Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


01 Oct 2017

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File List, RICO

1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:
TruthCures.org
badlymeattitude.com/
immune2lies.com/
researchfraud.com/
may12.org
meadvocacy.org/
truthbetoldx81
lymecryme
CrymeDiseaseNorway
crymedisease
theothersideofthestretcher
rjspiritualityandtuth
LymeTruthSite

JC-LilnkedIn
KD-Linkedin.com
LD-LinkedIn
JC-academia.edu

KD-academia.edu

 


CDC "SPIDER"

Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"

RICO_filed_USDOJ

BlumenthalAntiTrust Lawsuit

Exosomes, Blebs

Spirochetal_Dementia


PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994
BarbourFishpdf.pdf
 

Pathogenic Fungi

Bush's warcrimes, Oct 2000

Trainer

170708

 

 

ACTIONLYME PRE-HISTORY-  all about me and my famous self!!! (NOT)

1993, Joe Burrascano, Congressional Oversight Hearing  Lyme disease- MD Harassment

1998 New London Day Article May by KMDickson

After dealing with the abuse and neglect by the State of Connecticut, ACTIONLYME founded Sep 1999

 

1999, e-Petitions, First ActionLyme, anti-Conflicts of Interest Campaign/Report/Summary to "authorities,"  by K. M. Dickson:

http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=Petition+Dattwyler+Kathleen+group%

http://groups.google.com/groups?q=Pataki+Rowland+Kathleen+group:sci.med.diseases

 

1999, ActionLyme Reporting Adverse Events Reporting Campaign Begins, Summer

Allen Steere, the "Astute Clinician"

 http://groups.google.com/groups?q=kathleen+Parenti+group:sci.med.diseases.lyme+group:sci.med.diseases.lyme

 

1999, Vikay Sikand, East Lyme, CT  ("Ha, Ha, Aren't we all getting old and forgetful"), reporting Sikand to the FDA

LDF and Lymerix, April 2001     

Vijay's LYMErix Blow-Off and Lewis Bull

 

1999, Fall:  The Poughkeepsie Lyme Initiative.  The Bard Conference nearly was caved due to pressure from New York Medical College (source of NY DOH’s OPMC “Experts”)  THE SPIN, second publication of conflicts of interest >>>   http://www.lymenet.de/aktive/pli.htm     compiled by K.M. Dickson   (Medical Detectives>>  Xxxxxx- who wishes to remain anonymous, Vanderhoof-Forschner, Dickson)

Mass. Lyme's ActionItem:  REPORTING Allen Steere for Medical Misconduct:  SteereReport

----

Edward McSweegan DCF-like stalking and harassment

2000, NOVEMBER, First ActionLyme Website, "The Lyme Disease Dilemma"
http://www.geocities.com/kmdickson0308/lyme-dilemma.html,  by K.M. Dickson

===

2001,  January 31, FDA LYMErix Vaccine Meeting, KMDickson, and ActionLyme, the sum of complaints brought about FDA's call for a hearing- OspA associated with activation of something like Lyme disease and the lack of Asymptomatically infected in the Vaccine (rOspA) group.  We ratted out VIJAY SIKAND (above, documented mistreatment of a trial participant in East Lyme, CT)  http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf  

Edward McSweegan attended this FDA Meeting and was FURIOUS at what I told the FDA  LOL

because the bogus Lyme vaccine was all his idea  (see the Barry Goldwater Letter)

Pam Weintraub:  http://www.whale.to/m/lymerix8.html    "The Bitter Feud over LYMErix  Big Pharma Takes on the Wrong Little Osp"

OTHER FDA TESTIMONY, at the Jan 31, 2001 Vaccine Meeting, See Lobet's and TRLA as persisting infection

http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2.htm

 

TRANSCRIPT of Jan 2001 FDA Vaccine Meeting:

http://www.fda.gov/ohrms/dockets/ac/cber01.htm#Vaccines%20&%20Related%20Biological

Choose:  3680t2.rtf  at the very bottom, center of the page.

          

LYME FOUNDATION      Lyme Foundation.  Vaccine withdrawn 2/27/02

LYME ASSOCIATION:    http://www.lymediseaseassociation.org/Vaccine.html

 

BELOW, Submission to the OPMC, November 2001, Albany, NY Medical Licensing Board (OPMC) Abuse of Lyme-Treating Physicians  Hearings (submitted by K.M. Dickson, below--  Includes Bransfield/Brand's  Rebuttal to Klempner, July 12, 2001, NEJM and "The Chronic Lyme Study" which was anything butt...)***

From/For the Albany OPMC Hearing:  Spirochetes, their Nature  More below

            OPMC Hearing Testimony, Kenneth B. Liegner, MD, and “social pathology”:

                http://www.aapsonline.org/testimony/liegtest.htm

Other Testimony at Albany, November 27, 2001

http://www.lymeinfo.net/part1.html

 

ActionLyme.50megs (second homepage—see especially, the “Planet CDC” Explainer.)

http://www.actionlyme.50megs.com   by K.M. Dickson

 

Trouble in Rhode Island, the R.I. Tick Borne Diseases Management Plan-- by K.M. Dickson            (link, see partial report in Pathologies.)

