include demyelination or loss of neurons leading to atrophy.
Neurologic complications in earlier reports were said to occur in 20% of LD cases. In my experience, and as published by Dr. Logigian, 90% of patients have one or more of encephalopathy, cranial neuritis or psychiatric changes. Early in the course of LD, these problems may be absent or muted, but eventually intrude and can become dominant aspects of LD.
Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS and LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination. In Miklossy's study above, senile plaques stained avidly for Bb spirochetes. Vincent Marshall reviewed the MD literature in Medical Hypothesis (Vol 25: 89-92, 1988) and advances the notion that LD is causing MS! His survey revealed that multiple studies prior to 1951 were able to demonstrate spirochetes in the spinal fluid of MS patients (by inoculation into animals and on silver stain of CNS tissues). Dr. Coyle has documented the presence of antibodies to Bb in MS patients (Neurology Vol. 39:760-763, 1989). The encephalopathy attributed to MS is very reminiscent of LD. Both MS and LD are associated with sinusitis (Lancet, 1986). Dr. Leigner has reported a case of LD which fulfilled all criteria for MS. The epidemiology of MS and the geographic distribution parallels that of LD. The symptoms of both LD and MS can be aggravated if the patient takes a hot bath. Anecdotally, patients with LD, who previously had been identified as MS, responded to antibiotic therapy.
LD has been documented to cause strokes, paralysis, a variety of seizures, transient or permanent blindness, Parkinsonian-like movement disorders, motor and/or sensory neuropathies, mononeuritis multiplex, radiculoneuritic pains, meningitis and encephalitis. It has been affiliated with Lou Gehrig's disease and the Guillain-Barre Syndrome.
Recent reports suggest that the spectrum of neurologic LD is actually similar in both Europe and the USA (Jacqueline, MS; Surv Opthalmol 35:191-204, 1990) and belies the assertion that European LD research holds no relevance for LD in the USA.
The more commonly noticed neurologic deficits involve one or more cranial nerves (I thru XII), most often the sensory divisions of the trigeminal (V) and the motor components of the facial (VII) nerves in my patients. In declining order, deficits to pain sense are detected in V2, V3, and V1. V2 neuritis appears as paraesthesias or dullness in the central face and cheeks. Gum and tooth pain can be another manifestation of trigeminal neuritis. Rule out dental abscess or sinusitis which can present with similar tooth pain.
The most common cranial neuritis I see is that of the VII nerve. Abnormalities of the VII nerve can be varied. Usually there is symmetry of the central facial creases, the lips at rest or in motion, or overt deviation of the mouth or smile to one side. Colleagues have dismissed these asymmetries as normal findings, saying "well, everyone has those". I feel there is significance when antibiotics cause these so-called innate or normal findings to resolve.
When Bell's palsy is present, there are the facial defects described above for VII neuritis plus a wider eye on the same side as an elevated eyebrow, often attended by complaints of tearing and drooling (usually at night) on the affected side. 10.6% of 951 LD cases were found with Bell's palsy and 25% of those have had bilateral Bell's palsy (Clark, JR et al. Laryngoscope 1985: 95: 1341-45). Bilateral Bell's promulgated as pathognomonic for LD, actually can be associated with intrapontine lesions, diabetes mellitus, syphilis, sarcoid, leukemia, Guillain-Barre, viruses or diphtheria. Considering the incidence of Bell's palsy in LD, it is improper to treat it as viral in origin without a work-up for LD.
Incidentally, hyperaccusis (sound sensitivity) can be a feature of VII neuritis. Olfactory neuritis (I) is attended by dysosmia (unusual smells). Neuritis of the III, IV and VI cranial nerves will show up as double vision. When the VIII nerve is involved, vertigo and impaired hearing can result. I have had at least two cases of Meniere's Disease respond to treatment for LD. Dysphagia (difficulty swallowing) can be associated with X neuritis but not invariably. More often in my experience, a deviated uvula or soft palate is perceived. Dysphonia (altered voice) can occur with X neuritis when the branches that serve the larynx are affected. Recurrent laryngeal nerve paralysis has been seen with LD (Schroeter, V. et al. Lancet 2:1245, 1988). IX neuritis (glossopharyngeal) can cause a unilateral sore throat which was reported by 3 of my patients. XI neuritis (spinal accessory) presents as trapezial or sternocleidomastoid muscle weakness resulting in a drooped shoulder or weakness on resisted head rotation respectively. Do not confuse this with a unilateral dystonia where the affected shoulder girdle will be elevated with preserved motor strength on both sides. Hypoglossal (XII) neuritis can be associated with a heaped up tongue on the unaffected side or deviation of the tongue on protrusion toward the abnormal side.
