It seems some Lyme disease activists are unhappy (via My Left Nutmeg) with the new IDSA guidelines on Lyme disease because of the guidelines’ recommendation for specific objective diagnostic criteria, the non-recommendation of months to years of antibiotic treatment and the non-recommendation of “alternative” nutritional supplements. Armed for battle, they even have the Connecticut Attorney General involved.
Lyme disease has been quack-fodder for too long and guidelines such as these are badly needed.
9 comments:
The IDSA did not based its new guidelines on science. In fact, they have ignored practically all of the scientific evidence there is on Lyme when creating these new guidelines. It's absurd.
Certainly.
The IDSA's Inadequate Treatment of Lyme disease
Lit. Analysis
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In addition to the various studies and articles used to determine the Infectious Diseases Society of America's (IDSA) 2000 and 2006 guidelines on Lyme disease diagnosis and treatment, there also exist a great deal of valuable data that the IDSA has either ignored or far too readily discounted. Among such data is evidence that the IDSA has not only failed to provide adequate guidelines for Lyme disease diagnosis and treatment both in the past and in the present, but also that the IDSA is responsible for the pain and suffering of many chronic Lyme disease sufferers.
In constructing their 2006 IDSA guidelines, its writers state that "the panel weighed both the risks and consequences of developing late complications of Lyme disease and the economic costs and possible adverse effects of antimicrobial therapy"[1]. More importantly, they add that "also considered were the inconvenience of prolonged therapies, the potential impact of the indiscriminate use of antibiotics on the development of antibiotic resistance in the community, and the economic costs." Unfortunately, a great deal of chronic Lyme disease patients now exist due to vague diagnostic definitions set by the IDSA's 2000 guidelines. With the choices of issues addressed in their 2006 guidelines, one must ask: how much has the IDSA really done over the years to improve the standard of care Lyme disease patients receive, to ensure an acceptable quality of testing procedures, or to develop safer and more effective treatment protocols?
The IDSA's vague and subjective guidelines on Lyme disease diagnosis and treatment have, according to the International Lyme and Associated Diseases Society (ILADS), "f[allen] short of meeting the needs for diagnosis and treatment of individuals with chronic Lyme disease"[2]. Stated in discussion surrounding issues addressed in U.S. Public Law 107-116, signed in 2002 by President Bush, the Departments of Labor, Health, and Human Services, and Education, and Related Agencies:
The Committee is distressed in hearing of the widespread misuse of the current Lyme disease surveillance case definition. While the CDC does state that 'this surveillance case definition was developed for national reporting of Lyme disease: it is NOT appropriate for clinical diagnosis,' the definition is reportedly misused as a standard of care for healthcare reimbursement, product (test) development, medical licensing hearings, and other legal cases[3].
None of the IDSA's guidelines, including the 2006 "updated" text, address the above complaint. E.J. Mundell of HealthDay News writes one month after the release of the IDSA's 2006 guidelines: "while there's no rule that physicians must follow IDSA recommendations when treating Lyme disease, insurance companies often base their treatment coverage on these types of guidelines. State medical boards might also consult the recommendations when reviewing alleged malpractice cases"[4]. For years the need to change the way physicians, insurance companies, and other agencies use the CDC's reporting guidelines has been addressed, and still absolutely nothing has been done to implement said change.
Even if change were to occur today, there are still a great number of people who now suffer chronic Lyme disease because of vague or incomplete information proposed within the IDSA's previous guidelines. Unlike in the 2006 guidelines, the IDSA's Lyme disease diagnostic and treatment guidelines set in 2000 do not detail the full range in which Lyme disease is considered to be endemic, nor does it give any definitions or examples with which to identify the erythema migrans (EM) rash or any Lyme disease vector other than Ixodes scapularis. Because of this, notes Ginger Savely, RN, "misinformed health care providers in the southern and western states consider [Lyme disease] rare and non-endemic"[5]. The 2006 IDSA guidelines finally do include more specific information about the prevalence of Lyme across the nation, pictures of multiple tick species, the inclusion of Ixodes pacificus as a known Lyme disease vector, and two photographs of confirmed EM lesions. The updated guidelines also describe, in detail, the IDSA's official description of the EM rash:
Primary erythema migrans is a round or oval, expanding erythematous skin lesion that develops at the site of deposition of B. Burgdorferi by an Ixodes tick. These skin lesions typically become apparent approximately 7-14 days (range 3-30 days) after the tick has detached or was removed and should be at least 5 cm in largest diameter for a secure diagnosis. ... secondary erythema migrans skin lesions can be <5 cm in largest diameter, but like primary lesions, they may expand.
