Your Newsgroup Leader's Daily Alert July 25, 2005

FOR DISTRIBUTION TO ALL THE LYME LISTS.

Thank you, all my volunteers.

Carry on,
Keep up the good work.

Newsgroup Leader
============

Borreliosis is a stealth disabler, and largely only affects
people with weakened immune systems. Parents of
children with weakened immune systems are not informed
that childhood immunizations are a risk for such encephalitis
because this, childhood immunizations' damage,
is form of genocide, as is untreated borreliosis.

(I have the other kind of autism:)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11897815&query_hl=6

CDC completely aware of these genetic risks. Such
disabled people will not be likely to reproduce.


M just posted a series of articles on Kaiser, vaccines and the
CDC one of which was this:
http://www.909shot.com/History/Newsletters/nlr696.htm

CDC is clearly aware of genetic risks for most diseases.
(Tuskegee Bad Blood, we can add to the above experiments,
as well as Lyme.)

The Authors of the ISDA Guidelines, did "a 180" on Lyme
because they were threatened.
http://www.geocities.com/kmdickson0308/1-2.txt

People with our kind of borreliosis, are being selected out
of the gene pool, as are vaccine damaged kids. That was the
element of the "cost-risk analysis" that we hadn't considered
before, when we said it was more expensive to have a population
of disabled kids, than to pre-screen children for immune competence
before giving them vaccines.


Klempner found the genetic correlation to Neurologic Lyme,
HLA-DQB1*0602, just like Roland Martin found the other MS
type before that:
http://neuroscience.nih.gov/Lab.asp?Org_ID=98

We were never told of Klempner's *real* "results," we got
the usual garbage instead:
http://www.ilads.org/position2.html


Thus, Roland Martin was recruited by the NIH to come to America from
Germany. I wonder if that was the reason Steere disappeared
into Germany in the early 1990s. Steere published that Borreliosis
produced two syndromes: One like Rheumatoid Arthritis, and
one that mimicked Multiple Sclerosis.... in 1991.

Borreliosis is a stealth disabler of people with inherently
incompetent immune systems (incompetent to tropical
infections) of Northern European decent.

The same is probably true of children who, during adolescence
acquire some other form of encephalitis, that is called
"schizophrenia," just to generalize. It is also a state of reduced
consciousness.

NIH had at one time published an article about the "wildfire"
process of adolescent onset schizophrenia, in which they had
brain scans showing the progression of brain damage, which
looked like an infectious process. They took it off their website
and removed most of the references to that article from the web:
http://www.google.com/search?hl=en&q=wildfire+schizophrenia+NIMH+adolescents&btnG=Google+Search


Kissinger was into depopulation and bioweapons.
You know, together.

The primary evidence that all of the above is true, is CDC's
clear lack of response to our direct attempts to communicate
to them - when they don't respond with their usual garbage.

Note that CDC had nothing to say about the sanctioning
and persecution of Lyme-treating physicians and patients.

The only thing they did in response to Blumenthal's request
to straighten out their website, was the total opposite of
what they promised him:
http://www.hhs.gov/asl/testify/t040129.html
http://www.cslib.org/attygenl/health/0129lyme.pdf

http://www.cdc.gov/ncidod/dvbid/lyme/

The thing about Lyme is that it is not a communicable disease.

It just nicely selects people out, but you can't sneeze on
someone and give them this permanent brain infection.
Although congenital Lyme happens. In seronegative
cases, mostly, so who cares. These cases will never be
detected.

Especially with Wormser pulling THIS crap for the CDC:
1999 Blood borne dissemination:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9986813&query_hl=8

2005 Blood borne dissemination:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15867407&query_hl=9

Kathleen
===============
To: SpinLyme@xxxxxxxxxxxxxxx
Subject: [SpinLyme] Lyme disease patients getting the runaround ! (Ltr
Cape Cod Times 7/21)
Date: Sat, 23 Jul 2005 20:12:44 +0000

http://www.capecodonline.com/cctimes/edits/letts.htm

Cape Cod Times
Letters

July 21, 2005

Lyme disease patients getting the runaround

I feel I can ask this question as I have had Lyme disease for more
than 13
years: Why can't we all (public, patients, doctors and HMO's) work
together to
find a cure for this extremely debilitating disease?