LD related headaches can have a wide variety of patterns and can broadcast the early onset of LD or a flare of LD. The headaches incorporate the characteristics of migraines, muscle tension or cervical/radicular headaches. Pseudotumor cerebri (elevated CSF pressure with normal CSF analysis in the absence of intracranial masses) can complicate the course of LD and cause headaches. Papilledema (swelling) of the optic disc is usually present when CSF pressures are elevated, but not invariable. A spinal tap will have high opening pressures and be therapeutic as well. Depending on the characteristics of the headaches, sinusitis and brain tumors may have to be ruled out. Cluster headaches have characteristics compatible with some LD headaches including responsiveness to 100% oxygen.
Immunosuppression due to LD has been reported. Therefore, it is not surprising that recurrent or intractable upper respiratory tract infections (URI's) have been noted. LD can cause or worsen pre-existing sinusitis, asthma, bronchitis, otitis, mastoiditis. Frequently, the pediatric history of LD contains a pattern of repetitive URI's. Mastoiditis can also be associated with a Bell's Palsy. LD can be affiliated with the appearance of new onset allergies for the first time in a patient's life or magnify an atopic predisposition. The usual medications for sinusitis and allergies will have a predictably diminished effect, when LD is operant.
Another concomitant reported by an incidental patient is the occurrence of motion sickness which can be reversed with LD treatment.
Eye related problems in LD are commonplace and can include conjunctivitis, ocular myalgias, keratitis, episcleritis, optic neuritis, pars planitis, uveitis, iritis, transient or permanent blindness, temporal arteritis, vitritis and periorbital edema (Jacqueline MS; Ibid). Horner's syndrome, ocular myasthenia gravis, and an Argyll-Robertson pupil are also reported. Optic neuritis has been observed to become recurrent or intractable after treatment with steroids. Given the earlier remarks about the detrimental effects of steroids on LD, recidivous optic neuritis may be due to occult LD.
Lyme hepatitis occurs in approximately 15-20% of patients. Liver tenderness is inconstant and the elevated liver enzymes respond to antibiotics. Sometimes, the hepatitis appears temporarily in the early phases of treatment with subsequent resolution.
In many of my patients, cysts are found not uncommonly in various locations: thyroid, breast, liver, bone, ovary, skin, pineal gland, and kidney. Some forms of Polycystic Kidney and Fibrocystic Breast Disease may be LD manifestations.
LD can cause an interstitial cystis leading to bladder pain relieved by urination. A neurogenic bladder can develop with either hesitancy, frequency, loss of bladder awareness, urinary retention, incontinence or the symptoms of UTI (urinary tract infection). I suspect that some cases of chronic pyelonephritis are actually LD. Pediatricians may want to consider that nocturnal enuresis (bedwetting) is secondary to LD.
Constipation severe enough to cause fecal impaction can occur. Many LD patients will experience a spastic (irritable) colon and that diagnosis should spark a search for LD. I have treated LD attended by ulcerative colitis with substantial remission of the colitis when antibiotics were inaugurated. Fecal incontinence due to impaired rectal sphincter tone can occur. Dr. Martin Fried has demonstrated Bb spirochete in the gastric and duodenal mucosa of children with LD who complained of abdominal pain and who were documented to have gastritis and/or duodenitis. It is appropriate to work up LD when confronted by these clinical entities.
Among untreated patients with LD, arthritis can ultimately develop in up to 60%. The joint swelling, which may or may not be painful, frequently is episodic, recurrent and migratory if multiple joints are involved. Any joint can be affected including the TMJ (temporomandibular) and small joints of the fingers (contrary to earlier reports). Up to 10% of untreated LD arthritis can develop into destructive/deforming synovitis almost identical to Rheumatoid Arthritis (RA). Dr. Lavoie has published the coincident findings of LD with RA, and SLE (lupus) with LD. The SLE was associated with positive DS-DNA (double stranded DNA) which is considered diagnostic for lupus.
The tabulation of rheumatologic syndromes, either caused by LD or affiliated with it, is growing. Drs. Weber and Schwartzberg have reported Polymyalgia Rheumatica apparently caused by LD. Sjogren's Syndrome with LD has been published. Antibodies to Bb in the context of Psoriatic arthritis, systemic sclerosis and Reiter's Syndrome have been documented.
An expanding cohort of patients in my practice appear to have long-standing LD that dates to their "growth spurt" years and their past medical history contains the previous development of Osgood-Schlatter's Syndrome (water on the knee) in their teens. A relationship to LD can't be excluded.
