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09 Feb 2012
HOME
Pharma/CDC on Brain
damage from vaccines, Fauci, Phages, Bioweapons manufacture
HHS.gov is
Incompetent; BMJ calls fraud "crime.")
Official: CFIDS and MS-Lyme are the
same disease; Epstein-Barr
CDC Greed
(won't answer the FOIA)
ELISA = arbitrary cutoff.
Disclaimer
Overview
TUSKEGEE - By Jerry Leonard
1998, CIA Oilmen & Israelis plan to overthrow
Saddam for the oil.
Bush/Gore Oil/War-(Oct,2000)
Bush's own explainer (Oct
2000):
Iraq Oil
Iraq was an oil-theft war.
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Updated. Please use
CRYMEDISEASE_CHP3_B.htm
Steere:_The_Original_Serodiagnosis--Changing
antibody bands over time. The same
as it is now, and has always been.
Lyme borreliosis is just a tissue-based
version of the Relapsing Fever Borrelia.
Steere: A MILITARY OFFICER OF
THE CDC---- Draft-dodging his way to
Medical Infamy:
"In 1972, his final year of medical
school at Columbia College of Physicians
and Surgeons,
Allen
Steere learned epidemiology,
as a
dodge, after hearing from an Army
recruiter that some 90 percent of new
doctors would be drafted and shipped
out to Southeast Asia, unless they found
alternative service. Dr.
Steere discovered the Epidemic
Intelligence Service, the C.D.C.
division that investigates
outbreaks of new diseases, like AIDS and
Legionnaires' disease. From 1973
to 1975, he practiced the science of
epidemiology across America."-David
France, NYTimes
==================
Steere and Brains:
Borrelia burgdorferi
and Escherichia coli lipopolysaccharides
induce nitric oxide and interleukin-6
production in cultured rat brain cells.
Tatro JB, Romero LI, Beasley D,
Steere AC, Reichlin S.
Division of Endocrinology, New England
Medical Center Hospitals, Boston, MA
02111.
Borrelia burgdorferi, the spirochetal
agent of Lyme disease, infects the
central nervous system (CNS), but the
factors that mediate inflammation and
neurologic dysfunction are not known.
Sonicated B. burgdorferi stimulated in a
concentration-dependent manner the
production of nitric oxide (NO) in glial-enriched
primary cultures of neonatal rat brain
cells via induction of NO synthase
activity. Lipopolysaccharide (LPS) of
Escherichia coli also stimulated nitrite
accumulation in a
concentration-dependent manner.
Stimulation of NO production by B.
burgdorferi sonicate and E. coli LPS was
associated with increased levels of mRNA
coding for the cytokine-inducible form
of NO synthase. B. burgdorferi sonicate
also stimulated release of
interleukin-6, with a
concentration-response relationship
similar to that for its stimulation of
nitrite production, as did E. coli LPS.
A competitive antagonist of E. coli LPS,
Rhodopseudomonas sphaeroides lipid A,
inhibited LPS-induced stimulation of NO
synthase activity but markedly
potentiated that of B. burgdorferi,
indicating that the initial triggering
mechanism of B. burgdorferi is distinct
from that of E. coli LPS. Induction of
NO synthase by bacterial agents within
the brain may represent a common pathway
of CNS inflammation and neurotoxicity.
PMID: 7513330 [PubMed - indexed for
MEDLINE]
Reporting Steere to Medical Board
K.M. Dickson
Steere to 1990
Steere's original observations, before
Yale had a vaccine to try, the results
of which were spun.
Remember that this guy is a
Rheumatologist, and would not be
inclined to understand the genetics of
vector borne diseases, nor be aware
that he did not have the entire picture
in his mind of a borreliosis, even
though the US drafted the best
Spirochetologist in the world, at that
time, Willy Burgdorfer.
Unfortunate arrogance and greed, for
which the two continents of the Western
world must continue to suffer.
"Stalking
Steere"-- He changed his tune, as you
will see, after LymeRIX was patented, in
1989
Same
(next link). I saved a copy
because that Stalking Steere article is
hilarious. Steere, a Poor Thing,
and Peter Welch defending him.
Steere's depressed. Imagine?
That article is a definite Keeper.
http://www.vaccinationnews.com/DailyNews/June2001/StalkDocSteereReLymeDis.htm
Steere and Immune complexes
Strain Tricks:
1)
CDC's Dearborn IgG criteria was derived
from strain G39/40, but Barbara Johnson
of the CDC, at the conclusion of
Dearborn conference, and as part of the
CDC's recommendations, recommended not using this G39/40 strain because
it failed to express enough antigen of
diagnostic value.
2)
SmithKline, MarDx (had the contract for
both vaccine trials), and Quest use B31,
which does not express much OspC, which
is the Osp associated with
Neuroonvasiveness. So if you are
infected, and are tested by Quest, and
have neurologic Lyme disease, you may be
given a "waste basket" diagnosis.
The History of
"Lyme Disease" It's
actually LymeRIX Disease, or Yale's
disease or Steere's disease, and is
imaginary.