By this definition, no lesion noted at the site of a tick bite may be considered a primary EM rash unless it expands to be larger than 5 cm. Although the above definition at least provides some guideline for physicians, it still leaves question about the diagnosis of patients who experience multiple EM lesions, when all of which fail to expand beyond 5 cm in diameter and therefore no primary "diagnostic" lesion can be identified. Both the IDSA and ILADS do agree that the appearance of EM rashes can vary; contrary to popular belief, there is no single "classic" EM rash, and appropriate identification can be a difficult call.
Not all cases of Lyme disease begin with the patient's recollection of a rash, either. According to Dr. Joseph Burrascano Jr., President of East End Medical Associates and Board Member of ILADS, less than half of Lyme patients even remember seeing any rash at all[6]. Even the IDSA admits that "seventh nerve palsy due to Lyme disease can develop in patients who have no recollection of an erythema migrans lesion or of a tick bite." With this in mind, a great many patients who might fit other IDSA clinical criteria for Lyme diagnosis might still slip through the proverbial cracks due to lack of recollection of a tick bite, no memory of an EM rash, or the presentation of an atypical EM rash. Given this diagnostic hurdle, the IDSA 2006 guidelines state that "diagnostic testing performed in laboratories with excellent quality-control procedures is required for confirmation of extraneous Lyme disease."
The IDSA has long required two-tier process for the testing of Lyme disease, using first an ELISA titer and then a Western blot; the first test is used for its supposed sensitivity and the second for its specificity. If both tests are interpreted as positive, then the patient can be diagnosed. While this practice would seem simple enough, a number of researchers claim yet another flaw:
Many of the commercially available assays [for Lyme disease] have been plagued by a lack of sensitivity, specificity, and reproducibility. Furthermore, the absence of free antibodies to B. burgdorferi components has been documented in well- characterized erythema-migrans-positive cases of Lyme disease, including those with prominent neurologic involvement[7].
According to ILADS guidelines, the process required by the IDSA is so flawed that it "fails to detect up to 90% of cases." The IDSA even notes in its 2000 guidelines that "serological assays for Lyme disease have substantial limitations"[8]. So why would the Committee who signed Public Law 107-116 agree two years after the drafting of these guidelines that "the current state of laboratory testing for Lyme disease is very poor. The situation has led many people to be misdiagnosed and delayed proper treatment. ... the ramifications of this deficit in terms of unnecessary pain, suffering and cost is staggering," and why are similar complaints being raised to this day? Discrepancies between ELISA and Western blot results often are interpreted as an immediate negative for Lyme disease. Tom Grier of the Canadian Lyme foundation points out of this accepted practice:
A misconception about Western Blots and ELISA tests is that they have as many false positives as false negatives. This is not true. False positives are rare. Negative serologies despite a rash or positive culture is routine. ... when the ELISA or Western Blot tests are positive, they are significant[9].
Wikipedia Encyclopedia notes that "false positive Lyme diagnosis is most commonly due to false positive serology in a subset of patients who may suffer from syphilis, rheumatologic diseases, or infectious mononucleosis"[10]. So, in essence, if there exists question as to the validity of a positive titer, a short list of diseases can be ruled out with further testing, which, when weighed against patients' lists of symptoms, might either further validate or rule out suspected cases of Lyme disease. Barring these other diseases, a positive ELISA titer should not be discounted simply because of a subsequent negative Western blot.
Yet another problem with the two-tiered testing system for Lyme disease is the interpretation of the Western Blot, itself, which is determined by the number of diagnostic "bands" counted in the completed test. ILADS guidelines state:
The CDC considers a western blot positive if at least 5 of 10 IgG bands or 2 of 3 IgM bands are positive. However, other definitions for western blot confirmation have been proposed to increase sensitivity. In fact, several studies showed that sensitivity and specificity for both the IgM and IgG western blot range from 92 to 96% when only two specific bands are positive.
Greer and others, such as independent laboratory IGeneX, who agree with this assessment, point out that certain bands, such as 31kDa, 34kDa, and 39kDa, reflect proteins that are specific only to B. burgdorferi; IgeneX claims that 31kDa and 34kDa not only indicate Lyme disease, but that they are actually specific to late stage Lyme disease[11]. The Lyme Disease Association points out that, not only do these bands have said significance, but they often can explain a number of false-negative tests found in commercial Western blots:
Even more puzzling was the omission from consideration of bands 31 and 34 kDa [from commercial tests], corresponding to OspA and OspB, among the most species-specific proteins of the [Lyme] organism. Often absent in early disease, Osps A and B tended to come into prominence as patients became increasingly ill. Although the absence of either of these bands from a patient's immunoblot did not rule out Lyme disease, their presence was hardly meaningless[12].
Wikipedia Encyclopedia adds: "it is important to note that [31 and 34 kDa]...are so specific to Borrelia burgdorferi that they are being used/studied for the development of a Lyme disease vaccine." P.J. Malloy et al. of the IDSA found, when testing patients who had been administered a Lyme vaccine based on the OspA protein, bands 16, 18, 20, 30, 32, 34, 40, 50, 60, and 65 kDa all frequently came up positive in response to just that one protein being introduced to the patients' systems[13].