Arthralgias and bone pain in LD can be excruciating. It is the imprudent clinician or parent who lackadaisically attributes these symptoms to "growing pains" or aging.
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Another patient of mine recalled recurrent and migratory polyarthritis since he was 18 (1966). Monthly Medrol Dose Packs (steroids) failed to alter the clinical picture. In 1987, he was hospitalized with an acute exudative synovitis of the knee, whereupon ear lobe biopsy demonstrated the classic histologic feature of Relapsing Polychondritis, a very rare disorder with a peak onset in the 5th decade of life. In spite of continual high dose steroid treatment, (and later methotrexate with non-steroidal anti-inflammatory agents), he eventually developed a deforming arthropathy in his hands which progressed slowly between 6/90 to 12/92. Earlier physicians had discounted the significance of a positive Lyme Elisa = 1.09 in 4/91 as "low titer". An unsuspected encephalopathy betrayed its existence as memory and concentration impairment beginning 1/91. The patient presented for LD evaluation 1/93. Laboratory values include: an IgG by Elisa = 14.7, IgM by IFA = 80 and the Western Blot had bands at 31 and 41 KDA. the polysynovitis and encephalopathy proved rapidly responsive to antibiotics for LD. The patient was quickly emancipated from the other medications although steroids had to be slowly tapered and are now down to an inconsequential dose without recurrence of rheumatologic complications. The patient, although symptom free while on antibiotics, has permanent crippling deformities of the hands.
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Cardiac complications arise in 8-12% of LD cases. Conduction defects and heart block, of which first-degree is the most common, can be discovered on EKG. A long rhythm strip should be employed to detect intermittent blocks. Higher degrees of heart block can result in fainting or death and may require cardiac pacemaker.
Sudden death can also result from arrhythmias. Fast and slow heart rates occur, usually at the time of symptom flares, and sometimes in the manner of Sick Sinus Syndrome (tachy/brady). Ventricular tachycardia has been documented to attend LD infection in the heart, confirmed on cardiac biopsy. The cardiomyopathy may be complicated by congestive heart failure (CHF) as the following case might illustrate.
Mitral valve prolapse is not uncommonly found in LD. MVP can be associated with confounding chest pain and ventricular arrythmias. It is often accompanied by Mg++ deficiency and LD can cause Mg++ levels to be low. In a few of my patients, MVP developed only after the onset of LD and resolved with LD treatment. Chest pain due to LD may arise from numerous causes: myocarditis, pericarditis, angina, asthma, bronchitis, periostitis of the ribs, pectoral myositis and tendinitis, sternoclavicular and costochondral arthritis, esophagitis and esophageal spasm, stomach acid reflux, and gastritis.
Elevated ACE (angiotensin converting enzyme) levels have been detected in LD (Leigner, 1990). The relationship between high ACE levels and heart disease may provide a mechanism to explain LD's anecdotally suspected tendency to accelerate Coronary Heart Disease and incite hypertension. Possibly, Syndrome X (angina with normal coronary arteries at catheterization) is due to LD induced arterial spasm, an event that might be enhanced by direct perivasculitis and/or Mg++ deficiency (see Grisold, M abstract No. 55F, V Int'l Lyme Symposium).
Potassium deficiency without an obvious origin irregularly evolves in LD. Rarely, the K+ losses are profound. This could be due to Mg++ deficiency. New onset or difficult to control hypertension is more likely to be seen. LD should be part of the evaluation of hypertension. LD treatment has permitted easy BP control in several patients, some of whom were able to forego using their traditional hypertension medications. Increasingly, I am encountering thyroid disease in LD. A local endocrinologist has remarked to me privately that the incidence of thyroid involvement in LD may be greater than expected from the normal population. A final judgement awaits formal statistical analysis. In many of these patients, the thyroid dysfunction was seen to originate in the pituitary or hypothalmus. Remaining alert to the possibility of thyroid disease is essential because there can be considerable clinical overlap with LD. Subacute thyroiditis is the most prevalent thyroid phenomenon I see in LD. Hypoadrenalism can uncommonly develop. Uncorrected hormonal aberrations can vitiate otherwise effective LD therapy. Like any infection, LD can provoke the onset of hyperglycemia and alter the facility with which diabetes is managed.
Impaired fertility and a loss of libido is not infrequent in LD. A reversible cause of infertility should be sought and ought to include LD. Reduced sexual interest without an ostensible justification is usually misinterpreted by the partner with predictable social and psychological turmoil. LD infection in the CNS or in the sex glands may be causal. In a few female LD patients, disturbed estrogen and progesterone levels were found. Early "menopause", skipped menses, and heavy menstrual flow represent a few of the perturbations in LD.