 

ILADS Position Paper on Klempner  (authors: RC Bransfield, VT Sherr, Se Phillips, KM Dickson, RB Stricker, HA Smith, S Brand)

 

REPORTING Lenny Sigal for Medical Misconduct :        SIGAL

=============================

*** ALBANY, November, 2001

ASSEMBLY COMMITTEE ON HEALTH

CORRECTED VERSION 7/14/02 Replaced Phylum with Order (see Lynn Margulis’ work)
 

Richard N. Gottfried Chair
Lara Kassel
Legislative Associate
Assembly Member Gottfried's office
822 Legislative Office Building
Albany, NY 12248

 

From: ActionLyme, International Patient Advocacy Group, by K. M. Dickson

ActionLyme Mission: To influence planning and policy in Vector Borne Diseases founded upon a complete presentation of the dynamic and extensive evidence of both spirochetal diseases, in general, and Borreliosis, more specifically, in humans.

Introduction: 

"Lyme disease" is infectious arthritis in a joint, with a high antibody response (i.e, 5 of 10 bands on a Western Blot), according to the CDC.  It is culturable Borrelia burgdorferi organisms from joint fluid.

Neuroborreliosis, or Lyme borreliosis is the chronic neurologic illness that is more commonly, and historically, (i.e., before Lyme, CT's Polly Murray discovered a cluster of juvenile arthritis) associated with spirochetal infections of mammals.  The simplest analogy is tertiary syphilis, a late neurologic spirochetal illness.

It is extremely uncommon for there to be a spirochetal infection that results in joint inflammation alone.  "Lyme disease" may be unique among spirochetal infections, in that respect.

Part I.

VALIDATION OF THE SCIENCE

In answer to the question, Do the NY OMPC investigated Lyme treating physicians have valid reason to believe Lyme borreliosis is a persisting infection, such that they treat and retreat Lyme Borreliosis according to methods that match the extensive evidence of how spirochetal microbes in general, and Borrelia burgdorferi, in particular, behave,” ActionLyme has provided a summary of scientific articles which support not only the Borreliae as persisting organisms, but support the ruggedness and persistence of the representatives of the entire Order Spirochaetales against environmental extremes, including chemical or antibiotics.

Part I of this ActionLyme response, examples of persistence from Nature, are only part of the picture of persistence across the Order. The greater bulk of confirming scientific publications are available to be read on the ActionLyme website:

http://actionlyme.50megs.com/OPMC.htm

 

In summary, Spirochetes are capable of:

-Morphological changes- spheroplast or "cyst" form, which is infectious/regenerates to intact form

-Dessication or near-Dessication

-Antimicrobial resistance-gene sharing, via plasmid

-Lateral gene transfer

-Intracellular persistence resulting in immune and antibiotic evasion (Klempner)

-Antigenic variation resulting in immune evasion

-Freezing.   Lyme patients cannot donate blood, per the Red Cross

-Porins- >> Confer resistance to antimicrobials, are possibly superantigens

Spirochetes do not behave like other bacteria. They are their own Order, the next degree of taxonomic classification under the Animal Kingdom is Class considerable uniqueness from other bacteria (Linnaean System: Kingdom, Phylum, Class, Order, Family Genus, Species).. 

Part II is a summary of publications and testimony on "Autoimmunity" in Neuroborreliosis.  The argument that treatment-resistant Lyme arthritis is an autoimmune disorder is commonly known, although still a hypothesis; there is a known association to T cell haplotypes, or the genetic code for Major Histocompatibility Complex class II "antigens", or antigen-presenting molecules in autoimmune disease and in autoimmune Lyme arthritis.  Simply put, people with HLA-DR4 or -DR2, the arthritis-prone individuals, tend to have a high antibody response and prolonged and extensive joint inflammation from B. burgdorferi, or, they have "Lyme disease".

There are now 2 known associations with persistent Neuroborreliosis as an autoimmune disorder, HLA-DR1*1501 and HLA-DQB1*0602, which are the two primary class II haplotypes associated with Multiple Sclerosis.  Klempner found that Chronic Lyme patients tend to have this *0602 haplotype much more than would be expected, and therefore, believes may be a correlate in this illness.  This discovery was not reported in the New England Journal last summer.  It is still a hypothesis, that these antigen-presenting molecules have "molecular mimicry" or similarity to, and attack self, but there is an increased prevalence of at least one of these two haplotypes expressed in Multiple Sclerosis/Lyme and is therefore, now a current area of discovery.

Multiple Sclerosis is a Central Nervous System disease.  Lyme borreliosis patients have been accused of exhibiting behavior that is not rational (Steere), neurotic (Weld), may be Munchausen and Munchausen-by-Proxy (Sigal), paranoid (Schoen), anxious

(Shapiro), ignorant (Benach), neuropsychiatric illness without objective evidence (Klempner), etc.,…

Rather than publicly stating that Lyme borreliosis patients have a CNS disorder, rather than providing the evidence of the association in MS haplotypes, rather than providing the evidence in the pathophysiology that these researchers have found, this data is withheld, and instead, it is publicly suggested that Neuroborreliosis patients exhibit severely psychopathology.

It is said, by these researchers, that Neuroborreliosis symptoms are "vague", but actually, they are only "vague" when the physician doesn't look at symptoms with the available objective tools. 

"Lyme disease" is not vague.  A swollen, red knee does not require anything more than human eyes to detect.  It is Lyme borreliosis, that requires more sophisticated perceptive abilities and analytical equipment.

The medical and social respect, care, and deference given to MS, Lupus, Narcolepsy, HIV and other neurological patients are being denied Lyme borreliosis patients.  Instead, these researchers invoke the stigma of mental illness as a deliberate means to deny the validity of our complaints and our access to treatment for a medical condition.  This denial of 1) our basic human dignity and 2) access to medical care for a medical condition, are Human Rights Abuses.

