Allen Steere Caught in His Lies (Letter to Volkman)
Mort Zuckerman
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Subject: Allen Steere Caught in His Lies (Letter to Volkman)
Date: Aug 23, 2011 2:31 PM
ARTICLE BELOW
======================================
See where Steere says Volkman was
talking about Seronegative Lyme
Arthritis.
We all know there is no such thing.
"Lyme Disease" was defined as the
Arthritis (HLA-linked hypersensivity
response) by Allen Steere on behalf
of the insurance companies in 1992.
http://www.actionlyme.org/STEERE_AT_ACADEMY_OF_INSURANCE_MEDICINE.htm
See that he informed the Academy of Insurance
Medicine of the Dearborn lies (throw out
all IgM antibodies, and to do an ELISA
first, to screen out all neurologic cases)
before Dearborn happened. Look at the
date he gave this lecture:
http://www.actionlyme.org/STEERE_AT_ACADEMY_OF_INSURANCE_MEDICINE.htm
That was the same year he went to Europe to
falsify the disease definition (1992):
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
That same year, also, CDC officer Barbara
Johnson claimed 5 patents with SmithKline in
Europe in which it is revealed that CDC officer
Barbara Johnson knew that there were two
kinds of Lyme - the arthritis and the deadly
Great Imitators:
http://www.actionlyme.org/CDCS_PARTICIPATION_IN_LYME_CRIMES.htm
SAY BARBARA JPHNSON'S 1992 PATENTS:
"Summary of the Invention
"In one aspect, the invention provides isolated B. burgdorferi
antigens which are regulated and differentiated by growth of the B.
burgdorferi in a tick vector. Novel antigens of the invention are
listed below in Table I.
"Certain of these antigens are characterized as being B. burgdorferi
B31 strain specific and major histocompatibility complex (MHC) ***
nonrestricted. Certain other of these antigens are characterized as
being MHC restricted***...."
- - -
"Restricted to HLA and non-restricted."
As shown here in the RICO complaint to
the USDOJ:
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm
The too-many-antibodies characteristic of the
HLA-restricted arthritis on the right and everyone
else on the left (the non-arthritis or the
"seronegative")
Thence, CDC officer Barbara Johnson also does
not want to be charged for murder. She was
present at Dearborn and approved Steere's
proposal to change the definition of "Lyme
Disease" to "JUST AN HLA-RESTRICTED, ARTHRITIC
KNEE", as you can see here:
http://www.actionlyme.org/Dearborn_Who_Approved.htm
***Later*** in 1994, this single, narrowed
disease definition (arthritis only) was adopted
at Dearborn, while Allen Steere knew
the non-arthritis forms were deadly.
So, that's the crime.
Volkman wasn't talking about Lyme Arthritis in
his letter trashing Steere, et al:
http://groups.google.com/group/sci.med.diseases.lyme/msg/94f8c535ee2a8139?hl=en&dmode=source
Volkman was talking about this:
http://www.actionlyme.org/STEERES_SERONEG_LYME_ASSAY.htm
and this:
http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm
All the murderous ALDF.com crooks knew seronegative
(means NOT ARTHRITIS) Lyme was the deadly
neurologic outcome, with the ALS, the MS,
and especially the Lupus:
http://www.actionlyme.org/110228_IOM_LYME_TUSKEGEE.htm
http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm
because *they* were the ones who described
these outcomes.
:)))
That there would even *be* "Lyme Wars" and
3 class action lawsuits, the Blumenthal AntiTrust
lawsuit, and the obvious viciousness on the
part of the cabal - the ALDF.com (see who is on the board:
http://www.actionlyme.org/ALDF_BOARD.htm )...
should be a red flag to the common everyday
Joe New York Times Science Tuesday writer
like Jane Brody or Lawrence Altman.
Being beholden to BigMoney, Big Insurance,
Kaiser-Permanente, the individual CDC officers
and NIH employees, and Erol Fikrig at Yale
who refuses to attend any Blumenthal Lyme
Hearings without their lawyers present... ???
That's the Widespread Whore Story that allowed
the Chinese to create stealth, antibiotic
resistant mycoplasma and to grab the EBV
vaccine.
And not only did the Chines grab the EBV vaccine,
they stated that this EBV LMP-2A antigen - the
thing that activates Allen Steere's partner Bridgette
Huber's famous Human Endogenous Retrovirus...
the HERVs spoken about last week in the NYTimes
by Harold Varmus, blowing up all of US and
Global Medicine...
could not be a vaccine because it is immunosuppressive:
http://www.cmi.ustc.edu.cn/6/6/423.pdf
Like LYMErix.
- - -
Allen Steere, et al, does not want to spend
the rest of his life in prison. Not only for
mass murder but for the treachery to "US
National Security (the Corporations; BigPharma)."
A final thought: Why would any CDC officer,
NIH staff member, or Yale employees want to
speak only through their lawyers?
Must have been a private enterprise.
Kathleen M Dickson
http://www.actionlyme.org
=====================================
http://onlinelibrary.wiley.com/doi/10.1002/art.24242/full
To the Editor:
In a recent letter to the editor (1) about our article on Borrelia
burgdorferi antibody responses in patients with antibiotic-refractory,
antibiotic-responsive, or non–antibiotic-treated Lyme arthritis (2),
Dr. Volkman states that seronegative disease may occur after one
course of antibiotic therapy for Lyme arthritis. In 1988, Dr. Volkman
and colleagues described a small number of patients who received short
courses of antibiotic therapy for early Lyme disease and subsequently
developed “seronegative late Lyme disease” (3). This concept has been
discredited as understanding of Lyme disease has increased, and it is
certainly not applicable to Lyme arthritis, a late manifestation of
the disorder. Current thinking is that all patients with neurologic,
cardiac, or joint abnormalities associated with Lyme disease have
antibody responses to B burgdorferi (4), and patients with Lyme
arthritis have the strongest responses, exhibiting reactivity with
many spirochetal proteins.