Women with symptomatic LD can experience new onset or heightened PMS (ballistic mood swings and irritability), or perimenstrual headache or cramps. The last of these theoretically could also be due to Pelvic LD infection (ooperitis or salpingitis) and/or elevated PGE-2 (prostaglandin E-2) levels, the latter having been reported in LD. A surfeit of PGE-2, free radicals, altered fat metabolism and general immunosuppression by LD may contribute to a predilection (stimulate or predispose) for oncogenesis (forming cancer). Carcinomas are not unknown in LD: melanoma, thyroid cancer, and lymphoma have been published. Free radicals, by engendering connective tissue cross-linking, could be responsible for intra-abdominal adhesions to form, and for some LD patients to appear older than their stated age, or have a haggard facial appearance.
Breast pain due to mastitis and testicular pain from orchitis have been described by some of my patients. So far, there are 3 men in our files whose chief complaint with LD was pelvic pain due to chronic prostatitis.
Flawed studies have created the impression that pregnancy outcomes are not influenced by LD. There is substantial documentation to suggest a causal relationship between LD and stillbirths, congenital abnormalities, spontaneous abortion, low birth weight babies, prematurity and intrauterine fetal infection acquired from the mother. An outcome of untreated LD arising from Mg++ deficiency could be pre-eclampsia (hypertension) or eclampsia (hypertension with seizures). Magnesium is often relied on to treat these problems. Women with LD in pregnancy can experience severe morning sickness, gestational diabetes mellitus and prominent flares of Lyme related symptoms. As both LD and Sudden Infant Death Syndrome are attended by sleep apnea, this should impel further research to determine if some babies with SIDS are actually suffering from LD. Bb can appear in the breast milk.
Lyme patients very often complain of heel pain. This may be due to an underlying plantar fasciitis, with or without a heel spur, or periostitis of the heel. Epicondylitis (tennis elbow) is another complication. Carpal Tunnel Syndrome can also develop in untreated LD.
Lyme patients tend to heal slowly and are prone to musculoskeletal injuries, sometimes without the usual antecedents. One patient sustained a vertebral facet dislocation while shaving ( the usual context is athletic). Even in the well conditioned athlete, there can be an unexpected spate of muscle cramps, sprains, tendinitis and bone or joint pains at the sites of load bearing.
Muscle weakness occurs in some LD patients, More commonly, exertional performance is limited by shortness of breath, poor coordination, musculoskeletal discomfort, or fatigue. Exercise without or early in treatment can precipitate a flare of fatigue, especially the following day.
Low back ache can arise from sacroilitis, paravertebral lumbosacral muscle strain/spasm, and herniated vertebral discs. In a few patients, spinal stenosis is encountered.
Inflammation of the abdominal wall muscles, in particular the rectus abdominus is not an infrequent problem. Usually the tender sites are focal, involving more often than not, the lateral borders of the rectus abdominus muscle. Nausea is often present as well. The sites are best located when the patient is performing a Valsalva maneuver or doing a partial sit up. Failure to appreciate the abdominal myositis may lead to avoidable extensive GI workup.
A very helpful diagnostic maneuver is palpatory tenderness of the medial tibia shaft due to periostitis (inflammation of the tissue around the bone if not the bone itself). Periostitis is also common in another spirochetal disease, syphilis (Textbook of Medicine, Ed: Kelley, 1989, p. 1587) and is responsible for the bone pain that both syphlitic and Lyme patients experience. Tenderness is easily elicited in 95% or more of LD patients simply by pressing the bony aspect of the thumb joint against the medial aspect of the tibia about 3-6 inches above the ankle. The intensity of the pain experienced by the patient can vary, but is often exquisite and will cause the leg to recoil abruptly. The pain often lingers after this procedure. In a minority of LD cases, periostitis is generalized and I have appreciated skull involvement in a few instances. A small proportion of LD patients have periostitis.
As a result of fibrositis, myositis, periostitis, is it any wonder that the ill LD patient view hugs as potential torment? The chagrin of mystified family members is understandable. Self-examination for periostitis can be unreliable. Periostitis pubis (of the pubic bone) can mimic bladder pain or be the origin of lower midline abdominal pain, especially in children.
Lyme (and Brucella) should be included in the differential diagnosis of Desert Storm Syndrome, with which LD shares many features.
The abundant research opportunities should be clear to all. It is unnecessary to give Lyme Disease the "Galileo" treatment.
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Posted: Wed Nov 16th, 2005 14:59 |
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IV Rocephin treatment for chronic Lyme/borreliosis
(filelink)
Rocephin is a Beta-Lactam antibiotic. It is totally the wrong antibiotic for Chronic Lyme.