Whether Lyme borreliosis becomes a form of Multiple Sclerosis, or Lyme borreliosis is a cause of multiple sclerosis in the absence of persisting organism, or that any infectious cause of Multiple Sclerosis is either persisting infection or is true autoimmunity, are subjects of current scientific debate.

The evidence in Neuroborreliosis is that spirochetes persist past antibiotic treatment.  The evidence is that patients have one of three outcomes:  1) Lyme arthritis and high antibody response, 2) signs of infection resolve and the patient becomes asymptomatic, 3) patients develop a chronic neurologic syndrome clinically indistinguishable from Multiple Sclerosis.

It is scenario 3 that Lyme treating physicians treat, primarily; the chronic fatigue/ chronic musculoskeletal/ chronic neurocognitive disorder. That they treat with longer antimicrobial therapies than would meet with the intentions of Managed Care bottom line, is because the evidence from the Order is that spirochetes do not behave like other bacteria- they undergo physical changes which protect them from enviromental extremes. 

We have no data that says spirochetal infections are not persistent.  There is no specific antibiotic cure for Borreliosis, nor are there any specific antibiotic cures for Syphilis, Leptospirosis, or Brachyspirosis.  That is the state of the science:  There is no specific, targeted, antibiotic known to kill all these organisms in any mammal.

ActionLyme will provide evidence from the scientific research that, indeed, Neuroborreliosis results in a CNS disease with similarities to Multiple Sclerosis, and is the presence of real pathology, rather than is a psychogenic/hypochondriacal syndrome.

Table of Contents:  (HARD COPY of these will be hand-delivered Tuesday Nov 27 to Assembly)

Part I.  THE CAUSE OF CHRONIC NEUROBORRELIOSIS, Evidence from Nature. The Order, on persistence.

1) "Composite, large spirochetes from microbial mats: spirochete structure review."

Morphological changes may be responsible for relapsing, persisting illness.

http://www.pnas.org/cgi/reprint/90/15/6966.pdf

2) "Conversion of Borrelia garinii cystic forms to motile spirochetes in vivo."

Transfer of the spheroplast results in infection.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11478686&dopt=Abstract

3) “Effects of Penicillin, Ceftriaxone, and Doxycycline on Morphology of Borrelia burgdroferi

Conversion to spheroplast may not be the end stage.

http://aac.asm.org/cgi/reprint/39/5/1127.pdf

4) - "The Complexity of Vector-borne Spirochetes (Borrelia spp)"

Willy Burgdorfer   12th International Conference on Lyme Disease and Other Spirochetal and Tick-Borne Disorders  April 9, 1999 Keynote Address

Dr. Burgdorferi recognizes the older data on morphological variants.

http://www.medscape.com/medscape/cno/1999/lyme/Story.cfm?story_id=534

5)  "Detection of Borrelia burgdorferi DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis."-  Steere

Standard antimicrobial therapy does not kill all spirochetes.  The longer the therapy, the lower the DNA concentration in Lyme arthritis.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8272083&dopt=Abstract

6) "Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from Ceftriaxone in vitro."-- Klempner

14 days exposure to ceftriaxone does not kill all B. burgdorferi due to intracellularity of the organism.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1634816&dopt=Abstract

7)  “Relapsing Fever—Treatment and Control”  Chapter by Jay P. Sanford, from Biology of Parasitic Spirochetes, Academic Press, 1976, edited by Russell C. Johnson Jay P. Sanford, Uniformed Services University School of Medicine, Bethesda, Maryland p. 390

"There are aspects of the treatment of relapsing fever, syphilis, leptospirosis that illustrate similarities and from which therapeutic principles may be developed.  The ability of borrelia, especially tick-borne strains, to persist in the brain and in the eye during remission after treatment with arsenic or with penicillin or even after apparent cure is well known (1).  The persistence of treponemes after treatment of syphilis is a major area which currently requires additional study (3,5,10,11)."

8) "Central nervous system manifestations of Lyme disease." -Duray, Steere, Pachner

Brain biopsy from patient with subacute Lyme encephalitis produced an organism morphologically compatible with B. burgdorferi.  It appears spirochetes infect human brain tissue.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2742551&dopt=Abstract

9) "In vivo activities of Ceftriaxone and Vancomycin against Borrelia spp. in the mouse brain and other sites." – Barbour

After 7 days delay, vancomycin treatment failed to eradicate Borrelia from the brains of immune compromised mice.

http://aac.asm.org/cgi/reprint/40/11/2632.pdf

 

Part II. THE EFFECT OF NEUROBORRELIOSIS

Multiple Sclerosis and Persisting Infection? Evidence from the laboratory.

(More, again, on the ActionLyme website.)

1) Martin (NIH) and T cells and HLA-DR1*1501:

"Identification of candidate T-cell epitopes and molecular mimics in chronic Lyme disease"

http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v5/n12/full/nm1299_1375.html

2) Klempner (Tufts) quoting Martin (NIH),  "Is it thee or me?-autoimmunity in Lyme disease"

Autoreactive T cells to human nerves.

http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v5/n12/full/nm1299_1346.html

3)  Klempner to Rhode Island Doctors and HLA-DQB1*0602

South County Hospital, "Diseases of Summer Conference", July, 2001

What was discovered, but not published in NEJM

The validity of the Fibromyalgia Impact Questionnaire or SF-36 as assessment tools for outcomes of standard treatment, over re-examining and re-reporting cerebrospinal fluid Matrix- Metalloproteinases- enzymes seen in the pathophysiology of Multiple Sclerosis, and previously reported by Klempner in Neuroborreliosis patients.