Considering the fact that five out of ten IgG bands need to show up as reactive to be considered positive, many chronic Lyme sufferers are being told their tests are negative simply because some of the bands specific to their stage of the disease are not recognized by the CDC. Also, under CDC criteria, tests that show even two or three CDC-accepted bands as positive, but lack the required number of positive bands, are still interpreted as negative. Considering the fact that these bands are reactive only to B. burgdorferi, and considering the rarity of false positive reactions, it defies all logic for a test with at least two reactive Lyme-specific bands to be interpreted as negative for Lyme, no matter how many other bands do or do not react.
In light of the obvious diagnostic pitfalls set by both past and current IDSA guidelines, IgeneX claims:
The diagnosis of Lyme disease must be made based on history, signs (such as erythema migrans), symptoms, and other laboratory data, in addition to the presence of antibodies to B. Burgdorferi. Negative [test] results should not be used to exclude Lyme disease.
Even the IDSA's 2006 guidelines states of early Lyme disease: "patients should be treated on the basis of clinical findings." This completely contradicts the statement that "diagnostic testing is ... required for confirmation of extraneous Lyme disease," even though Public Law 107-116 complained four years earlier that "the vaccine clinical trial has documented that more than one third (36 percent) of the people with Lyme disease did not test positive on the most sophisticated tests available." Given both of the above criteria, the chances of an infected individual with no history of an EM rash has less than a one in three chance of getting diagnosed or treated at all.
One must question the motives behind much of what was added (and not added) to the IDSA's 2006 update, given many of the specifics to its text. For example, the 2006 guidelines' addressing of "post-Lyme disease" appears to be in response to ILADS demand that new guidelines incorporate information on the diagnosis and treatment of chronic Lyme disease; the IDSA's response seems to be inspired more by contempt than peer-reviewed study, offering clearly one-sided information on the pathology, or rather apparent lack thereof, of the chronic form of the disease. The Lyme Disease Association (LDA) responds to this by stating in its Petition against the current guidelines on Lyme disease:
[The 2006 IDSA] guidelines fail to meaningfully address the needs of patients with chronic Lyme disease, who are now relegated to the pile of diseases with unknown etiology, like CFS and FMS, and who are provided with only symptomatic relief, while the underlying infectious disease is allowed to progress unabated[14].
The IDSA's current suggestions for Lyme disease treatment also conflict with the findings of ILADS and a number of other private researchers. While the IDSA recommends a maximum of 28 days for any and all manifestations of Lyme disease, stating "to date, there are no convincing published data that repeated or prolonged courses of either oral or iv antimicrobial therapy are effective for [chronic Lyme] patients," the text then slightly varies from this stance by stating, "response to treatment is usually slow and may be incomplete. However, unless relapse is shown by reliable objective measures, repeat treatment is not recommended." So first the IDSA does not recommend long-term or repeated therapy at all, but then states that it is acceptable only if "relapse is shown by reliable objective measures." The guidelines do nothing to explain what falls under the definition of reliable objective measures, however, and so once again the physician is left to assume to the best of his or her ability what diagnostic restrictions this leaves him or her to work with.
The IDSA further confounds its recommendations by the even more contradictory statement made in regard to those suffering from Lyme-related arthritic conditions: "we recommend repeat treatment with another 4-week course of oral antibiotics or with a 2- to 4-week course of iv ceftriaxone" and by noting of late stage Lyme disease: "the response to treatment ... is typically slow, and improvement or resolution of symptoms may take weeks or months." ILADS members believe that repeated or prolonged courses of antibiotics might be necessary for some patients to recover, claiming "reports show failure rates of 30-62% within 3 years of short-course treatment using antibiotics thought to be effective for Lyme disease." J. Oksi et al. report in the Annals of Medicine: "we conclude that the treatment of Lyme borreliosis with appropriate antibiotics for even more than 3 months may not always eradicate the spirochete"[15].
The IDSA even lists studies in which large numbers of patients claim either relapse or continuing symptoms, but then dismisses any evidence of chronic infection by questioning the legitimacy of diagnostic criteria used in said studies. However, studies such as that documented by J. Oksi et al. in the Annals of Medicine beg to differ: "of 165 patients treated for disseminated Lyme borreliosis with three months or more of antibiotics ... 32 had treatment failure. At follow-up 13 patients with clinical relapse were PCR culture positive"[16]. Although "clinical relapse" is left a subjective term by the IDSA, it is safe to assume that the positive PCR cultures would qualify at least 13 out of 32 alleged treatment failures, close to 8% of the patients in that study. Considering the possibility that all 32 of those patients were properly diagnosed, the failure rate would jump to 30%. In another study published in Brain, J. Oksi et al. describe finding B. burgdorferi in the brain tissue of a patient who died after over six months of potent antibiotic therapy[17]. The 2006 guidelines further note:
Studies indicate that antibiotics can cure B. burgdorferi infection in infected animals ... but rare animals may remain culture positive, and a substantial proportion of animals will remain PCR positive in some, but not all, studies.