Note what this study (below) found about Beta-Lactams
"these forms without cell walls can be a possible reason why Borrelia survive in the organism for a long time (probably with all beta-lactam antibiotics) and the cell-wall-dependent antibody titers disappear and emerge after reversion."
That is why Rocephin does not reduce the chronic bacterial load, why it does not reduce the Bowen titre.
There is nothing fundamentally wrong with the Bowen test, patients on the MP have experienced a dropping titre.
Lida Mattman used Beta-Lactams and Vancomycin in her lab to make active-phase bacteria turn into the persistent L-form chronic variants.
Trevor Marshall, PhD
===============================================
EICS of Kansas City, MO, hosted the 2004 "Emerging Infectious Diseases" conference in Kansas City MO on November 19,2004.
At ILADS Dr Fallon was unable to talk about the results from the $5 million, 4-year, NIH study he had conducted into Chronic Lyme therapy with IV Rocephin, but at this conference he gave us the detailed results, together with a request that we not publish the details until they appear in print next September.
So here is my summary of only the key points:
1. Chronic Lyme is real, and is measurable with objective neurological and physical indicators
2. 10weeks of IV Rocephin makes the patients feel better, and returned their objectively measurable deficiencies towards 'health,' but the neural indicators relapsed within 3 months. Some of the skeletal and physical indicators retained some improvement.
3. MRI scans are no use whatsoever in diagnosing or tracking the disease.
The Fallon study found that the MRI scans showed "MRI hyperintensity burden does not change between time 1 and time 2. Hyperintensities appear to represent fixed damage." IMO, the corollary is that, at least based on the MRI data shown by Dr Fallon at this conference, IV Rocephin does not change any irreversible brain damage. "Fixed Damage" is likely a long-term phenomena, IMO, only loosely related to the symptoms.
4. SPECT scans are of little use without analysis way beyond the means of a typical physician.
5. In answer to a direct question, how did anticoagulants seem to help the neurolyme, Brian said that the changes are not vascular, that they are metabolic, and opined that anticoagulants are not likely to do any longterm good
6. This study was so meticulous that they even matched education level of patients and controls, as well as age and sex.
Further, Dr Fallon's group found from SPECT data that the main metabolic changes in the brain were in the region of the Parahippocampal Gyrus. This is responsible for receiving sensory input from the outside world, integrating it, and projecting it onto the Hippocampus (memory) and Amygdala (fear, aggression, mood).The Insula was also affected.
Further, the Para-Lymbic dysfunction noted on SPECT
1. disrupts attention, memory and learning
2. alters emotional response to sensory stimuli
3. distorts links between visceral states and mood, and may lead to increased stress responses
4. depresses the immune response and alters endocrine function
5. alters perception and emotional valence of pain, smell and taste
Six of the 37 patients and 37 controls had significant adverse events during the trial, including two cases of serious thrombus, one MRSA infection and one Gall Bladder removal.
This was an amazing presentation, and made the whole conference a memorable one for me. I felt as though I was part of history - now we know the data on IV Rocephin, so we can start focusing on the 'why' of how this therapy affects the body in chronic Lyme.
============================================
Infection. 1996 May-Jun;24(3):218-26.
Related Articles, Links
Formation and cultivation of Borrelia burgdorferi spheroplast-L-form variants.
Mursic VP, Wanner G, Reinhardt S, Wilske B, Busch U, Marget W. Max von Pettenkofer-Institut, Ludwig-Maximilians-Universitat Munchen, Germany.
**As clinical persistence of Borrelia burgdorferi in patients with active Lyme borreliosis occurs despite obviously adequate antibiotic therapy**, in vitro investigations of morphological variants and atypical forms of B. burgdorferi were undertaken. In an attempt to learn more about the variation of B. burgdorferi and the role of atypical forms in Lyme borreliosis, borreliae isolated from antibiotically treated and untreated patients with the clinical diagnosis of definite and probable Lyme borreliosis and from patient specimens contaminated with bacteria were investigated. Furthermore, the degeneration of the isolates during exposure to penicillin G in vitro was analysed. Morphological analysis by darkfield microscopy and scanning electron microscopy revealed diverse alterations. Persisters isolated from a great number of patients (60-80%) after treatment with antibiotics had an atypical form. The morphological alterations in culture with penicillin G developed gradually and increased with duration of incubation. Pleomorphism, the presence of elongated forms and spherical structures, the inability of cells to replicate, the long period of adaptation to growth in MKP-medium and the mycoplasma-like colonies after growth in solid medium (PMR agar) suggest that B. burgdorferi produce spheroplast-L-form variants. With regard to the polyphasic course of Lyme borreliosis, these forms without cell walls can be a possible reason why Borrelia survive in the organism for a long time (probably with all beta-lactam antibiotics) and the cell-wall-dependent antibody titers disappear and emerge after reversion.