Why are we reading statements from Drs. Sugar and Wormser saying Lyme
disease is highly overstated, and we as sufferers have to fight it out
in the
press
because we need for everyone to know the real truth?

Why do we have to fight for what we know? Why do we have to travel
hundreds
of miles to be treated because Dr. Donta and a few sacred others are
overloaded with patients?

Why do we as sufferers continue to be told we're psychosomatic or any
other
range of theories and have to fight with all our strength to be
properly
diagnosed and treated?

Richard W. Sylver
East Dennis

_Letters@xxxxxxxxxxxxxxxxxx (mailto:Letters@xxxxxxxxxxxxxxxxx)



[Non-text portions of this message have been removed]


-----Original Message-----
From: Kathleen <janmusinski@xxxxxxxxxxxxx>
Sent: Jul 25, 2005 12:32 AM
To: Kathleen <janmusinski@xxxxxxxxxxxxx>, ami.klin@xxxxxxxx,
fred.volkmar@xxxxxxxx, tommaurer@xxxxxxxxxxxxxxxxxx,
gary_wormser@xxxxxxxx, greatcod@xxxxxxxxx, rlord@xxxxxxxxxxxxxxxxx,
custserv@xxxxxxxxxxx, m_aguero-rosenfeld@xxxxxxxx,
mas1@xxxxxxxxxxxxxx, public@xxxxxxxxxxx, SpinLyme@xxxxxxxxxxxxxxx,
letters@xxxxxxxxxxx, krugman@xxxxxxxxxxx, tb-petitions@xxxxxxxxx,
public@xxxxxxxxxxx, scilyme@xxxxxxxxxxxxxxx, fbinhct@xxxxxxx,
gerard.baker@xxxxxxxxxxxxxx, lou@xxxxxxx, pressbox@xxxxxxxxxxx,
ny@xxxxxxxxxx, igenex@xxxxxxxxxx, friends@xxxxxxx, hurleydan@xxxxxxx
Cc: jgerberding@xxxxxxx, pmead@xxxxxxx, thomas.carson@xxxxxxxxx
Subject: NO INTEGRITY

If the CDC or the NIH had any *integrity* at all, they would call
off the Yale/ALDF dogs.


McSweegan would like to call me a liar and a crazy person, considering
how
enormous are these crimes of theirs that I have revealed.

It is so transparent, that it is juvenile.

McSweegan and Fish conspired to do the same thing to Karen Forschner.

The LymeRIX vaccine is GONE, because it was never a vaccine:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7729870&query_hl=1

The whole thing was a FRAUD, and still is.

Otherwise, there would not be this army of McSweegan sock puppets out
here, on the newsgroup, displaying their abundant fear.

I would not have had my crimes invented for me, and I would not have a
YALE
"psychiatrist" determine I am *crazy* to be saying I am innocent,and
lying
about, and *inventing* the things I said, and perjuring himself.

As did DMHAS.

The whole thing was orchestrated.

This concept of inventing people's crimes and then slamming them away
forever, was not
news to any law enforcement officer I spoke with, including Austin
McGuigan, the
former CT Chief State's Attorney.

I am not a synthetic chemist, I am an analytical methods development
chemist,
contrary to what the Yale "psychiatrist" informed the "court."

'Far more capable of solving this crime than these ALDF criminals ever
anticipated.

FDA did not do their job.

This is the crime:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf

LymeRIX did not prevent asymptomatic Lyme, it made asymptomatic Lyme
*symptomatic.* The Rahn and Evans text book "Lyme Disease, AP Key
Diseases
Series" was meant to deflect even more adverse events: "BLAME THE
VICTIM."

*Munchausen's*

When I read Douglas Dodge's LymeTruth in May of 1998, I knew there was
no controversy,
but that "Lyme Disease" was one big Yale/Steere *LIE*.

CDC and NIH know I am right. They haven't the integrity to admit it.

They haven't the integrity to call off the McSweegan, Nowakowski and
ALDF-related dogs, and admit the truth.