See separate pages ___;Bransfield/Brand Rebuttal to Klempner, July 12, NEJM.

4) "Matrix metalloproteinases in the cerebrospinal fluid of patients with Lyme neuroborreliosis."

Klempner reports MMPs- enzymes found in the CSF of Multiple Sclerosis patients, as well as Borreliosis patients.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9466528&dopt=Abstract

5)  "Clonal expansion is a characteristic feature of the B-cell repertoire of patients with rheumatoid arthritis”

B cells and "Autoimmunity"-  The picture involves more than T cells.  It could be there is continually presented antigen- from somewhere.

http://arthritis-research.com/content/2/1/50

6) "Lyme Disease and the Clinical Spectrum of Antibiotic Responsive Chronic Meningoencephalomyelitides"

Ken Liegner's autopsy results.  Many sad stories.  Probably not psychogenic.

http://www.medscape.com/SLACK/JSTD/1997/v04.n03/jst0403.04.lieg/jst0403.04.lieg-01.html

7) THE EARLY HISTORY OF LYME TREATMENT:

At one time, all of the Authors of the IDSA Guidelines, except Durland Fish who is an entomologist, believed there was evidence to provide longer treatment.  See “Early Treatment History Data” set. Page___

8) So where are we?   Some researchers are still dedicated, despite the harassment by the OPMC and similar controlling entities elsewhere in the US, and the frustrations of dealing with Managed Care, to figuring out  how to help patients with borreliosis.  There were two studies completed in the United States that have shown improvement with longer term therapy; outside imaginary, and as yet, un-validated, standards of care.  One is an ongoing study by Dr. Brian Fallon of Columbia, See: http://www.columbia-lyme.org/

a) "Repeated Antibiotic Treatment in Chronic Lyme Disease"- Fallon, et al.

http://www.medscape.com/SLACK/JSTD/1999/v06.n04/std0604.02.fall/std0604.02.fall-01.html

b) "Tetracycline therapy for chronic Lyme disease."  Sam T. Donta, Boston University School of Medicine, Infectious Diseases Faculty.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9233665&dopt=Abstract


Mark Klempner, Tufts,  to Rhode Island Doctors: South County Hospital, "Diseases of Summer Conference", July, 2001

What was discovered, but not published in NEJM.  An audio transcript.

"Um, There, these patients obviously, are very, very much interested in that question, as we are, and I just want to highlight a preliminary piece of data of where we think we're going from here, unpublished*, and not for large, uh, dissemination, but here is the preliminary data.

And, that is, that when you look for the possibility of an autoimmune disease, the best way to look is to see if there is any genetic clustering in HLA haplotypes. The reason for that is the way antigens get presented in the context of who you are, that is, your HLA haplotype.  And we can talk in some detail about that.  Those diseases that I think everybody would agree are so called Autoimmune: lupus, rheumatoid arthritis, type 1 diabetes, and perhaps MS, have some clear genetic clustering that leads us to believe that these are indeed autoimmune diseases, although we do not satisfy so-called co-postulates of autoimmune disease that we've written about.  And the odds ratio for your having that particular HLA type, in the case of Rheumatoid arthritis, a DR4.  Or a DQB0602 to protect you from type 1 diabetes, are on the  order of 3 to 6.  One of the ones that is probably  highest, of course,  is B27, in patients with alkyloiding spondolytis and the like.  It turns out that if you look at the first 51 patients with post- treatment chronic Lyme disease, the patient population that participated in our study, there was a very high incidence of DQB0602 with an odds ratio of 770%.  So it may well be that exposure to THAT organism with THAT background of HLA haplotype may lead you to develop chronic symptoms.  That is a hypothesis that needs to be tested.  It would obviously lead to an entirely new form and approach to therapy."

 

"There were also many outcomes that were done in the laboratory.  I won't focus that much on them.  They are still a focus of great interest for us. And that is these serial plasma samples for PCR, at the dates that I mentioned here to try to determine if we could pick up sequestered infectious organisms.  Urine samples on multiple days for antigen testing and I'll comment on perhaps at the end of there's time, about the Lyme Urine Antigen Test- what we found in that regard.  Um, a new test that we're still working on, looking in the spinal fluid for a particular matrix-metalloproteinase, a CSF gelatinase, which I won't have time to comment on.  We published on this before, we're still looking at it, and it may be an interesting marker in these patients."

 

Early Treatment History Data set

TITLE: Treatment of Lyme disease.,  Schoen RT,  Conn Med 1989 Jun;53(6):335-7

ABSTRACT: Lyme disease, a tick-transmitted spirochetal infection, can be divided into three stages that can overlap or occur alone. The goals of antibiotic therapy in stage one are to shorten the duration of early disease and to prevent the development of later stages of the illness. This can usually be accomplished with oral antibiotic therapy.  Later stages of the illness are frequently more difficult to treat,  requiring prolonged oral or intravenous antibiotic therapy.