In our article, my colleagues and I described the pattern of IgG
antibody responses to Bburgdorferi proteins in 3 groups of patients
with Lyme arthritis. Among non–antibiotic-treated patients who were
seen in the 1970s, before the cause of the disease was known, titers
of antibody to B burgdorferi antigens remained high throughout a 2–5-
year period of arthritis, whereas the antibody titers in antibiotic-
treated patients, whether they had an antibiotic-responsive or
antibiotic-refractory course, declined gradually over a period of 6–24
months after therapy.
Even so, antibody titers in Lyme arthritis patients often remain
positive at low levels for years (5). Cell-mediated immunity to B
burgdorferi antigens is also found in patients with Lyme arthritis,
and the frequency of Borrelia-specific T cells declines with
antibiotic therapy (6). Although a Jarisch-Herxheimer reaction may be
seen in ∼15% of patients during the first 24 hours after antibiotic
therapy for early, disseminated Lyme disease (7), a reaction in
antibiotic-treated patients with Lyme arthritis, a manifestation of
late infection when fewer organisms are present, has not been
observed.
Prior to current knowledge about antibiotic treatment of Lyme disease,
untreated patients with erythema migrans, the initial skin lesion of
the infection, often developed Lyme arthritis later (8). Today, early
Lyme disease is usually recognized and treated appropriately, and
these patients do not develop late manifestations of the illness.
However, in a small percentage of patients, the early period of
infection is asymptomatic, and arthritis is the presenting
manifestation of the illness. This was the case in the majority of the
patients in our study, all of whom were seen from 1987 through 2005
(2). In such patients, the duration of infection prior to arthritis
cannot be calculated with certainty.
We support the recommendations of the Infectious Diseases Society of
America for the treatment of Lyme disease (9). Approximately 90% of
patients with Lyme arthritis show response to a single 4-week course
of oral doxycycline or amoxicillin (10). If arthritis persists, a 2–4-
week course of intravenous antibiotic therapy is recommended. If
arthritis still persists and if the results of polymerase chain
reaction testing for B burgdorferi DNA in joint fluid are negative,
the patient is treated with antiinflammatory agents (11). Regardless
of the outcome of treatment, patients do not develop “seronegative
late Lyme disease.”
* 1
Volkman DJ. Seronegative disease after inadequate therapy in
Lyme arthritis: comment on the article by Kannian et al [letter].
Arthritis Rheum 2008; 58: 2212–3.
Direct Link:
o Abstract
o Full Article (HTML)
o PDF(42K)
* 2
Kannian P, McHugh G, Johnson BJ, Bacon RM, Glickstein LJ, Steere
AC. Antibody responses to Borrelia burgdorferi in patients with
antibiotic-refractory, antibiotic-responsive, or non–antibiotic-
treated Lyme arthritis. Arthritis Rheum 2007; 56: 4216–25.
Direct Link:
o Abstract
o Full Article (HTML)
o PDF(120K)
o References
* 3
Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ, Thomas J,
Golightly MG. Seronegative Lyme disease: dissociation of the specific
T- and B-lymphocyte responses to Borrelia burgdorferi. N Engl J Med
1988; 319: 1441–6.
o CrossRef,
o PubMed,
o ChemPort,
o Web of Science® Times Cited: 310
* 4
Steere AC, McHugh G, Damle N, Sikand VK. Prospective study of
serologic tests for Lyme disease. Clin Infect Dis 2008; 47: 188–95.
o CrossRef,
o PubMed,
o Web of Science® Times Cited: 5
* 5
Kalish RA, McHugh G, Granquist J, Shea B, Ruthazer R, Steere AC.
Persistence of immunoglobulin M or immunoglobulin G antibody responses
to Borrelia burgdorferi 10–20 years after active Lyme disease. Clin
Infect Dis 2001; 33: 780–5.
o CrossRef,
o PubMed,
o ChemPort,
o Web of Science® Times Cited: 38
* 6
Kannian P, Drouin EE, Glickstein L, Kwok WW, Nepom GT, Steere
AC. Decline in the frequencies of Borrelia burgdorferi OspA161 175-
specific T cells after antibiotic therapy in HLA-DRB1*0401-positive
patients with antibiotic-responsive or antibiotic-refractory Lyme
arthritis. J Immunol 2007; 179: 6336–42.
o PubMed,
o ChemPort,
o Web of Science® Times Cited: 4
* 7
Steere AC, Hutchinson GJ, Rahn DW, Sigal LH, Craft JE, DeSanna
ET, et al. Treatment of the early manifestations of Lyme disease. Ann
Intern Med 1983; 99: 22–6.
o PubMed,
o ChemPort,
o Web of Science® Times Cited: 345
* 8
Steere AC, Schoen RT, Taylor E. The clinical evolution of Lyme
arthritis. Ann Intern Med 1987; 107: 725–31.
o PubMed,
o ChemPort,
o Web of Science® Times Cited: 399
* 9
Wormser GP, Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC,
Klempner MS, et al. The clinical assessment, treatment, and prevention
of Lyme disease, human granulocytic anaplasmosis, and babesiosis:
clinical practice guidelines by the Infectious Diseases Society of
America. Clin Infect Dis 2006; 43: 1089–134.
o CrossRef,
o PubMed,
o Web of Science® Times Cited: 135
* 10
Steere AC, Levin RE, Molloy PJ, Kalish RA, Abraham JH III, Liu
NY, et al. Treatment of Lyme arthritis. Arthritis Rheum 1994; 37: 878–
88.
KMDickson