PMID: 8811359 [PubMed - indexed for MEDLINE]
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Posted: Sat Dec 10th, 2005 04:51 |
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How to remove a tick
(filelink)
Here are step-by-step instructions on how to remove a tick.
Click here for an evaluation of commercially available tick-removal devices.
This article discusses controlled studies on the various methods of tick removal.
Here are tips on tick removal from a veterinarian.
Here is info on a tick remover device.
The CDC website info on tick removal is surprisingly brief and reassuring. Perhaps this reflects their official stance the borreliosis/Lyme disease is not a big problem in the US.
The general concensus seems to be to NOT use heat to try to make the tick come out. There is no agreement on the technique that works best and whether or not it is vital to ensure the head is removed.
========================================================
I have used the Pro-Tick Remedy Tool that is shown at the Ohio State University website....
http://www.biosci.ohio-state.edu/~acarolog/tickgone.htm
It is the one on the right side without any name just below the picture of the three tools.
I have had the opportunity to use it on adult size and nymph size ticks.
It works excellently!!!! I highly recommend it!!!
I do not have any faith in a tweezer type apparatus. There is too much chance that the gut will be squeezed, forcing bacteria into the person.
George Howell
Last edited on Mon Jan 9th, 2006 06:05 by Foundation Staff
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Posted: Wed Apr 19th, 2006 14:26 |
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Q: Why do some Lymies recover in just a few weeks on IV antibiotics?
No Lymie has "gotten well" in just a few months of therapy. Never.
There are two issues. The first is the definition of "gotten well." The problem here is that if there is no definitive agreement on how to measure the disease severity itself, then there is no way to measure the change in the disease itself.
One is dependent on reports of patients "feeling better." And patient reports are inherently unreliable.
Think of yourself - think what you would give to be able to have a week, or maybe two, of a clear mind. Able to think clearly again. Wouldn't you declare that you are "feeling much better?" You would still be far from cure, but just getting from day to day is your aim right now. But that is not our aim. Our aim is nothing short of cure - full recovery.
The second problem is that many physicians, even experts, do not understand that all antibiotics do not necessarily kill all bacteria. Some antibiotics actually help bacteria survive. In fact, many antibiotics have been isolated from bacterial species, and their function is exactly that - to allow one species to survive while killing its competitors.
For example, Demeclocycline, a close cousin of Minocycline, was first isolated from a mutant Strep species. It doesn't harm the Strep as much as it harms competitive species.
So this lack of understanding has led to the concept that people taking IV Rocephin are in fact killing the bacteria which cause their chronic Lyme. But Rocephin does not do that. It actually protects the Th1 bacteria from the immune system, and in so doing, makes the patient feel better. But the patients relapse when they stop the Rocephin infusion.
Brian Fallon's study at Columbia showed that definitively. Any benefits from IV Rocephin are lost within a few months after discontinuing treatment.
One of my presentations at our upcoming June 2006 conference is going to be exactly on this topic - "Why do all Antibiotics not kill all Bacteria?"
..Trevor..
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Posted: Sun Jun 4th, 2006 18:47 |
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Jun 04 2006 9:03 AM
Pesky Lyme disease hangs on
Medical professionals disagree on treatment
By Robert Miller
THE NEWS-TIMES
If you get bitten by a black-legged tick, what's your next move?
If you start showing symptoms of Lyme disease, one school of treatment argues you should take at least two months of antibiotics for the simplest case and much more for complicated ones.
You can also expect the tick to be carrying more than the strain of bacteria that causes the disease.
Dr. Richard Horowitz of Hyde Park, N.Y., president-elect of the International Lyme and Associated Diseases Society (ILADS), said "99.9 percent of the patients I see with Lyme disease are co-infected. There are 10 other diseases we should be looking for."
Horowitz spoke last week at a forum held by the Newtown Lyme Disease Task Force.
The second school of thought would argue that the longest you should ever take antibiotics is 28 days — even if you've got the painful arthritis that's a symptom of Lyme.
It also questions whether there's a condition called chronic Lyme disease — a persistent infection that can last for years — and discounts the threat of omnipresent co-infection.
"The evidence does not support that — far from it," said Dr. Gary Wormser, chief of the infectious diseases division at New York Medical College in Valhalla, N.Y., and vice-chairman of its department of medicine.
The differences between the two approaches and the implications for the way patients are treated for Lyme disease are profound. And this comes at a time of increasing threat from the disease.