And the US Attorney Kevin O'Connor should step down. We don't need
such a person protecting these NeoCon Yale/Rowlandgate Jail-Building
criminals.
http://www.cslib.org/attygenl/press/2004/other/corruption%20juvenile%20tr%20school%20contracts.htm

How O'Connor got his job:
http://www.corporatecrimereporter.com/curryinterview.htm


Everything I said about them was more true than I knew:
http://en.wikipedia.org/wiki/Paul_Wolfowitz

http://www.cnn.com/2005/POLITICS/07/23/dems.radio/
"We deserve people who work in the White House who are committed to
protecting classified information, telling the truth to the American
people and living by example the idea that a country at war with
Islamic extremists cannot focus its efforts on attacking other American
citizens who simply tried to tell the truth," Johnson added.

Kathleen
===================================
1) Lyme is a borreliosis (a permanent brain infection), and we're not
"CRAZY"

Alan Barbour:
http://www.ucihs.uci.edu/microbio/index.html?top.html&menu.html&facultyResearch/faculty/barbour.html
"These tick-borne infections are notable for multiphasic antigenic
variation through DNA recombinations in the case of relapsing fever,
the occurrence of chronic arthritis in the case of Lyme disease, and
invasion of and persistence in the brain in the case of both
diseases."

Borrelia and Brain (MedLine): (nearly 200 citations)

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=PureSearch&db=pubmed&details_term=%28%22borrelia%22%5BMeSH%20Terms%5D%20OR%20borrelia%5BText%20Word%5D%29%20AND%20%28%22brain%22%5BMeSH%20Terms%5D%20OR%20brain%5BText%20Word%5D%29


2) The blood testing standard for Lyme is bogus. Steere knows there
is a different antibody profile for neuroborreliosis, and that OspA
(LymeRIX) and B produced strong antibodies in people with arthritis, so
it never should have been left out of the standard.

Borrelia is a "stealth pathogen," thus there is not typically a
high antibody response.


ALAN BARBOUR:
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/srchnum.htm&r=1&f=G&l=50&s1=6,719,983.WKU.&OS=PN/6,719,983&RS=PN/6,719,983

"Multiclonal populations therefore can exist in an infected patient
so that immunological defenses are severely tested if not totally
overwhelmed."


(1986) "Antigens of Borrelia" Allen Steere, in which he states that
antibodies to
borrelia include OspA and B, and that these bound strongly in persons
with Lyme arthritis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3531237&query_hl=1

1: 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]



(1988) "Changes in Infectivity and Plasmid Profile of the Lyme
Disease Spirochete..." National Institute of Allergy and Infectious
Disease , (1988)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3397175&query_hl=2
1: Infect Immun. 1988 Aug;56(8):1831-6.

Changes in infectivity and plasmid profile of the Lyme disease
spirochete,
Borrelia burgdorferi, as a result of in vitro cultivation.

Schwan TG, Burgdorfer W, Garon CF.

Laboratory of Pathobiology, Rocky Mountain Laboratories, National
Institue of
Allergy and Infectious Diseases, Hamilton, Montana 59840.

In vitro cultivation of Borrelia burgdorferi, the etiologic agent of
Lyme
spirochetosis, allows for the isolation and growth of this bacterium
from
infected tissues. However, continuous cultivation in modified Kelly
medium
causes a reduction in the number of detectable plasmids and the loss of
infectivity in the white-footed mouse, Peromyscus leucopus. In an
unpassaged
culture of B. burgdorferi, nine plasmids were present, including seven
linear
plasmids ranging in size from 49 to 16 kilobases (kb) and two circular
plasmids
of 27 and 7.6 kb. The 7.6-kb circular and 22-kb linear plasmids were no
longer
detectable in spirochetes noninfective in white-footed mice, suggesting
that a
gene(s) encoding for factors responsible for infection may be present
on one or
more of these extrachromosomal elements. Furthermore, changes in
spirochetal
proteins and lipopolysaccharide-like material were observed also during
early
cultivation and may be related to loss of infectivity.
PMID: 3397175 [PubMed - indexed for MEDLINE]


NIH: Don't use high passage strains: They lose OspA and B plasmid
expression


(1988) European Patent Application Number 93201345.1
Assigned to Alan Barbour, Louis Magnarelli, Sven Bergstrom


USA Patent #
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/srchnum.htm&r=1&f=G&l=50&s1=5,582,990.WKU.&OS=PN/5,582,990&RS=PN/5,582,990

"It has been shown that the earliest IgM antibodies formed against
antigens of the B. burgdorferi strain B31, which was deposited in the
American Type Culture Collection in 1983 with the accession number ATCC
35210, are directed against a genus-specific flagellar poly-peptide
termed flagellin having a molecular weight of 41 kd (10) and which
reacts with monoclonal antibody H9724 (22). IgG antibodies are also
first directed to the 41 kd flagellin, but with advancing disease IgG
antibodies form against other immunogens, especially against two
abundant proteins with molecular weights of 31 kd and 34 kd. These two
proteins, which have been denoted OspA (31 kd) and OspB (34 kd), have
been found to be located at the B. burgdorferi surface and embedded in
its outer fluid cell membrane (11).