The above statement clearly shows that the IDSA does, indeed, acknowledge studies in which animals remained ill after antibiotic therapy, and even that "a substantial proportion of animals will remain PCR positive" after said therapy. The guidelines' authors are quick to add that this result is found "in some, but not all, studies." This tags such studies with an undue sense of inconclusiveness, although ultimately it does also contradict the guidelines' insistence that "a single 28-day course of antibiotics is sufficient to eradicate the spirochete in most cases."
A number of researchers have found that Lyme disease can be so difficult to eliminate because of the spirochete's ability to change into a self-defensive cystic form:
B. burgdorferi has the ability to make cystic forms both in vivo and in vitro, e.g. when exposed to antibiotics commonly used for treating Lyme borreliosis. This phenomenon, combined with the ability of the cysts to reconvert to normal mobile spirochetes, may explain a reactivation of the disease after an illusory cure - and not a "post Lyme syndrome" as postulated by other researchers[18].
Here, the researchers suggest a viable alternative to the common belief that Lyme disease might easily be eradicated with a single course of appropriate antibiotic treatment. The IDSA's current response to this theory is that "the 'cystic' forms of B. burgdorferi that have been seen under certain growth conditions have not been shown to have any clinical significance." The guideline's authors appear hesitant to address this idea at all, quoting the word "cystic" as if it were a novel concept, despite the fact that researchers have known about the spirochete's defensive capabilities throughout the better part of the past century[19]. The IDSA also claims that the cysts observed "under certain growth conditions have not been shown to have any clinical significance;" there are no claims that cysts observed under all growth conditions lack clinical significance.
Drs. Broroson and Broroson explain their findings, which illustrate that the cysts do, indeed, have clinical significance, in that B. burgdorferi often goes dormant while in its cystic form: "the effectiveness of antibiotics requires active metabolism by the bacteria, and therefore it is likely that cystic forms of B. burgdorferi may be resistant to antibiotic treatment"[20]. Drs. Broroson and Broroson add that the cystic form might also explain why Lyme disease tests have such low serological and PCR sensitivity[21].
Because of B. burgdorferi's amazing defensive capabilities many top researchers, such as Dr. J. Burrascano Jr., recommend against the findings of the IDSA, suggesting the long-term use of a number of antibiotics, including metronidazole and others specifically not approved for use against Lyme disease in the IDSA's 2006 updated guidelines. Although it is clear that Lyme disease is not as easy to treat as the IDSA would like to report, its authors are adamantly against long-term treatments, which contrary to the IDSA's findings do show promise in treating late stage Lyme disease.
The limitations on antibiotic use and treatment length is likely due to the restrictions based on IDSA findings indicating simply that "the development of resistant strains of bacteria limits the long-term market potential for an antibiotic"[22]. It is stated, however, in the 2000 IDSA guidelines: "it has not been shown nor is it anticipated that B. burgdorferi will develop resistance to antibiotics, but the indiscriminate use of antibiotics exacerbates the problem of antibiotic-resistant community-acquired infections with other bacteria." Given these two pieces of information, it is evident that the IDSA is more concerned with the possibility of creating an antibiotic-resistant strain of streptococcus than it is with the actual treatment benefits of long-term antibiotic use against Lyme disease[23,24]. While this may seem to be the fair and logical concern, and a small population of chronic Lyme sufferers might appear to be a small consequence in comparison, one must consider the extent to which some people are suffering due to the effects of untreated or under-treated Lyme disease.
Lyme disease causes a wide variety of physical and mental complications. According to HealingWell.com, common symptoms of Lyme disease are arthritis, stiff neck, headaches, Bells' palsy, poor concentration, memory loss, and varying degrees of pain and weakness[25]. Its authors add that "less commonly, Lyme disease can result in eye inflammation, hepatitis, and severe fatigue." B.A. Fallon, et al. write of neuropsychiatric Lyme disease: "the psychiatric presentations of Lyme borreliosis may be as diverse and debilitating as occur with neurosyphilis"[26]. The LDA notes in its 2006 Petition against the IDSA's guidelines: "studies have shown that patients with chronic Lyme disease suffer a degree of debility equal to that of patients with congestive heart failure. Failure to address the underlying infectious disease etiology keeps these patients sick, which is inhumane and immoral." Is the lesser of two evils destroying the lives of thousands of men, women, and children with justifiable cause, or are these people, instead, being wrongly denied proper antibiotic treatment and being forced to suffer undue complications as a result of said denial?