Lyme disease is at the epidemic stage in the state. There were 1,810 cases reported to the state Department of Public Health in 2005, compared to 1,348 in 2004 — a 26 percent increase.
Connecticut has the highest per capita rate of Lyme disease in the country with about 136 cases per 100,000 people.
But by all accounts, the disease is underreported by a factor of 10 or more.
"The Centers for Disease Control and Prevention reported there were 19,804 cases (nationwide) of Lyme disease in 2004," said Pat Smith, president of the Lyme Disease Association, a patient advocacy group, who also spoke at the Task Force meeting.
"That means there were about 200,000 cases, and that doesn't count the ones that don't fit the CDC requirements."
Lyme disease is caused by a cork-screw-shaped bacteria, Borrelia burgdorferi. The black-legged tick — also known as the deer tick — ingests the bacteria when it feeds on deer, white-footed mice and small rodents, which act as sort of moveable reservoirs of Borrelia. When an infected tick bites a human, the human can get infected as well.
The initial symptoms of the disease can include a bull's-eye rash, fever, headache and sore joints — like a case of the flu without a cough. If the disease is diagnosed early, it can usually be treated successfully with a month of antibiotics.
"We've found there's a six-week window where treatment is really successful," said Thomas Forschner, executive director of the Lyme Disease Foundation based in Tolland, Conn.
But only about half the people infected by a tick bite get the telltale rash. Some have no symptoms at all. Others are treated with antibiotics, but relapse. They can develop much more severe symptoms, including swollen joints.
But because the most common blood tests for Lyme disease are highly inaccurate, doctors who rely on them can easily misdiagnose or disregard the symptoms. The CDC says doctors should not base a diagnosis on those tests but on clinical observations.
"You only use the blood tests to support your diagnosis," said Horowitz of ILADS, whose members are often doctors whose practices are devoted to treating the disease.
What's most controversial is the diagnosis of chronic Lyme disease.
Doctors in the ILADS and patient advocates like Smith insist that people can develop long-term, recurring Lyme infections that can manifest themselves in a host of symptoms — chronic fatigue, sight and hearing loss, memory loss, depression and personality changes, heart damage and arthritic pain that can flare up in different places.
"It's a multi-system bacterial infection," Horowitz said at the Newtown Lyme Task Force meeting. "There are 300 different strains of Borrelia burgdorferi internationally and 100 in the United States. The symptoms can come and go and they can migrate. It's a gestalt of symptoms."
Doctors who are convinced chronic Lyme disease exists treat those patients with long-term courses of antibiotics, often lasting months or years. The ILADS criteria do not limit how long patients should be on antibiotics, leaving that up to the doctors' discretion.
Horowitz said his rule of thumb is to continue antibiotics until a patient is symptom-free for two months.
Horowitz also said ticks carry several other illnesses, including anaplasmosis, the malaria-like babesiosis, and bartonella, commonly known as Cat Scratch fever. All of these come with their own set of symptoms, which must be treated as well. This means patients must get a mix of antibiotics.
"When I see a patient with chronic Lyme disease, I see a patient with chronic Lyme and co-infection," he said.
But Wormser of New York Medical College follows the guidelines of the Infectious Diseases Society, or IDSA. He said there's no evidence for so much co-infection in Lyme patients. IDSA also says there's no scientific proof for a diagnosis of chronic Lyme disease, and thus no need whatsoever for long-term antibiotic therapy.
"Study after study has shown this," he said. They've tested patients who claim they have chronic Lyme disease. Half never had Lyme disease to begin with.
"Another study at Yale showed that half the people being treated for chronic Lyme actually had other treatable diseases," Wormser said.
Wormser co-authored the IDSA Lyme disease guidelines. The society represents about 8,000 infectious disease specialists in the United States.
The society is now rewriting those guidelines. Wormser said he does not expect them to be substantially different than they are now .
But proponents of more liberal use of antibiotics to treat Lyme said last week that they expect, if anything, the new IDSA guidelines will be even more conservative than they are now.
"It doesn't make any sense," said Forschner of the Lyme Disease Foundation about any reduction in the IDSA guidelines, which now allow 14 to 28 days of antibiotic treatment. "What difference does a little bit more of antibiotics make?"
Forschner said the scientific literature does not support long-term antibiotic therapy for early Lyme disease, which some doctors now prescribe.
"I think the new IDSA guidelines are in reaction to that. But why swing the pendulum so far in the other direction?" Forschner said.
There is one substantial change to the IDSA guidelines, Wormser said. It will advise doctors that, on a selective basis, they can prescribe a single large dose of antibiotics to a patient immediately after a black-legged tick bite, before the patient starts exhibiting any symptoms of the disease.