-OspA is meant to be a diagnostic antigen (it is now not)


1990 CDC Publication Lyme blood testing standard: Perform serial
Western blots


(1991)- Yale, Fikrig, Borrelia specific flagellin fragment is 94.4%
accurate and does not cross react (is specific)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1894359&query_hl=3
1: Infect Immun. 1991 Oct;59(10):3531-5.

Molecular characterization of the humoral response to the 41-kilodalton
flagellar antigen of Borrelia burgdorferi, the Lyme disease agent.

Berland R, Fikrig E, Rahn D, Hardin J, Flavell RA.

Section of Immunobiology, Yale University School of Medicine, New
Haven,
Connecticut 06510.

The earliest humoral response in patients infected with Borrelia
burgdorferi,
the agent of Lyme disease, is directed against the spirochete's 41-kDa
flagellar
antigen. In order to map the epitopes recognized on this antigen, 11
overlapping
fragments spanning the flagellin gene were cloned by polymerase chain
reaction
and inserted into an Escherichia coli expression vector which directed
their
expression as fusion proteins containing glutathione S-transferase at
the N
terminus and a flagellin fragment at the C terminus. Affinity-purified
fusion
proteins were assayed for reactivity on Western blots (immunoblots)
with sera
from patients with late-stage Lyme disease. The same immunodominant
domain was
bound by sera from 17 of 18 patients. This domain (comprising amino
acids 197 to
241) does not share significant homology with other bacterial
flagellins and
therefore may be useful in serological testing for Lyme disease.
PMID: 1894359 [PubMed - indexed for MEDLINE]


(1992) "Western blotting in the Serodiagnosis of Lyme Disease"
1992, July Dressler/Steere

Steere knowingly using a weakened strain intending to leave OspA and B
out of the serologic standard, decreasing the likelihood that people
will be diagnosed with Lyme disease, and with the intention of
capturing all the post-LymeRIX or ImmuLyme approval testing for Lyme.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8380611&query_hl=7
1: J Infect Dis. 1993 Feb;167(2):392-400.

Western blotting in the serodiagnosis of Lyme disease.

Dressler F, Whalen JA, Reinhardt BN, Steere AC.

Division of Rheumatology/Immunology, Tufts University School of
Medicine, New
England Medical Center, Boston, Massachusetts 02111.

There are currently no accepted criteria for positive Western blots in
Lyme
disease. In a retrospective analysis of 225 case and control subjects,
the best
discriminatory ability of test criteria was obtained by requiring at
least 2 of
the 8 most common IgM bands in early disease (18, 21, 28, 37, 41, 45,
58, and 93
kDa) and by requiring at least 5 of the 10 most frequent IgG bands
after the
first weeks of infection (18, 21, 28, 30, 39, 41, 45, 58, 66, and 93
kDa). When
these definitions were tested in a prospective study of all 237
patients seen in
a diagnostic Lyme disease clinic during a 1-year period and in 74
patients with
erythema migrans or summer flu-like illnesses, the IgM blot in early
disease had
a sensitivity of 32% and a specificity of 100%; the IgG blot after the
first
weeks of infection had a sensitivity of 83% and a specificity of 95%.
Among
patients with indeterminate IgG responses by ELISA, 6 of 9 patients
with active
Lyme disease had positive blots compared with 2 of 34 patients with
other
illnesses (P < .001). Thus, Western blotting can be used to increase
the
specificity of serologic testing in Lyme disease.
PMID: 8380611 [PubMed - indexed for MEDLINE]




(1993) "Antibody Responses to Three Genomic Groups.."
Dressler/Steere
1: J Infect Dis. 1994 Feb;169(2):313-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8106763&query_hl=1

Antibody responses to the three genomic groups of Borrelia burgdorferi
in
European Lyme borreliosis.