As quoted in Human Pathology: "high doses of parenteral antibiotics, or combination therapies with long duration may be needed to kill the living spirochetes"[27]. While the educated consensus outside the IDSA holds to these values, the medical community in whole has become powerless to treat Lyme disease in a way which many believe is the only means of ensuring their patients' future health and quality of life. The IDSA is strictly against combination therapies for Lyme disease, as noted in their 2006 guidelines, just as it is, albeit with just caution, against long-term use of any antibiotics. Because of these guidelines, and because proving the existence of persistent Lyme infection has been very difficult up until now, countless patients have been left to suffer without recourse.
Up until recently there has been no means whatsoever of proving the existence of chronic or persistent Lyme infections, other than the subjective observations vaguely implied by the IDSA and the interpretation of Western blot bands the IDSA refuses to acknowledge. Drs. Raphael Stricker and Edward Winger recently isolated a test which so far has proved to be a good indicator of patients' B. burgdorferi bacteria load, the CD-57 NK test. "Just as AIDS patients have always held great store in their CD4 T-cell count, Lyme patients now have a fairly reliable marker of the status of their illness," notes Ginger Savely, RN. She also claims that a low CD-57 count, which indicates an active Lyme bacterial load, cannot be caused by MS, lupus, and other diseases Lyme tends to mimic.
Dr. Burrascano writes: "our ability to measure CD-57 counts represents a breakthrough in [Lyme borreliosis] diagnosis and treatment." He adds, "if the CD-57 count is not in the normal range when a course of antibiotics is ended, then a relapse will almost certainly occur." More research into the CD-57 test is needed, as it is not yet recognized by the mainstream, but it may prove to be the "reliable objective measures" needed to prove the necessity of ongoing antibiotic treatment for Lyme disease.
While there exist very real consequences to inadequately diagnosed, untreated, or under-treated Lyme disease patients, the IDSA finds it necessary to err on the side of caution, limiting diagnosis and antibiotic use because of "the potential impact of the indiscriminate use of antibiotics on the development of antibiotic resistance in the community." Turn the Corner Foundation, an affiliate of ILADS, sees this as a morbid error in judgment, stating: "the very real consequences of untreated chronic, persistent Lyme infection far outweigh the potential consequences of long-term antibiotic therapy"[28]. Furthermore, is it admissible to define long-term antibiotic therapy for Lyme disease as "indiscriminate," considering its potential benefits to late stage and chronic Lyme disease sufferers?
While the potential for serious repercussions exists with long-term antibiotic use in Lyme disease treatment, the denial of diagnosis and proper treatment to thousands of sick individuals is not the way to go about addressing the problem. Considering for a moment that the proposed risks of properly treating Lyme disease patients truly do outweigh the benefits, these patients still deserve to know the truth about their illness, just as they deserve some type of recourse if they have been made to suffer unduly. More importantly, Lyme patients deserve to have all phases of the disease further researched, so that viable treatment alternatives might be discovered and a cure actually found. It is imperative that legislators and researchers work together to rectify the IDSA's mismanagement of this issue and establish a new set of guidelines that reflects all relevant available data.
References
1. Wormser, Gary P., et al. The Clinical Assessment, Treatment,
and Prevention of Lyme Disease, Human Granulocytic
Anaplasmosis, and Babesiosis: Clinical Practice Guidelines
by the Infectious Diseases Society of America. CID 2006; 43:1090-1121.
2. Cameron, David., et al. ILADS Guidelines for Lyme disease,
2004:4-7,9,11.
3. Public Law 107-116 Signed by President Bush on 1/10/02. Departments of Labor, Health, and Human Services, and Education, and Related Agencies Appropriations act of 2002.
Found at www.lyme.org/legislative/letter107-116.pdf.
4. Mundell, E.J. "New Lyme Disease Guidelines Spark Showdown". HealthDay News. http://news.healingwell.com/?p=news1&id=
535816. November 9, 2006.
5. Savely, Ginger. "Everything You Wanted to Know About the
CD-57 Test...but were too sick to ask!".
www.publichealthalert.org, 2006.
6. Burrascano, Joseph J. Jr. "Managing Lyme Disease". 15th Edition, 2005:7,8,12-21.
7. Coyle, PK., et al. Detction of Borrelia burgdorferi-specific
antigen in antibody negative cerebrospinal fluid in
neurologic Lyme disease. Neurology 1995; 45:2014.
8. Wormser, Gary P., et al. Practice Guidelines for the
Treatment of Lyme Disease. CID 2000; 31 (Suppl 1):3,5,9,11.
9. Grier, Tom. "Lyme Disease Test, Is Testing Flawed?".
Canadian Lyme Foundation. www.canlyme.com/flawedtest.html.
10. "Lyme Disease". http://en.wikipedia.org/wiki/Lyme_disease.
2006.
11. "IgeneX Innovations". www.igenex.com/innovations3.htm, 2003.