 

Dattwyler and Luft

TITLE: A perspective on the treatment of Lyme borreliosis., Luft BJ; Gorevic PD; Halperin JJ; Volkman DJ; Dattwyler RJ,  Department of Medicine, University of New York, Stony Brook 11794-8153. SOURCE:  Rev Infect Dis 1989 Sep-Oct;11 Suppl 6:S1518-25

 ABSTRACT:  Lyme borreliosis has become the most common tick-borne infection in the United States.  Although both beta-lactam and tetracycline antibiotics have been shown to be effective in the treatment of this spirochetosis, the development of optimal therapeutic modalities has been hampered by the lack of reliable microbiologic or immunologic criteria for the diagnosis or cure of this infection. In vitro sensitivity studies have been performed by several laboratories, but there has been no standardization of the methodology for measuring either inhibitory or bactericidal levels. Clinical studies have documented the efficacy of antibiotics, but therapy has failed in as many as 50% of cases of chronic infection.  Although new antibiotic regimens appear promising, the optimal treatment of this infectious disease remains to be determined. In this report we review the clinical and experimental rationale for the antibiotic regimens that we currently use and the need for a more standardized approach to treatment trials.

 

CONTRAST quote to New York Times by Dattwyler:

“In contrast, antibiotics have been shown to work extraordinarily well when, for instance, the Lyme organism has demonstrably infected the brain, Dr. Dattwyler said.”

 

Coyle

 

TITLE:  Seronegative chronic relapsing neuroborreliosis [see comments], Lawrence C; Lipton RB; Lowy FD; Coyle PK,  Department of Medicine, Albert Einstein College of Medicine,   New York, N.Y., USA. Eur Neurol 1995;35(2):113-7

ABSTRACT: We report an unusual patient with evidence of Borrelia burgdorferi infection who experienced repeated neurologic relapses despite aggressive antibiotic therapy. Each course of therapy was associated with a Jarisch-Herxheimer-like reaction. Although the patient never had detectable free antibodies to B. burgdorferi in serum or spinal fluid, the CSF was positive on multiple occasions for complexed anti-B. burgdorferi antibodies, B. burgdorferi nucleic acids and free antigen.

 

Coyle on long term effects

 

TITLE: Cognitive functioning in late Lyme borreliosis [see comments], Krupp LB; Masur D; Schwartz J; Coyle PK; Langenbach LJ; Fernquist SK; Jandorf L; Halperin JJ, Department of Neurology, State University of New York, Stony Brook 11794., Arch Neurol 1991 Nov;48(11):1125-9

ABSTRACT: Lyme borreliosis, a tick-borne multisystem disease, may cause a variety of neurologic complications, including meningoencephalitis and encephalopathy. To evaluate neurobehavioral function following treated Lyme borreliosis, 15 patients with Lyme disease and complaints of persistent cognitive difficulty a mean of 6.7 months following antibiotic treatment underwent neuropsychological evaluation and were compared with 10 healthy controls, matched in aggregate for age and education, who underwent the identical neuropsychological assessment. Compared with controls, patients with Lyme disease exhibited marked impairment on memory tests and particularly on selective reminding measures of memory retrieval. The memory impairment did not correlate with serum or cerebrospinal fluid anti-Borrelia burgdorferi antibody titers and was not explained by magnetic resonance imaging findings or depression.  The cause of this encephalopathy is currently unknown; however, indirect effects of systemic infection or other toxic-metabolic factors may be partly responsible.

 

 

Wormser and Nadelman

 

TITLE: Isolation of Borrelia burgdorferi from the blood of seven patients with Lyme disease., Nadelman RB; Pavia CS; Magnarelli LA; Wormser GP: Department of Medicine, New York Medical College, Valhalia.,  Am J Med 1990 Jan;88(1):21-6

ABSTRACT: PURPOSE: Borrelia burgdorferi, the etiologic agent of Lyme disease, has rarely been successfully cultured from blood. We report on seven patients from Westchester County, New York, with B. burgdorferi bacteremia diagnosed between April 1987 and August 1987. PATIENTS AND METHODS: One hundred thirty-two attempts to isolate spirochetes were made on blood specimens obtained from 104 patients. Twenty-two of these specimens were obtained from nine patients who had recently been bitten by Ixodes ticks but who were asymptomatic. Heparinized blood or serum specimens (0.2 to 0.4 mL) were inoculated onto 6 mL of modified Barbour-Stoenner-Kelly medium. Lyme serology was performed by enzyme-linked immunosorbent polyvalent, IgM, and IgG assays, fluorescent immunoassay, and microhemagglutination.  RESULTS: Four of the seven patients had erythema migrans, two had facial nerve palsy, and one had a flu-like syndrome without rash. These patients represented 21% (four of 19) of all patients with the characteristic skin lesion who had blood cultures for B. burgdorferi, and 40% (two of five) of all those with facial nerve palsy. Serologic testing was frequently nonreactive; two patients had no detectable antibody on multiple sera by five different assays. All patients improved with antibiotic treatment, and had negative subsequent blood cultures, but five of seven had persistent complaints after completion of therapy.  CONCLUSION: Culturing blood for B. burgdorferi may be useful in confirming the diagnosis of Lyme disease in selected patients. Use of spirochete blood cultures may facilitate a better understanding of the pathogenesis and natural history of Lyme disease.