Dearborn
Quite famous Farce of the CDC
"Rare"
Diseases, Neuroborreliosis Conference
Also a Keeper. Save to your hard
drive.
"Session 11
The humoral response to B.
burgdorferi – how it relates to
protection and to disease in human
infection
Dr Allan Steere, Division of
Rheumatology/Immunology, Tufts
University School of Medicine,
Association of Neurologic Signs and
Symptoms with IgA Responses to Borrelia burgdorferi in Patients
with Early Lyme Disease"
Borrelia and IgA Of course, no
one tests for this. It's not a
KeyStone Kops situation.
===================
STEERE, 1986
PREGNANCY: 5/19
advserse outcomes
| JAMA 1986 Jun
27;255(24):3394-6 |
|
Lyme disease during pregnancy.
Markowitz LE, Steere AC, Benach JL,
Slade JD, Broome CV.
Lyme disease is an increasingly
recognized tick-borne illness caused by
a spirochete, Borrelia burgdorferi.
Because the etiologic agent of Lyme
disease is a spirochete, there has been
concern about the effect of maternal
Lyme disease on pregnancy outcome. We
reviewed cases of Lyme disease in
pregnant women who were identified
before knowledge of the pregnancy
outcomes. Nineteen cases were identified
with onset between 1976 and 1984. Eight
of the women were affected during the
first trimester, seven during the second
trimester, and two during the third
trimester; in two, the trimester of
onset was unknown. Thirteen received
appropriate antibiotic therapy for Lyme
disease. Of the 19 pregnancies, five
had adverse outcomes, including
syndactyly, cortical blindness,
intrauterine fetal death, prematurity,
and rash in the newborn. Adverse
outcomes occurred in cases with
infection during each of the trimesters.
Although B burgdorferi could not be
implicated directly in any of the
adverse outcomes, the frequency of such
outcomes warrants further surveillance
and studies of pregnant women with Lyme
disease.
PMID: 2423719 [PubMed - indexed for
MEDLINE]
THE ORIGINAL SERODIAGNOSIS, STEERE:
OspB and 41 kilodaltons (flagellin), and
persisting and expanding IgM and IgG,
means chronic infection:
| J Clin Invest 1986
Oct;78(4):934-9 |
|
Antigens of Borrelia burgdorferi
recognized during Lyme disease.
Appearance of a new immunoglobulin M
response and expansion of the
immunoglobulin G response late in the
illness.
Craft JE, Fischer DK, Shimamoto GT,
Steere AC.
Using immunoblots, we identified
proteins of Borrelia burgdorferi bound
by IgM and IgG antibodies during Lyme
disease. In 12 patients with early
disease alone, both the IgM and IgG
responses were restricted primarily to a
41-kD antigen. This limited response
disappeared within several months. In
contrast, among six patients with
prolonged illness, the IgM response to
the 41-kD protein sometimes persisted
for months to years, and late in the
illness during arthritis, a new IgM
response sometimes developed to a 34-kD
component of the organism. The IgG
response in these patients appeared in a
characteristic sequential pattern over
months to years to as many as 11
spirochetal antigens. The
appearance of a new IgM response and the
expansion of the IgG response late in
the illness, and the lack of such
responses in patients with early disease
alone, suggest that B. burgdorferi
remains alive throughout the illness.
PMID: 3531237 [PubMed - indexed for
MEDLINE]
And what does THIS
mean? Hyporeactive T cells in Lyme
arthritis?
Immune responses to
Borrelia burgdorferi in patients with
reactive arthritis.
Weyand CM, Goronzy JJ.
Department of Medicine, University of
Heidelberg, Federal Republic of Germany.
In reactive arthritis (ReA), including
Reiter's syndrome, a close relationship
between chronic enteric and
genitourinary infections and the
clinical features of enthesitis has been
described. In contrast, in Lyme
arthritis, a distinct clinical entity,
chronic infection with the
tick-transmitted spirochete Borrelia
burgdorferi has been associated with the
disease. In a prospective study, 51
patients with ReA were tested for
evidence of chlamydial and spirochetal
infection. The presence of Chlamydia was
determined by culture in 8 patients, and
7 additional patients had markedly
elevated antibody titers. In 9 patients,
antibodies specific to B burgdorferi
were found. Purified peripheral blood T
lymphocytes of all 9 patients
proliferated specifically to stimulation
with macrophages pre-pulsed with B
burgdorferi antigens. Compared with
other protein antigens, higher numbers
of antigen-pulsed macrophages were
necessary to activate B
burgdorferi-specific T cells. Although
antibody titers decreased in response to
antibiotic treatment in 8 of 9 patients,
second-line therapy with sulfasalazine
or methotrexate was required to obtain
clinical remission. These data suggest
that chronic infection with B
burgdorferi can cause ReA. In
predisposed individuals, the
arthritogenic immune response might be
triggered by persisting infectious
agents independent of their antigenic
specificities.
PMID: 2476133 [PubMed - indexed for
MEDLINE]
Steere, 1986, alone:
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