12. Lyme Disease Association. Conflicts of Interest in Lyme Disease: Laboratory Testing, Vaccination, and Treatment Guidelines. Www.lymediseaseassociation.org/
ConflictReport.pdf. 2001.
13. Molloy, P.J., et al. Detection of Multiple Reactive Protein Species by Immunoblotting after Recombant Outer Surface Protein A Lyme Disease Vaccination. CID 2000; 31:45,46.
14. Lyme Disease Association, Inc. Petition.
www.lymediseaseassociation.org/referral/Petitions/
Petition.php?id=1. 2006.
15. Oksi, J. et al. Borrelia burgdorferi detected by culture and PCR in clinical relapse of disseminated Lyme Borreliosis. Annals of Medicine 1999; 31(3):232.
16. Oksi, J. et al. Borrelia burgdorgferi detected by culture
and PCR in clinical relapse of disseminated Lyme borreliosis. Annals of Medicine 1999; 31(3):225.
17. Oksi, J. Et al. Inflammatory brain changes in Lyme borreliosis, A report on three patients and review of literature. Brain 1996; 119(Pt 6):2143-54.
18. Broroson, O., and Broroson, S. An In Vitro Study of the Susceptibility of Mobile and Cystic Forms of Borrelia burgdorferi to Metronidaxole. APMIS 1999; 107(6):566.
19. Balfour, Andres. The Infective Granule In Certain Protozoal Infections, as Illustrated By The Spirochetaetosis of Sudanese Fowl. The British Medical Journal. April, 1911.
20. Broroson, O., and Broroson, S. Transformation of Cystic Forms of Borrelia burgdorferi to Normal, Mobile Spirochetes. Infection 1997; 25(4):245.
21. Broroson, O., and Broroson, S. A Rapid Method for Generating Cystic Forms of Borrelia burgdorferi, and Their Reveresal to Mobile Shirochetes. ARMIS 1998; 106(12):1139.
22. IDSA. "Facts About the Antibiotic R&D Pipeline".
www.idsociety.org/Template.cfm?Section=Antimicrobials&
Template=ContentManagement/ContentDisplay.cfm&ContentID=
9715. 2006.
23. IDSA. "Facts About Antibiotic Resistance".
www.idsociety.org/Template.cfm?Section=Antimicrobials&
Template=ContentManagement/ContentDisplay.cfm&ContentID=
9714. 2006.
24. IDSA. "Bad Bugs, No Drugs White Paper Executive Summary".
www.idsociety.org/Template.cfm?Section=Antimicrobials&
Template=ContentManagement/ContentDisplay.cfm&ContentID=
9770. 2006.
25. HealingWell.com. "Introduction to Lyme Disease".
www.healingwell.com/library/lymedisease/info1.asp
26. Fallon, B.A., et al. "Late State Neuropsychiatric Lyme Borreliosis Differential Diagnosis and Treatment".
Psychosomatics 1995; 36:299.
27. Nanagara, R. Et al. Ultrastructural demonstration of spirochetal antigens in synovial fluid and synovial membrane in chronic Lyme disease; possible factors contributing to persistence of organisms. Human Pathology 1996; Vol27(10):
1032.
28. Turn the Corner Foundation. ILADS Lyme Disease Treatment Guidelines Summary. www.turnthecorner.org/lyme-guidelines.htm, 2006.
Disclaimer: This analysis is for informational purposes only, and should not be used in place of professional medical advice.
Copyright 2006. All Rights Reserved.
Questions/Comments: lymeanalysis@zoomshare.com
Excellent science supported by evidence that clearly consigns the IDSA guidelines to the trash pile.
I think the new IDSA guidelines are... how did you put it... oh, yes-- "quack-fodder". How dare they allow thousands of people to suffer. I hope they are all put in prison. These people must pay for their crimes. These poor people have suffered needlessly because a group of so-called doctors cannot open their eyes to how insidious this disease is. They are downright ignoring the facts. I winder what will happen when themselves or their loved ones get infected. And it's bound to happen. Lyme is the fastest growing infectious disease in the country-- it has even surpassed HIV. That will certainly change the tune, eh?
Doctor, how exactly is Lyme disease "quackfodder", to you? How can you dismiss such a debilitating disease? I have Chronic Lyme... I wasn't dignosed for years after being infected. I am in my 15th month of antibiotic treatment, and I'm slowly starting to get better. I have a lot of cognitive problems and I am always in pain. Have YOU ever had Lyme disease? What if you or one of your loved ones fell ill with Lyme symptoms after a tick bite? Would you tell yourself or them that Lyme is just a bunch of quackfodder? Seriously, you doctors have got to start opening your eyes. This is a national health crisis. It's getting worse with each passing year. Come on now.
