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Borreliosis Basics ALDF/CDC Patents USDOJ RICO Complaint AIDS-like EBV-Borreliosis; UN Complaint (2003) Bioweapons Attributes
Lyme Facts CDC's Patents w/ GSK Blumenthal (AntiTrust) Great Imitator, IDSA, 1989 Antics Crazy Eddy & Durl Lyme as a bioweapon?
Persist.Historical, IDSA's UConn Assaults Children 30 reports; Sepsis = Autism OspA / Pam3Cys Tolerance Munchausen's Libel Army says Bioweapon
DNA Shell Game Congenital Lyme by Yale Dattwyler: Seroneg Lyme Failed Other Fungal Vax Sweeg's Munchausen's Russians@NYMC (HLAs)
Steere Falsifies test Halperin: Lyme & ALS Steere: Seronegative Lyme PubMed: OspA >> EBV ALDF.com files Plum Island Evidence
Yale's Vaccine Conspiracy Steere: Lyme >> Lupus Klempner on hidden tape LYMErix causes neurologic Fish @ Internat.Spy Firm EXOSOMES/BLEBS
IDSA&CDC Biomarkers Klempner & "Guidelines" False Claims Act refs NIH:  CLD is active herpes Durland Fish's "Attack" Lyme Mafia Alpert
Plum Stupid, referenced Cryme Disease Videos .CORIXARICO

ME/CFS is active herpes

IDSA Reviews Lyme Mafia Sepkowitz


08/25/2015 13:57:41
 

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"LLMDs" reveal they have no clue what they are talking about...  Lyme/CFIDS is post sepsis syndrome.  OspA-ish blebs are  toxins inflaming brain & turn off the humoral immune system.  Lyme = like AIDS.


Bagging the
Whistleblower AmericanCowardiceŽ  dot NAZI dot mil 
AmericanFascismŽ

FibroLies, unbelievable, what the truth is !!

CDC/Yale/IDSA: "LYMErix causes  same multisystem disease" as 'Chronic Lyme'"  OspA is a fungal toxin causing immunosuppression


Benach/IDSA, brain damage in Lyme, 1992 (scanned)

Exosomes, Blebs turn off the immune response and inflame the brain

SASH vaccines paper (Common Mechanisms)

Spirochetal Dementia

OhioActionLyme, USDOJ criminal charge sheets

Cryme Disease
Norway Site


Bad Ass Cryme Blog



 

 


 

1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.

ActionLyme/Kathleen Dickson predicts all of Bushie's outcomes in Oct 2000

ActionLyme/Kathleen Dickson predicts Bush will have us worshipping his bombs (Shock and Awe"), in Oct 2000 during the Gore Debates    



Steere's "Seronegative Lyme" Hysteria about OspA-induced Antibody Inhibition
Read about it also in the 1998 FDA LYMErix meeting transcript:
http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf


1990
; Steere using Dattwyler and Volkman's Seronegative Lyme Assay (developed because Dattwyler knew fungal antigens produced immunosuppression) to evaluate "Chronic Neurologic Lyme" cases:


http://www.nejm.org/doi/pdf/10.1056/NEJM199011223232102


See Also, CRYMEDISEASE_CHP3_B.htm  where we show Steere in 1991 actually used this seronegative Lyme assay on his own lab
workers, 101016.htm (
http://www.ncbi.nlm.nih.gov/pubmed/1883122)  where we see Steere knowingly falsely advising the Academy
of Insurance Medicine a year later (1992), and the Plum Island Chapter of Cryme Disease where Justin Radolf demonstrates in 2001
that OspA vaccination (or autovaccination via blebbing), results in inhibition of antibody production via downregulation of HLA.

N  1988 Dec 1;319(22):1441-6.

Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.

Source

Department of Medicine, State University of New York, School of Medicine, Stony Brook 11794-8161.

Abstract

The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients. We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls. The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean ( +/- SEM) stimulation index of 17.8 +/- 3.3, similar to that (15.8 +/- 3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1 +/- 0.5; P less than 0.001). 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.

Comment in

http://www.ncbi.nlm.nih.gov/pubmed/3054554