 

Wormser and Nadelman

 

TITLE: A clinical approach to Lyme disease., Nadelman RB; Wormser GP, Department of Medicine, New York Medical College, Valhalla.,  Mt Sinai J Med 1990 May;57(3):144-56

 ABSTRACT: Lyme disease (also known as Lyme borreliosis) is an emerging, newly described infectious disease with diverse clinical manifestations.  The disease is caused by the spirochetal agent Borrelia burgdorferi, which is transmitted to humans by the bite of certain species of Ixodes ticks harboring the organism. The most readily identifiable clinical feature is the distinctive skin lesion, erythema migrans. If recently infected patients go untreated, approximately 15% will develop neurologic conditions (most commonly facial nerve palsy), 8% will develop myocarditis (typically with heart block), and 60% will develop migratory mono- or pauci-articular arthritis. Diagnosis depends on clinical suspicion, recognition of the characteristic signs and symptoms, and appropriate testing for antibody to B. burgdorferi.  Serology for Lyme disease, although in need of better standardization, is most useful in diagnosing patients with manifestations of Lyme disease other than erythema migrans. All manifestations of Lyme disease are potentially treatable with either a beta-lactam antibiotic (for instance penicillin, amoxicillin, or ceftriaxone) or a tetracycline preparation. However, the optimal antimicrobial regimen, including choice of drug, drug dose, route of administration, and length of therapy, is unknown. Other important areas for future research include Ixodes biology and control, improved laboratory tests for diagnosis and for assessing response to therapy, and vaccine development.

 

Rush

 

This study was about the treatment results of acute disseminated Lyme disease, which is within the first month of infection AND NOT DISSEMINATED INTO THE CNS. This is not a treatment study about Chronic Lyme disease.  There are no other publications by this scientist other than the Guidelines and possibly one on AIDS.

 

TITLE:  Ceftriaxone compared with doxycycline for the treatment of acute

disseminated Lyme disease., Dattwyler RJ; Luft BJ; Kunkel MJ; Finkel MF; Wormser GP; Rush TJ; Grunwaldt E; Agger WA; Franklin M; Oswald D; Cockey L; Maladorno D,  Department of Medicine, State University of New York, Stony Brook, 11794-8161, USA., N Engl J Med 1997 Jul 31;337(5):289-94

ABSTRACT:

BACKGROUND: Localized Lyme disease, manifested by erythema migrans, is

Usually treated with oral doxycycline or amoxicillin. Whether acute disseminated

Borrelia burgdorferi infection should be treated differently from localized infection is unknown. METHODS: We conducted a prospective, open-label, randomized, multicenter study comparing parenteral ceftriaxone (2 g once daily for 14 days) with oral doxycycline (100 mg twice daily for 21 days) in patients with acute disseminated B. burgdorferi infection but without meningitis. The erythema migrans skin lesion was required for study entry, and disseminated disease had to be indicated by either multiple erythema migrans lesions or objective evidence of organ involvement.  RESULTS: Of 140 patients enrolled, 133 had multiple erythema migrans lesions. Both treatments were highly effective. Rates of clinical cure at the last evaluation were similar among the patients treated with ceftriaxone (85 percent) and those treated with doxycycline (88 percent); treatment was considered to have failed in only one patient in each group. Among patients whose infections were cured, 18 of 67 patients in the ceftriaxone group (27 percent) reported one or more residual symptoms at the last follow-up visit, as did 10 of 71 patients in the doxycycline group (14 percent, P > or = 0.05). Mild arthralgia was the most common persistent symptom. Both regimens were well tolerated; only four patients (6 percent) in each group withdrew because of adverse events. CONCLUSIONS: In patients with acute disseminated Lyme disease but without meningitis, oral doxycycline and parenterally administered ceftriaxone were equally effective in preventing the late manifestations of disease.

 

 

Rahn

 

TITLE:  Treatment of Lyme disease.,  Steere AC; Green J; Hutchinson GJ; Rahn DW; Pachner AR; Schoen RT; Sigal LH; Taylor E; Malawista SE,  Zentralbl Bakteriol Mikrobiol Hyg [A] 1987 Feb;263(3):352-6

 ABSTRACT: We compared phenoxymethyl penicillin, erythromycin, and tetracycline, in each instance 250 mg four times a day for 10 days, for the treatment of early Lyme disease  (stage 1). None of 39 patients given tetracycline developed major late complications compared with 3 of 40 penicillin-treated patients and 4 of 29 given erythromycin (p =  0.07).  However, with all three antibiotic agents, nearly half of patients had minor late symptoms. For neurologic abnormalities (stage 2), 12 patients were treated with high-dose intravenous penicillin, 20 million U a day for 10 days. Pain usually subsided during therapy, but a mean of 7 to 8 weeks was required for complete recovery of motor deficits. For the treatment of established arthritis (stage 3), 20 patients were assigned treatment with intramuscular benzathine penicillin (7.2 million U) and 20 patients received saline. Seven of the 20 penicillin-treated patients (35%) were apparently cured, but all 20 patients given placebo continued to have attacks of arthritis (P less than 0.02). Of 20 arthritis patients treated with intravenous penicillin G, 20 million U a day for 10 days, 11 (55%) were apparently cured. Thus, all 3 stages of Lyme disease can be treated with antibiotic therapy, but some patients with late disease may not respond.

 

Rahn, Steere, Schoen

 

TITLE: Treatment of refractory chronic Lyme arthritis with  arthroscopic synovectomy.  Schoen RT; Aversa JM; Rahn DW; Steere AC,  Department of Medicine, Yale University School of Medicine, NewHaven,Connecticut 06510., Arthritis Rheum 1991 Aug;34(8):1056-60

 ABSTRACT: Of 20 patients who underwent arthroscopic synovectomy for refractory chronic Lyme arthritis of the knee, 16 (80%) had resolution of joint inflammation during the first month after surgery or soon thereafter, and they have remained well during the 3-8-year followup period. Three of these 16 patients who were more disabled preoperatively, still had mild functional limitation at long-term followup.  The remaining 4 patients (20%) had persistent or recurrent synovitis.  We conclude that arthroscopic synovectomy is effective in treating chronic Lyme arthritis in patients in whom the disease does not respond to antibiotic therapy.