Dressler F, Ackermann R, Steere AC.

Division of Rheumatology/Immunology, New England Medical Center, Tufts
University School of Medicine, Boston, Massachusetts 02111.

The antibody responses to the three genomic groups of Borrelia
burgdorferi (B.
burgdorferi sensu stricto, Borrelia garinii, and Borrelia afzelii) were
determined in 97 German patients with various manifestations of Lyme
borreliosis. The geometric mean antibody titers in each patient group,
determined by ELISA, were similar with each antigen preparation. By
Western
blotting, however, patients with meningopolyneuritis tended to respond
to more
spirochetal polypeptides of B. garinii, the group 2 strain, whereas
those with
arthritis recognized more antigens of B. afzelii, the group 3 strain (P
< .03),
as did those with acrodermatitis. Only 1 patient each with erythema
migrans,
arthritis, or acrodermatitis had weak reactivity with outer surface
protein A
(OspA), and none responded to OspB. It is concluded that differences
among the
three groups of B. burgdorferi may result in variations in the antibody
response
in European Lyme borreliosis. PMID: 8106763 [PubMed - indexed for
MEDLINE]


G39/40 is high-passage (no good)

Steere demonstrates that there is a different antibody profile in
neurologic Lyme patients,
than there is for Lyme arthritis

Sequence described by Steere, kilodaltons (kD)

EARLY, with erythema migrans
41

1-5 months after disease onset
83
66

27
15
months to years
75
60
34 (Osp B)
31 (Osp A)
29
17

Page 936: 34, 31, 29, and 17 were "bound strongly," which means
there was a high antibody concentration. This was not the case later,
in Dressler/Steere, and OspA and B were left out of the serodiagnostic
standard (this is "bogus" science).
(See other notations in that text.)


The 1994 CDC Dearborn Conference criteria are supposed to be for
"early Lyme," but clearly "5 months to years," is not "early
Lyme," and no one agreed with Steere, except MarDx, who had been
given CDC Dearborn-positive arthritis blood to qualify their test kits,
and who also have been given the contracts for both vaccine trials.
http://www.cdc.gov/mmwr/preview/mmwrhtml/00038469.htm


The ImmuLyme trial began in March 1994, before Dearborn even convened,
and 6 years later, the principal investigator, Leonard Sigal reported
that he could not even read his Western Blots, in people who were
vaccinated.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9673299&query_hl=9
1: N Engl J Med. 1998 Jul 23;339(4):216-22.
Erratum in:
N Engl J Med 1998 Aug 20;339(8):571.

A vaccine consisting of recombinant Borrelia burgdorferi outer-surface
protein A
to prevent Lyme disease. Recombinant Outer-Surface Protein A Lyme
Disease
Vaccine Study Consortium.

Sigal LH, Zahradnik JM, Lavin P, Patella SJ, Bryant G, Haselby R,
Hilton E,
Kunkel M, Adler-Klein D, Doherty T, Evans J, Molloy PJ, Seidner AL,
Sabetta JR,
Simon HJ, Klempner MS, Mays J, Marks D, Malawista SE.

Department of Medicine, University of Medicine and Dentistry of New
Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019,
USA.

BACKGROUND: Lyme disease is a multisystem inflammatory disease caused
by
infection with the tick-borne spirochete Borrelia burgdorferi and is
the most
common vector-borne infection in the United States. We assessed the
efficacy of
a recombinant vaccine consisting of outer-surface protein A (OspA)
without
adjuvant in subjects at risk for Lyme disease. METHODS: For this
double-blind
trial, 10,305 subjects 18 years of age or older were recruited at 14
sites in
areas of the United States where Lyme disease was endemic; the subjects
were
randomly assigned to receive either placebo (5149 subjects) or 30
microg of OspA
vaccine (5156 subjects). The first two injections were administered 1
month
apart, and 7515 subjects also received a booster dose at 12 months. The
subjects
were observed for two seasons during which the risk of transmission of
Lyme
disease was high. The primary end point was the number of new
clinically and
serologically confirmed cases of Lyme disease. RESULTS: The efficacy of
the
vaccine was 68 percent in the first year of the study in the entire
population
and 92 percent in the second year among the 3745 subjects who received
the third
injection. The vaccine was well tolerated. There was a higher incidence
of mild,
self-limited local and systemic reactions in the vaccine group, but
only during
the seven days after vaccination. There was no significant increase in
the
frequency of arthritis or neurologic events in vaccine recipients.
CONCLUSIONS:
In this study, OspA vaccine was safe and effective in the prevention of
Lyme
disease. PMID: 9673299 [PubMed - indexed for MEDLINE]



(1993) March, Wormser and Nowakowski: Use Western blots for ELISA
negatives, Dressler/Steere proposal only 13-25% accurate. (The
standard adopted by the CDC is the opposite- It says not to do a
Western Blot on ELISA negatives.)

