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Attention: Genet B.
IDSOCIETY.org

CC: USDOJ 203-773-5376

CC: CT AG Richard Blumenthal
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Re: IDSA LYME “GUIDELINES” - PART II, CDC Officers’ Reports on Treatment Failure and Intracellular Spirochetal Persistence

First of all I would again like to thank youz for allowin us’n plain old regular scientists inputs to yer guidelines.

Today’s Topics, Part Two’s Topics is: CDC Officers Reporting Treatment Failure of Spirochetal Diseases:

CDC Officers Alan Barbour, Allen Steere, and Mark Klempner all have reported that treatment of spirochetal diseases fails. I will demonstrate those reports and their contents.

All members of IDSA’s new Lyme panel, the Blumenthal Panel, will look closely at these reports because I am sure, as Infectious Diseases Specialists, you have all seen this data before and know all about the History of Relapsing Fever and how it all jives with the current era, the Era-of-CDC-Officers Mark- Klempner-Alan-Barbour-and-Allen-Steere-All-Reporting-About-How-Antibiotic-Treatment of Spirochetal-Diseases-Fails, but only 1/6 to 1/3 remain ill. And I already wrote this report and sent it to the Albany Legislators in 2001 and talked in person to David Grann of “Stalking Steere,” while I was sending the Albany Legislators proof that IDSA/ALDF are a bunch of lying crooks and none of us was stalking Steere or Klempner. Except with a tape recorder:
http://www.actionlyme.org/Klempner_DQB1_0602.html (Transcript)
http://www.actionlyme.org/YOUTUBEVIDEOS.htm

http://www.youtube.com/watch?v=yPn_T9qy4C0&mode=related&search= Here it straight from the horse’s mouth.

As an aside, Gary Wormser and Mark Klempner published a report in 2005 where they reported that there was after all no association between the Neurologic or the NINDS-Roland Martin Multiple Sclerosis kind of Lyme and Haplotypes, as there is in the Steere/Dearborn-kind of Bad-Knee-Only-Kind-of-Lyme, the only kind that tests positive, as shown in the 2003 RICO Complaint against Yale et al:
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm

And as discussed by the CDC officers in their European patents with SmithKline:

http://www.journals.uchicago.edu/doi/pdf/10.1086/432733

They also published that the Steere/Dearborn kind of Lyme presents with no neurologic or brain or fatigue signs. Well, we knew that from Vijay Sikand who said so at the 1998 FDA Vaccine Committee Meeting where he said such people were “immune competent” or could produce enough antibodies to fight the infection:

Patients with this [Steere/s HLA or Dearborn positive Lyme] syndrome have recurrent episodes of arthritis/synovitus. Results of synovial fluid cultures and PCR for Bb are negative with the bogus primers we use, like OspA primers which we know undergo antigenic variation and are useless, and that is part of the PRIMERSHELLGAME:
http://www.actionlyme.org/PRIMERSHELLGAME.htm

We know, Okay? We get it about brains being complicated variables that apparently Yale throws out, even their own.

Alan Barbour published that OspA undergoes antigenic variation and is not a good vaccine candidate, despite being the patent owner of the ImmuLyme OspA, over which Gary Wormser is still being sued by Steve Sheller.
http://www.actionlyme.org/GARY_WORMSER_SUED.htm
http://www.actionlyme.org/BARBOUR_MUTANTS_1992.htm
And the RICO within the RICO gang of Dave Persing published in 1994 about TARGET IMBALANCE:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=8158048[uid]

However, despite equivalent or even superior analytic sensitivity for detection of cultured organisms, the reactivity of two genomic DNA targets was often weak or absent altogether in the clinical specimens. This apparent overrepresentation of B. burgdorferi plasmid sequences was found exclusively in clinical specimens and not in cultured organisms. The physiologic imbalance of genomic and plasmid DNA reactivity in B. burgdorferi infection may signal an underlying pathogenetic mechanism.

The pathogenic mechanism being the part where Relapsing Fever is called Relapsing Fever because of Antigenic Variation which means Osp primers are no good for DNA detection of spirochetes in humans, but IDSA already knowed this, as showed in the Primers Shell Game:
http://www.actionlyme.org/PRIMERSHELLGAME.htm
where all the IDSA crooks use the correct primers - the non-variable DNA or RNA - for searching for spirochetes in ticks when they’re REALLY looking for spirochetes… to patent (but not as regards humans whichin don’t count).