And doesn't it concern you that the doctors that wrote these guidelines are paid to testify against Lyme disease? They also refused to let ILADS be part of this process. Hmmm... methinks something is rotten here.
from Dr. RW:
One would hope that in those 400 articles was contained all the high level evidence....If you can cite what you believe to be the good evidence they ignored please post it here and we can open it for discussion.
Yes Dr. RW, one would hope. And I'll take you up on that invitation.
What is so bizarre is that the IDSA authors even ignored a great deal of research they authored themselves. For example, one of the reasons given against long-term antibiotic therapy is that Lyme is supposedly not an intracellular infection. Yet IDSA author Mark Klempner was the lead author on a study demonstrating that Lyme bacteria invade fibroblasts (PMID 8486939), and co-author of a study entitled "Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro." (PMID 1634816). Hardly consistent with the guidelines, which makes no mention of these studies.
In fact, Borrelia burgdorferi has been shown to invade a variety of cell types, most recently neuronal and glial cells in a study by CDC researchers. Perhaps the following list will interest you:
Ma Y, Sturrock A, Weis JJ (1991). "Intracellular localization of Borrelia burgdorferi within human endothelial cells" Infect Immun 59 (2): 671-8. PMID 1987083.
Klempner MS, Noring R, Rogers RA (1993). "Invasion of human skin fibroblasts by the Lyme disease spirochete, Borrelia burgdorferi". J Infect Dis 167 (5): 1074-81. PMID 8486939.
Dorward DW, Fischer ER, Brooks DM (1997). "Invasion and cytopathic killing of human lymphocytes by spirochetes causing Lyme disease". Clin Infect Dis 25 Suppl 1: S2-8. PMID 9233657
Montgomery RR, Nathanson MH, Malawista SE (1993). "The fate of Borrelia burgdorferi, the agent for Lyme disease, in mouse macrophages. Destruction, survival, recovery". J Immunol 150 (3): 909-15. PMID 8423346
Aberer E, Kersten A, Klade H, Poitschek C, Jurecka W (1996). "Heterogeneity of Borrelia burgdorferi in the skin". Am J Dermatopathol 18 (6): 571-9. PMID 8989928.
Girschick HJ, Huppertz HI, Russmann H, Krenn V, Karch H (1996). "Intracellular persistence of Borrelia burgdorferi in human synovial cells". Rheumatol Int 16 (3): 125-32. PMID 8893378.
Nanagara R, Duray PH, Schumacher HR Jr (1996). "Ultrastructural demonstration of spirochetal antigens in synovial fluid and synovial membrane in chronic Lyme disease: possible factors contributing to persistence of organisms". Hum Pathol 27 (10): 1025-34. PMID 8892586.
Livengood JA, Gilmore RD (2006). "Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi.". Microbes Infect [Epub ahead of print]. PMID 17045505.
It's not only Klempner who ignores his own work. Other authors of the IDSA guidelines apparently forgot their own published research on seronegative infection:
John Halperin:
"A small number of patients with Lyme borreliosis will lack serologic evidence of exposure to B. burgdorferi, despite a disease duration sufficient to develop a detectable immune response."
Halperin et al. "Practice parameters for the diagnosis of patients with nervous system Lyme borreliosis (Lyme disease).Quality Standards Subcommittee of the American Academy of Neurology." Neurology 1996 Mar;46(3):619-27. PMID 8618656.
Raymond Dattwyler and John Halperin:
"We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in seronegative patients with clinical indications of chronic Lyme disease."
Dattwyler et al. "Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi." N Engl J Med. 1988 Dec 1;319(22):1441-6. PMID 3054554.
Robert Nadelman and Gary Wormser:
Of seven patients with Bb cultured from the blood, "serologic testing was frequently nonreactive; two patients had no detectable antibody on multiple sera by five different assays.”
Nadelman et al. "Isolation of Borrelia burgdorferi from the blood of seven patients with Lyme disease." Am J Med. 1990 Jan;88(1):21-6. PMID 2294761.
Gerold Stanek:
"...each of the specific CSF parameters may be false negative in some cases... Neither can seronegativity exclude... the diagnosis of neuroborreliosis as in only 71% of group I [the group with specific evidence of Bb in CSF] serum B. burgdorferi antibodies were detected.”
Millner MM, Mullegger RR, Spork KD, Stanek G. "Lyme borreliosis of central nervous system (CNS) in children: a diagnostic challenge."
Infection. 1991 Jul-Aug;19(4):273-8. PMID 1917045.
Franc Strle:
"However, the absence of serologic evidence of Lyme disease in the initial stages, and even later (3, 4), cannot rule out the diagnosis.... Our case stresses the diagnostic value of clinical manifestations and of the course of illness and calls attention to seronegative forms of Lyme disease.”
Pikelj F, Strle F, Mozina M. "Seronegative Lyme disease and transitory atrioventricular block."
Ann Intern Med. 1989 Jul 1;111(1):90. PMID 2735630.