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8308100&query_hl=11

1: J Clin Microbiol. 1993 Dec;31(12):3090-5.

Erratum in:
J Clin Microbiol 1994 Mar;32(3):860.

Serodiagnosis in early Lyme disease.

Aguero-Rosenfeld ME, Nowakowski J, McKenna DF, Carbonaro CA, Wormser
GP.

Department of Pathology, New York Medical College, Valhalla.

Using a commercially available enzyme-linked immunosorbent assay
(ELISA) and an
immunoblot assay (IB), we tested sera from 100 patients with erythema
migrans
(EM) seen in 1991 a the Westchester County Medical Center Lyme Disease
Diagnostic Center. Convalescent-phase sera were available from 59
patients.
Fifty-five patients had EM of < 7 days' duration, 31 had EM of 7 to 14
days'
duration, and 14 had EM of > 14 days' duration. During the acute phase
of
infection, 35 patients had a positive ELISA result and 43 had a
positive IB
result by the recently published criteria of Dressler et al. (F.
Dressler, J. A.
Whalen, B. N. Reinhardt, and A. C. Steere, J. Infect. Dis. 167:392-400,
1993)
for interpretation of IB in patients with Lyme disease. A greater
sensitivity of
IB was observed in patients with EM of < 7 days' duration, as follows:
14 of 55
(25%) for IB versus 7 of 55 (13%) for ELISA (P = 0.144). Sera of all 14
patients
with EM of > 14 days' duration were reactive by both tests, as follows:
13
positive and 1 equivocal by ELISA and 12 positive and 2 indeterminate
by the IB.
The band reactivity most frequently observed in the IB was to the 41-
and 25-kDa
antigens, the latter being the most frequent band observed in
immunoglobulin M
blots. Seroconversion was observed in 74 and 64% of evaluable patients
by ELISA
and IB, respectively, despite the use of antibiotic therapy.
PMID: 8308100 [PubMed - indexed for MEDLINE]




(1993) "Overdiagnosis" article, Steere Patients not positive
"in our labs" - using bogus strains (high-passage G39/40, and
FRG- a German strain)

Most people will not have antibodies to these weakened or useless
strains.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8459513&query_hl=13

1: JAMA. 1993 Apr 14;269(14):1812-6.

The overdiagnosis of Lyme disease.

Steere AC, Taylor E, McHugh GL, Logigian EL.

Division of Rheumatology/Immunology, New England Medical Center,
Boston, MA
02111.

OBJECTIVE--To analyze the diagnoses, serological test results, and
treatment
results of the patients evaluated in a Lyme disease clinic, both prior
to
referral and from current evaluation. DESIGN--Retrospective case survey
of
prescreened patients. SETTING--Research and diagnostic Lyme disease
clinic in a
university hospital. PATIENTS--All 788 patients referred to the clinic
during a
4.5-year period who were thought by the referring physician or the
patient to
have a diagnosis of Lyme disease.
MAIN OUTCOME MEASUREMENTS--Symptoms and signs
of disease, immunodiagnostic tests of Lyme disease, and tests of
neurological
function. RESULTS--Of the 788 patients, 180 (23%) had active Lyme
disease,
usually arthritis, encephalopathy, or polyneuropathy. One hundred
fifty-six
patients (20%) had previous Lyme disease and another current illness,
most
commonly chronic fatigue syndrome or fibromyalgia; and in 49 patients,
these
symptoms began soon after objective manifestations of Lyme disease. The
remaining 452 patients (57%) did not have Lyme disease. The majority of
these
patients also had the chronic fatigue syndrome or fibromyalgia; the
others
usually had rheumatic or neurological diseases. Of the patients who did
not have
Lyme disease, 45% had had positive serological test results for Lyme
disease in
other laboratories, but all were seronegative in our laboratory. Prior
to
referral, 409 of the 788 patients had been treated with antibiotic
therapy. In
322 (79%) of these patients, the reason for lack of response was
incorrect
diagnosis. CONCLUSIONS--Only a minority of the patients referred to the
clinic
met diagnostic criteria for Lyme disease. The most common reason for
lack of
response to antibiotic therapy was misdiagnosis.
PMID: 8459513 [PubMed - indexed for MEDLINE]