A 2001 study in the New England Journal of Medicine showed that such treatment, given within three days of a deer tick bite, was 87 percent effective in stopping the disease in its tracks.
Smith of the Lyme Disease Association said what her group would like is for doctors to tell patients with Lyme disease that there are two established standards of care — the conservative one endorsed by the infectious diseases association, and the liberal one written by the International Lyme and Associated Diseases Society.
Then, at the very least, she said, patients would know the options. "We need to make sure the patients are aware of this."
Smith praised a bill in the U.S. Congress sponsored by Sen. Christopher Dodd, D-Conn., and Sen. Rick Santorum, R-Pa., that would provide an additional $100 million in federal funding for Lyme research over the next five years.
Smith said the federal government currently spends about $32 million a year for research on the disease and all its manifestations.
"Another $20 million a year will be a significant increase," she said.
The funding is also tied to specific goals, including finding a reliable blood test for Lyme infection.
"It took researchers five or six years to find a reliable blood test for AIDS," she said. "We've know about Lyme disease for 30 years and we still don't have a reliable blood test. That's outrageous."
Contact Robert Miller
at bmiller@newstimes.com
or at (203) 731-3345.
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Posted: Fri Aug 11th, 2006 03:39 |
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Is Lyme disease always poly microbial?-The jigsaw hypothesis.
(filelink)
Med Hypotheses. 2006;67(4):860-4. Epub 2006 Jun 30.
University of Wales, College of Medicine, Accident and Emergency, Heath Park, Cardiff United Kingdom, Cardiff, United Kingdom.
Lyme disease is considered to be caused by Borrelia species of bacteria but slowly evidence is accumulating which suggests that Lyme disease is a far more complex condition than Borreliosis alone. This hypothesis suggests that it may be more appropriate to regard Lyme disease as a tick borne disease complex. Over recent years numerous different microbes have been found in ticks which are known to be zoonotic and can coinfect the human host. The hypothesis suggests that multiple coinfections are invariably present in the clinical syndromes associated with Lyme disease and it is suggested that these act synergistically in complex ways. It may be that patterns of coinfection and host factors are the main determinants of the variable clinical features of Lyme disease rather than Borrelia types. An analogy with a jigsaw puzzle is presented with pieces representing Borreliae, coinfections and host factors. It is suggested that many pieces of the puzzle are missing and our knowledge of how the pieces fit together is rudimentary. It is hoped that the hypothesis will help our understanding of this complex, enigmatic condition.
PMID: 16814477 [PubMed - in process]
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Posted: Fri Aug 11th, 2006 23:11 |
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The politics of Lyme disease
(politicslymelink)
"Lyme is one of the infections found in Th1 immune dysfunction."
I don't want any patients to argue with me on this issue. It is a complex issue and currently closed to your participation. Please argue on the boards where Lyme dogma is discussed.
However, this is the current thinking of others, not just myself, including physicians who are well known in the Lyme community. As time goes by we will be able to develop the thinking behind the statement so that its support becomes obvious. Nevertheless, at this point I want to make it entirely clear that, for a host of reasons, Borrelia is not the sole cause of Th1 immune disease. Indeed, it might even just be a co-infection, like EBV. Time will tell.
..Trevor..
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Posted: Mon Dec 11th, 2006 02:46 |
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Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi.
(filelink)
Microbes Infect. 2006 Sep 22; [Epub ahead of print] Livengood JA, Gilmore RD Jr.
Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA.
Human infection by Borrelia burgdorferi, the etiological agent for Lyme disease, can result in serious acute and late-term disorders including neuroborreliosis, a degenerative condition of the peripheral and central nervous systems. To examine the mechanisms involved in the cellular pathogenesis of neuroborreliosis, we investigated the ability of B. burgdorferi to attach to and/or invade a panel of human neuroglial and cortical neuronal cells. In all neural cells tested, we observed B. burgdorferi in association with the cell by confocal microscopy. Further analysis by differential immunofluorescent staining of external and internal organisms, and a gentamicin protection assay demonstrated an intracellular localization of B. burgdorferi. A non-infectious strain of B. burgdorferi was attenuated in its ability to associate with these neural cells, suggesting that a specific borrelial factor related to cellular infectivity was responsible for the association. Cytopathic effects were not observed following infection of these cell lines with B. burgdorferi, and internalized spirochetes were found to be viable. Invasion of neural cells by B. burgdorferi provides a putative mechanism for the organism to avoid the host's immune response while potentially causing functional damage to neural cells during infection of the CNS.
PMID: 17045505 [PubMed - as supplied by publisher]
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