 ----Kathleen M. Dickson


 

The Klempner Article 

Bransfield and Brand

 

 

The recent article in the NEJM, "Two Controlled Trials of Antibiotic Treatment in Patients with Persistent Symptoms and a History of Lyme Disease," by Klempner, et. al. provides some interesting data, but the proper interpretation of this data is of little relevance to both clinical practice and guidelines related to chronic Lyme disease. It does, however, provide some interesting insight about the significance of PCR and IgG testing in Lyme disease, it demonstrates a poor quality of life is associated with a history of Lyme disease and it is an excellent example of the failure of objectivity in a peer reviewed article in a prestigious medical journal followed by misperceptions of the significance of this article by the media, resulting in the improper use of this article by the insurance industry. An objective review of this article is one issue, while the role of this article towards perpetuating false beliefs about Lyme disease is an additional and more significant issue.

 

Medicine today, is much like law. Both have adversarial qualities. Information is presented a manner that is most effective in arguing a point of view. When this technique is effective, guilt is proven to be innocence; black is proven to be white, etc. The technique is always the same. There are a series of statements and conclusions. Each statement is a 10-degree twist on the truth, so small that it can go below the radar of our ability to detect deception. After a series of complicated and related statements, there is a 180-degree twist to the truth.

 

The twists to this article began many years ago when a few rheumatologists involved in Lyme disease incorrectly attempted to apply their observations of acute Lyme arthritis to explain late stage Lyme disease and Lyme neuroborreliosis. The problem was compounded when Lyme disease was conceptualized from the perspective of an acute infection rather than recognizing the persistent relapsing nature of this microbe. These and many other similar twists set the stage to bias the researchers to confirm their prior views on the subject. A failure to recognize and comprehend that tick-borne diseases were often complex interactive infections involving multiple stealth and persistent pathogens, and an excessive reliance upon molecular mimicry hypotheses further added to the problem. As a result of these and other errors, a twenty-first century problem is approached with a nineteenth century view of infectious disease. The bias was further solidified as patent issues, competing diagnostic systems, research grants, reputations, lawsuits, and a need to defend prior consultant decisions that were provided to insurance companies as high paid consultants further clouded scientific objectivity. Anyone coming from this perspective would be highly motivated to design a study that would argue that persistent infection was not a significant issue in Lyme disease, and this is exactly what happened.

 

The study design guaranteed the study would fail. The design of the research protocol is the most critical step in the project. This study had a very restrictive inclusionary and exclusionary criteria. The vast majority of patients with chronic Lyme disease do not meet the criteria for inclusion into the study, therefore the findings and stated conclusions have no relevance to most patients with CLD. The other two NIH sponsored trials had much better study designs. I recall sitting in a meeting several years ago at NIH when the study design of the NIH intramural study was discussed. A pyramid was used as an analogy. At the bottom of the pyramid were the patients who had some of the features of Lyme disease with disagreement about whether or not these patients truly had Lyme disease. The intent was to select the patients at the tip of the pyramid who clearly had Lyme disease. This strategy was NOT used in the Klempner study. Patients who demonstrated DNA evidence of the presence of Borrelia burgdorferi by PCR testing were excluded from the study. There was only one short sentence in the journal article that discussed this, and this was the most significant sentence in the entire article.  PCR testing has been considered absolute proof in the legal system, why would a PCR positive patient ever be excluded? It was stated that it would have been unethical to give a placebo, rather than the antibiotic treatment to a PCR positive patient.  This is a clear endorsement that positive PCR testing is considered confirmation of persistent infection with Bb.  Depression, a major symptom of the neuropsychiatric manifestations of Lyme disease, was also an exclusionary criterion. Even though both PCR and depression were exclusionary criteria, the status of the study participants was measured by PCR testing on the spinal fluid and the Beck Depression Scale. Other means of evaluating the status of the patients were the SF-36 and other testing. Basically, the wrong tests and tests that lacked objectivity were used to evaluate the status of the patients. Although there were 12 authors, none were psychiatrists. Why? Neuropsychiatric symptoms are a major

part of the later manifestations of Lyme disease. How can a study, which is supposed to study late stage disease, not have the input of a psychiatrist with experience on working

with Lyme disease? The neuropsychological scales that were implemented in the study were notably insufficient to adequately assess the psychiatric symptoms and the executive functioning impairments, which are associated with persistent Lyme disease infections. The SF-36 scale was used. The scores were quite low, reflecting a poor quality of life for these patients. In addition, the SF-36 is only a subjective scale based solely upon patient opinion, and contains no objective criteria for the assessment of patients' status.

 

Rather than PCR, a positive IgG Western Blot test based upon five bands at only one laboratory was used as a reference point. No studies have ever demonstrated whether the absence of IgG reactivity had diagnostic significance in late stage disease.