(1993, Dec) US PATENT- Fikrig (Yale) 5618533 Bb Flagellin (94%
accurate, early, and specific test)

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/srchnum.htm&r=1&f=G&l=50&s1=5618533.WKU.&OS=PN/5618533&RS=PN/5618533

United States Patent 5,618,533
Flavell , et al. April 8, 1997

Flagellin-based polypeptides for the diagnosis of lyme disease
Abstract
Diagnostic means and methods for Lyme disease comprising B. burgdorferi
flagellin polypeptides and antibodies. Compositions and methods
comprising neuroborreliosis-associated antigens useful for the
detection, treatment and prevention of neuroborreliosis, arthritis,
carditis and other manifestations of Lyme disease.
Inventors: Flavell; Richard A. (Killingworth, CT); Fikrig; Erol
(Guilford, CT); Berland; Robert (Kingston, NY) Assignee: Yale
University (New Haven, CT) Appl. No.: 166160 Filed: December 10, 1993


1994, March through 1999, August- the ImmuLyme trial- A MUST READ


1994 June- FDA Meeting, Ray Dattwyler recommends using serial
Western Blots to assesss vaccines.


(1994, Oct 7) US PATENT- 5747294 Yale's OspA patent

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/srchnum.htm&r=1&f=G&l=50&s1=5747294.WKU.&OS=PN/5747294&RS=PN/5747294

United States Patent 5,747,294
Flavell , et al. May 5, 1998

Compositions and methods for the prevention and diagnosis of lyme
disease
Abstract
Methods and compositions for the prevention and diagnosis of Lyme
disease. OspA and OspB polypeptides and serotypic variants thereof,
which elicit in a treated animal the formation of an immune response
which is effective to treat or protect against Lyme disease as caused
by infection with B. burgdorferi. Anti-OspA and anti-OspB antibodies
that are effective to treat or protect against Lyme disease as caused
by infection with B. burgdorferi. A screening method for the selection
of those OspA and OspB polypeptides and anti-OspA and anti-OspB
antibodies that are useful for the prevention and detection of Lyme
disease. Diagnostic kits including OspA and OspB polypeptides or
antibodies directed against such polypeptides.

Inventors: Flavell; Richard A. (Killingworth, CT); Kantor; Fred S.
(Orange, CT); Barthold; Stephen W. (Madison, CT); Fikrig; Erol
(Guilford, CT)
Assignee: Yale University (New Haven, CT)
Appl. No.: 320161
Filed: October 7, 1994


"Early in human infection, antibodies are generated primarily against
a 41 kD flagella-associated antigen. Later on, high titers appear to
both OspA and OspB..."


(1994, Oct) Dearborn, MI CDC Conference data: Recommendations: DO
NOT USE HIGH PASSAGE STRAINS

Lists interest-conflicted parties


See my Jan 2001 FDA testimony (How to pass off a bogus vaccine: Make
its failure undetectable):

http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf



(1996, March) US PATENT- 6045804 Persing (Corixa) OspA-less
spirochete

United States Patent 6,045,804
Persing April 4, 2000

Method for detecting B. burgdorferi infection
Abstract
The present invention provides a method for detecting B. burgdorferi
infection utilizing an antigen preparation lacking a detectable level
of outer surface protein A (OspA). The antigen preparation is made from
an isolate of B. burgdorferi that lacks the plasmid encoding outer
surface protein A (OspA). The method of the invention discriminates B.
burgdorferi infection from OspA vaccination.

Inventors: Persing; David H. (Rochester, MN)
Assignee: Mayo Foundation for Medical Educational Research (Rochester,
MN)
Appl. No.: 612231
Filed: March 7, 1996



-Mentions problems with Immunoblotting

- Mentions there is a need for a test to detect Lyme in vaccinated and
non-vaccinated patients- WHICH IS THE ENTIRE NATURE OF THIS SCAM.