---------

Maybe tomorrow in Part III, where I’m helping IDSA, I will discussing what’s in their patents, including the patents of CDC-Officer-Barbara-Johnson-with-SmithKline in Europe and how it is clear that she knows the Dressler/Steere or Dearborn standard is scientifically bogus (or is only HLA-Steere’s-bad-knees-positive). For now, users can use this page:
http://www.actionlyme.orgCDCS_PARTICIPATION_IN_LYME_CRIMES.htm

Way, way back in 1986 CDC Officer and head of the NIH Rocky Mountains Bioweapons Lab in Montana that intended to- and dug a moat around it, like Plum Island and Long Island Sound, reported that a treatment for syphilis was to give people a fever through giving them High-Passage Relapsing Fever in an article entitled, The Biology of Borrelia Species. Here is the link it could be finded at:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=3540570

So, even at that time CDC officer Alan Barbour knew high-passage strains lost plasmids or virulence or would not generate the antigen necessary to detect specific antibodies via Western Blotting, as discussed in Part I of this complaint, whichin I calls: The Kathleen Dickson is Helpin IDSA’s, Too!! Series

There are several excerpts from that Barbour-Borrelia-Species report worthy of discussing mongst the genral publics, too!:

PAGE 394 of the pdf:

“A strain of B. duttonii that had been passed many times in mice was found to have lost virulence for humans (212). When using borrelia for pyrotherapy of neurosyphilis, the authors of this report [CDC Officers] recommend that no more than 30 to 40 passages in mice be made before inoculation of the strain back into humans (212).”

PAGE 391 of the pdf:

"The propensity for borrelia to go to the brain of infected mammals suggests that the relationship between these spirochetes and neural tissues is not trivial. Further study of this attraction and the interaction that follows may reveal the basis for the significant nerve and brain involvement in Lyme borreliosis"--

From Part I of this series, from Yale’s Steven Malawista, we know that it is “complicated” about the brain. Here we learning that that’s exactly where the spirochetes like to hang out:

PAGE 393 of the CDC-officer-Alan-Barbour pdf, bottom right:
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=373079&blobtype=pdf

Says Barbour: “Spirochetes are not found in the blood, but rodent brains are the best place to find them, so we used to use rodent brains as the primary spirochete storage area/media, before I, Alan Barbour, came up with the bogus BSK (B for Barbour) media, which everyone thinks is good for all Borreleae, not just Lyme Borrelia it’s sorta like the PrimersShellGame and I hope no one catches on…”

Says CDC Officer Alan Barbour in 1992:

http://www.actionlyme.org/BARBOUR_MUTANTS_1992.htm

PAGE 799 of the pdf that’s no longer available free-full-text online:

Says CDC officer Alan Barbour: “OspA undergoes antigenic variation due to the selection pressure of antibodies which means OspA is no good as a vaccine but buy mine, ImmuLyme, anyway.” And he gives three references to support this conclusion.

- - - - - -

SAYS CDC OFFICER ALLEN STEERE when he is discussing treatment failure even when playing a game with the primers (using the wrong primers) to detect Borrelia in humans:

http://www.actionlyme.org/BRAIN_PERMANENT.htm

1) The Long-Term Clinical Outcomes of Lyme Disease: A Population-based Retrospective Cohort Study:

http://www.annals.org/cgi/content/full/121/8/560

"Patient 12 had had high fever, meningeal symptoms, and subsequentarthritis in 1982. She was noted to have a positive serologictest result for Lyme disease 4 years later and was treated with2 weeks of parenteral penicillin. She later developed a progressivespeech disorder, bradykinesia, and abnormal ocular motor function.Magnetic resonance imaging of the brain showed scattered whitematter lesions in the hemispheres and pons, and she was diagnosedwith supranuclear palsy. Lumbar puncture showed no selectiveconcentration of antibody in the spinal fluid. Nevertheless,she was re-treated with 2 weeks of parenteral ceftriaxone in1989 that had no effect on her neurologic symptoms. During thetime of observation, this patient died. At autopsy, lymphoidmononuclear cells were observed surrounding the intracerebralvessels in one section. Using Dieterle silver stain, a spirochetewas present in the cortex and another was exterior to a leptomeningealvessel."

One of Steere's multiply-treated patients died anyway with spirochetes in her brain. How amazing that that suddenly doesn't happen any more, despite no new breakthroughs in antibiotic treatments or their delivery.