 

The study was designed to provide patients with "intensive antibiotics."  Although one month of ceftriaxone and two months of doxycycline would be considered intensive for the treatment of many acute infectious diseases, few physicians who shoulder the responsibility of treating chronic Lyme disease would consider this to be an adequate retreatment for a patient with late stage Lyme disease who had failed prior courses of significant treatment. Results, from recent scientific studies on dog models by Straubinger of chronic Lyme disease, indicate persistent infection even after 6 months of antibiotic treatment. Furthermore, experience in the treatment of human infections caused by other persistent bacteria, such as Treponema pallidum, Mycobacterium tuberculum and Helicobacter pylori demonstrates that prolonged antibiotic therapy and/or different combinations of antibiotics would result in greater improvement than was observed in this study.

 

Additionally, while the study tested patients for tick-borne coinfections, like babesiosis or ehrlichiosis, it failed to offer any treatment strategies.

 

The placebo and treatment groups appeared to start with significantly different scores on the primary outcome measures. In the group of seropositive patients, those in the placebo group had significantly better scores on the MOS Cognitive measures, and exhibited fewer neurocognitive symptoms at base-line, than the patients in the antibiotic group. In addition, within the seronegative group, patients in the placebo group had significantly poorer scores on the SF-36 Mental Component, the MOS Pain scale, and the Fibromyalgia Impact Questionnaire. The categorization of patients into Improved, Unchanged and Worse on each of the outcome components seems to lose a certain amount of information about the magnitude of change in functioning from base-line until post-treatment, and to be lacking in statistical power compared with other procedures for analyzing these data. In view of these two points, it would seem advisable to utilize Analysis of Covariance procedures to measure the impact of treatment on the outcome measures, after adjusting for patients' baseline scores on the measures of functioning. This procedure would take into consideration the baseline differences between groups,

would treat change in the outcome measures as a continuous rather than a categorical variable, and would afford more statistical power in testing differences between the placebo and antibiotic groups. Since the symptoms of chronic Lyme disease are different in different patients, some patients presented impairments primarily in specific areas of functioning, and change from treatment would be expected in the specific areas that were problematic for each patient. An analysis of change in the most problematic items on each of these scales would provide a more sensitive assessment of potential treatment effects. In addition, the small sample size raises concerns about statistical power, and further undermines the validity of the study.

 

The 35% improvement threshold, when combined with the other study design constraints would predict a failure, even before initiating the study. It should have been necessary to adjust the status assessment to make allowances for the Jarish-Herxheimer rection, but this was not a part of the study design. It would be important to know more details of the NIH NIAID Data Safety and Monitoring Board's termination of the study.

 

Since the patients with seronegative Lyme disease showed better improvement on antibiotics than their seropositive counterparts, it appears that negative IgG reactivity is not a useful criterion to deny the presence of persistent infection. If the investigators feel persistent infection was not a cause of the patient's current symptoms, then what else is a truly more plausible explanation?

 

A disclaimer reviewing the potential conflicts of interests of the authors was absent from the article, and would have been most appropriate in light of the significant political, financial, and ethical controversies surrounding chronic Lyme disease. This should have included disclosures of the authors' Lyme disease-related insurance consultations, roles as defendants in Lyme related law suits and their roles as paid expert witnesses, as well as their ownership of Lyme disease related patents, commercial diagnostic systems and their financial vaccine interests.

 

Along with three other related articles, the Klempner article was distributed on the Internet a month before the date of publication. The reason for the early release is a subject of considerable speculation. When the article was released, there was a well-orchestrated flood of articles in the media, which mostly interpreted the significance of the article out of context. Since the release, insurance companies have already used the article as proof to deny coverage for the treatment of Lyme disease.

 

In summary, the design of the research and the manner in which the article was written and promoted in the media even before it was published reflects many of the biases that have obstructed scientific objectivity and medical progress surrounding Lyme disease for decades. The study demonstrates that patients with a history of exposure to Lyme disease in the past, who probably do not have active infection at the time of the study as demonstrated by negative PCR's and a history of significant antibiotic treatment in the past, do not respond to inadequate antibiotic treatments as measured by incorrect and highly subjective criteria that are not representative of symptoms associated with CLD administered by physicians who appear to not know how to treat Lyme disease, some of whom have strong conflicts of interest to the contrary in a study that was never completed. In short, the study proves very little. It does, however demonstrate, that it is very easy to waste large amounts of Federal money for something of little benefit to taxpayers. In a backhanded way, it validates PCR testing as proof of persistent infection.  It suggests that IgG testing by Dearborn criteria is not a valid criterion to either confirm or refute the presence or absence of active infection. Most importantly it demonstrates that false beliefs can be self-perpetuating, information in the peer reviewed medical literature can be highly inaccurate and deceptive and it is very easy for medical information to be improperly interpreted by the media, insurance industry and potentially by the legal system.

 

Robert C Bransfield, MD

Private Practice of Psychiatry

Red Bank, NJ

 

Stephen Brand, Ph.D.

Assistant Professor (Research)

National Center on Public Education

University of Rhode Island

===

 

As we Lyme warriors cannot engage any earthly assistance;
As the entire US medical community chooses not to assist sick and abused people and put a stop to this;
As there is not one MD or group in the entire USA who will take these criminals to court;
As there is not one lawyer or Department of Justice official who will do the job they were hired to do and protect us from corporate crime;
As there are no men left among us:

http://www.ourladyswarriors.org/prayer/michael.htm

Saint Michael the Archangel,
defend us in battle.
Be our protection against the wickedness and snares of the devil.
May God rebuke him, we humbly pray;
and do Thou, O Prince of the Heavenly Host -
by the Divine Power of God -
cast into hell, satan and all the evil spirits,
who roam throughout the world seeking the ruin of souls.

Amen.

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