-Evidence of "partnership" between SmithKline, Corixa and Imugen
(also L2 Diagnostics, the Yale Lyme and Lupus clinic biotech spinoff.
This spinoff firm was funded by the Yale Endowment fund.


2000, "Detection of Multiple Reactive Species..." (Imugen's
Phillip Molloy,
Victor Berardi, and Leonard Sigal, with Dave Persing.).

http://www.journals.uchicago.edu/CID/journal/issues/v31n1/991200/991200.html?erFrom=-3186362707054415028Guest


Why weren't these unreadable blots reported to the FDA, and how could
Sigal have reported a 92% safe and effective vaccine with unreadable
blots?

Or is this just a promotion for use of their patented test, for which
only Imugen and L2 Diagnostics are licensed from Corixa to use?
http://www.yale.edu/opa/newsr/98-12-22-01.all.html

Yale, SmkithKline, Corixa, Imugen-THE PARTNERSHIP:

http://www.imugen.com/news_release1.htm

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=149722&tools=bot

Please see my notes in that report


Henry Feder (UCONN) ran a vaccine trial on European children, when
there is practically none of that kind of OspA in Europe, according to
Steere.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10547245&query_hl=1


1: J Pediatr. 1999 Nov;135(5):575-9.

Comment in:
J Pediatr. 1999 Nov;135(5):539-41.
J Pediatr. 2001 Apr;138(4):609-10.

Immunogenicity of a recombinant Borrelia burgdorferi outer surface
protein A
vaccine against Lyme disease in children.

Feder HM Jr, Beran J, Van Hoecke C, Abraham B, De Clercq N, Buscarino
C, Parenti
DL.

Department of Family Medicine, University of Connecticut Health Center,
Farmington, Connecticut 06030-1406, USA.

BACKGROUND AND OBJECTIVE: A recombinant lipoprotein vaccine against
Lyme
disease, containing 30 microg of Borrelia burgdorferi outer surface
protein A
(OspA) with aluminum adjuvant, has been shown in a large US field trial
of
subjects >/=15 years of age to offer 76% efficacy against clinical Lyme
disease
after 3 injections given at 0, 1, and 12 months. Lyme disease is also
an
important problem in children; thus, OspA vaccine trials in children
are needed.
The purpose of this study was to investigate the safety and
immunogenicity of 2
different doses of lipoprotein OspA with aluminum adjuvant vaccine in
healthy
children 5 to 15 years of age in a double-blind, randomized study.
STUDY DESIGN:
In a double-blind study, 250 children from the Czech Republic were
randomly
assigned to receive 15 microg or 30 microg of OspA vaccine at 0, 1, and
2
months. Serum samples, obtained before vaccination and 1 month after
the second
and third doses, were analyzed for antiOspA antibody. Solicited and
unsolicited
symptoms were collected from diary cards. RESULTS: Local pain at the
injection
site was reported by approximately 76% of the 250 children. Headaches
(after 5%
to 18% of the injections) and malaise (after 2% to 16% of the
injections) were
the most frequently reported general symptoms. Local and generalized
symptoms
were not different between the 15 microg and 30 microg groups, and all
symptoms
resolved within 4 days. Both doses were highly immunogenic, with the 30
microg
dose eliciting higher antibody levels. Seroconversion occurred in 99%
of the 250
children. CONCLUSIONS: The OspA vaccine against Lyme disease was well
tolerated
and highly immunogenic in children.
PMID: 10547245 [PubMed - indexed for MEDLINE]




2005, Feb- CDC releases more of their nonsense about what is a valid
test, and imply that we need "use of validated laboratory tests,"
but CDC's are hardly valid, FDA's own criteria.

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5405a6.htm


2005, May, Reponse to Dr. Raphael Stricker in which he states: "To
my knowledge, the CDC website does not state that the serological
criteria recommended by the CDC are not appropriate for use in clinical
diagnosis."

"Clinical" means signs and symptoms, independent of lab work.

It is on the Department of Health and Human Services' website, in
which CDC states that there is no substitute for sound clinical
judgment: PAUL MEAD: "For this reason, CDC has repeatedly stated
that the surveillance case definition is not a substitute for sound
clinical judgment."
http://www.hhs.gov/asl/testify/t040129.html

.

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