The rest of IDSA’s rejected, nearly-dead patients often end up in the care of Kenneth B. Liegner, of Armonk, New York, who is not too happy about being the last MD to see IDSA’s victims before the burial or more autopsies:
http://www.actionlyme.org/CDC_Spirochetes_Brain_Liegner_Autopsy.htm

^^^ Where the presence of spirochetes in IDSA’s victims after multiple course of antibiotics were found to have spirochetes in their tissues either by DNA methods or staining, by the CDC, Tulane, the Mayo Clinic or SUNY, StonyBrook.

2) http://content.nejm.org/cgi/content/full/330/4/229 (STEERE)

Detection of Borrelia burgdorferi DNA by polymerase chain reaction in cerebrospinal
fluid in Lyme neuroborreliosis.

"of 73 patients with Lyme arthritis who were untreatedor treated with short courses of oral antibiotics before testing,70 (96 percent) had positive PCR results. In contrast, of 19patients who received either parenteral antibiotics or longcourses of oral antibiotics, only 7 (37 percent) had positivetest results after treatment (P<0.001). In the 29 patientsfor whom serial samples were available, all pretreatment sampleswere positive."

3) http://www.ncbi.nlm.nih.gov/pubmed/8769624

Detection of Borrelia burgdorferi DNA by polymerase chain reaction in cerebrospinal fluid in Lyme neuroborreliosis.

: J Infect Dis. 1996 Sep;174(3):623-7.

Nocton JJ, Bloom BJ, Rutledge BJ, Persing DH, Logigian EL, Schmid CH, Steere AC.

Division of Rheumatology/Immunology, New England Medical Center, Boston, Massachusetts02111, USA.

A polymerase chain reaction (PCR) assay that detects Borrelia burgdorferi DNA in cerebrospinal fluid (CSF) was evaluated as a diagnostic test for acute or chronic Lyme neuroborreliosis. In one laboratory, 102 samples were tested blindly, and 40 samples were retested in a second laboratory. In the first laboratory, B. burgdorferi DNA was detected in CSF samples in 6 (38%) of 16 patients with acute neuroborreliosis, 11 (25%) of 44 with chronic neuroborreliosis, and none of 42 samples from patients with other illnesses. There was a significant correlation between PCR results and the duration of previous intravenous antibiotic therapy. The overall frequency of positive results was similar in the second laboratory, but concordance between the laboratories and among primer-probe sets was limited because many samples were positive with only one primer-probe set. Thus, PCR testing can sometimes detect B. burgdorferi DNA in CSF in patients with acute or chronic neuroborreliosis, but with current methods, the sensitivity of the test is limited.

KLEMPNER:

http://www.actionlyme.org/MarkKlempner_Fibroblasts.htm

or:
http://www.ncbi.nlm.nih.gov/pubmed/1634816?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

: J Infect Dis. 1992 Aug;166(2):440-4.Links

Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro.

Georgilis K, Peacocke M, Klempner MS.

Department of Medicine, New England Medical Center, Boston, Massachusetts.

The Lyme disease spirochete, Borrelia burgdorferi, can be recovered long after initial infection, even from antibiotic-treated patients, indicating that it resists eradication by host defense mechanisms and antibiotics. Since B. burgdorferi first infects skin, the possible protective effect of skin fibroblasts from an antibiotic commonly used to treat Lyme disease, ceftriaxone, was examined. Human foreskin fibroblasts protected B. burgdorferi from the lethal action of a 2-day exposure to ceftriaxone at 1 microgram/mL, 10-20 x MBC. In the absence of fibroblasts, organisms did not survive. Spirochetes were not protected from ceftriaxone by glutaraldehyde-fixed fibroblasts or fibroblast lysate, suggesting that a living cell was required. The ability of the organism to survive in the presence of fibroblasts was not related to its infectivity. Fibroblasts protected B. burgdorferi for at least 14 days of exposure to ceftriaxone. Mouse keratinocytes, HEp-2 cells, and Vero cells but not Caco-2 cells showed the same protective effect. Thus, several eukaryotic cell types provide the Lyme disease spirochete with a protective environment contributing to its long-term survival.

Or, said another way, “Fibroblasts protect spirochetes from ceftriaxone, which is why ceftriaxone fails to cure Lyme or Relapsing Fever.”

Thank you very much again and I will be back tomorrow with another famous topic because I make good researches in America, too!!

Kathleen M. Dickson

23 Garden Street, Pawcatuck, CT 06379

860-495-5298, 203-393-5148
ActionLyme.org, RelapsingFever.org,
Former Pfizer Analytical Methods Development Chemist