And on and on. Are you saying that all these IDSA authors were publishing "junk" in a prior lifetime?
On the diagnostic requirement of objective manifestations, I wonder if you've seen this study out of Tufts University:
"A mild chronic encephalopathy may be the most common neurologic symptom in patients with late stage Lyme disease. The symptoms tend to be diffuse and nonspecific, and patients typically report memory loss, sleep disturbance, fatigue, and depression.”
Kaplan RF, Jones-Woodward L. "Lyme encephalopathy: a neuropsychological perspective." Semin Neurol. 1997 Mar;17(1):31-7. PMID 9166957.
Or how about this from Yale:
"...it is important to have a high index of suspicion in early Lyme disease, because the rash may be atypical or absent, the early flu-like features can be nonspecific, and at this stage seroreactivity to B. burgdorferi may be lacking.”
Schoen RT. Identification of Lyme disease. Rheum Dis Clin North Am. 1994 May;20(2):361-9. PMID 8016416.
(Please recall that the new guidelines forbid this "high index of suspicion", as a rash or seropositivity is required for diagnosis.)
The IDSA guidelines offer one counter-argument to reports of documented, culture-confirmed persistent Lyme infection despite antibiotic therapy: "reinfection or laboratory contamination" could not be "excluded" in all of those studies. Does that sound convincing to you?
Finally, if you read the guidelines carefully, you will notice that two out of three NIH-funded, double blind controlled trials found a statistically significant, lasting benefit to long-term or repeated antibiotic therapy in chronic Lyme disease (Krupp and Fallon studies). This indisputable fact is disguised with distorted language to make it appear the antibiotics were ineffective.
For a description of these 3 NIH studies (including published critiques), and a great deal more of the published research the IDSA chose to ignore, see the Wikipedia Lyme disease page.
(Before you say Wikipedia isn't a reliable resource, forget the text if you like and look at the over 150 references which are hyperlinked to PubMed abstracts.)
Dr. Donnell...I found this post after a Google search re: CD-57 levels for diagnosing Lyme.
I, like you, am struggling with the plausibility of this boom of Lyme diagnoses, but my struggle is from a personal level, not a professional one.
My wife's doc diagnosed her w/Lyme over a year ago and has been treating her ever since...admittedly, there have been minor improvements, but nothing that's made her truly feel better.
She has bought in to everything he's said and she's convinced that all four of our kids have it too...even though they have never had tick bites.
Finally, I agreed to let them get tested and pretty much the only test they had done was the Stricker NK Panel CD-57 test offered by LabCorp.
The levels ranged from 25 to 46 in the four kids.
I'm wrestling with being supportive vs. being rational and, quite honestly, need someone to talk to who has exposure to this.
I'll get nowhere if I don't have some alternative suggestions for why those levels might be what they are. (What is a "normal" CD-57 level anyway???)
I'm in Kansas and will actually be driving through Arkansas for work next week...could you contact me via e-mail at jpjayhawk1993 at yahoo dot com? I know it's a long shot, but thought I would try.
Interesting that the doctor issued a challange, it was met and he is now silent. Has he read the information?? What are his thoughts??
The poster who wants to meet with the doctor. Did you read the article that was posted about the studies that were ignored?? You cannot rely on a doctor to answer you questions who refuses to look at the facts. You need to do your own research or ask your wifes doctor to meet with you and answer your questions.
The CD57 test is important in diagnosing Lyme. Normal levels range from 60-360. Lyme disease is the only disease to cause these levels to go down. Other diseases can affect the CD57, however, they make the count go up, not down. The lower the CD57 count, generally the sicker the patient.
Mine was 34 before treatment and is currently at 100 approximately 7 months into treatment. I have tested CDC positive for acute Lyme disease three times through LabCorp and once through IgeneX, with 8 bands positive, including 23, 31 and 34 bands -- 31 and 34 being the protein bands used in the making of the LymeRix vaccine.
Band 23-25 OspC is the current protein they are looking at for a future vaccine. The LymeRix vaccine was a failure due to the proteins having such a close similarity to HLA-DR4, an arthritis gene that some persons carry. Those who were vaccinated with LymeRix and who carried this gene (approximately 30%) ended up with an autoimmune disorder causing severe disability. Glaxo-Smith-Kline settled out of court and the FDA pulled LymeRix off the market citing, "not enough demand."
The research seems to be pointing in the direction of outer surface protein C (OspC) 23-25 being more likely the better option in the making of a vaccine for Lyme disease.
Your wife needs your support. This disease is difficult enough without a spouse who questions the believability of the illness and it's virulence. Two of my family members also tested CDC positive. Many do not test CDC positive, but I assure you our stories are the same. The proof is out there for those who are willing to do their homework.
If you choose not to do the homework and rely on what you hear rather than what is available for you yourself to research, then you have failed. This applies to physicians as much as it applies to patients and family members who refuse to be their own advocates.
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