Correct, "Late Lyme Arthritis in a Knee" is "Late Lyme Arthritis in a Knee"
Mort Zuckerman
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Subject: Correct, "Late Lyme Arthritis in a Knee" is "Late Lyme
Arthritis in a Knee"
Date: Dec 10, 2009 4:39 PM
WORMY/STEERE ARTICLE BELOW
============================
Thank you for forwarding this information.
We already know that the autoimmune response
to Pam3Cys caused by Steere's specific HLA group
binding the OspA-like antigens (hypersensitivity
or allergy or OspA is a superantigen to some
people) is "Lyme Disease" as shown by the USDOJ
RICO complaint:
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm
The USDOJ RICO complaint SHOWS - as in, you
can see the high concentration of antibodies
on the right, with your own eyeballs - in the
Steere's Knees People, by the darker set of
Western Blots. Darker bands means "MORE
ANTIBODIES."
Hypersensitivity, like allergy, means,
"too many antibodies." Lupus is a case
of "too many antibodies against phospholipids."
Lupus is a "rheumatological disease," like
arthritis, where Steere's RA kinda people
make too many antibodies against, like
mycoplasma in the knee or Lyme in the
knee. Same thing. Just ask Allen Steere:
http://www.ncbi.nlm.nih.gov/pubmed?term=steere%20AC[Author]%20AND%20%28%22radiography%22[Subheading]%20OR%20%22radiography%22[All%20Fields]%20OR%20%22ra%22[All%20Fields]%29&cmd=DetailsSearch&log$=details
Steere says,"Lyme arthritis in a knee
is a syndrome of too-many-antibodies against
the Lyme/mycoplasmal Pam3Cys antigens, and
some of them cross-react with collagen."
We, as previously mentioned, are not talking
about that disease. We are talking about
the kind of Lyme shown here:
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
Look at the ^^^ blots of the Meningitis patients.
They're ALL! IGM-type.
All IgM were thrown out at Dearborn and
by Allen Steere in Europe
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
because THAT disease requires intravenous ceftriaxone.
This difference, this false claim that
you have to have Steere's HLA in order to
have a disease is the specific cryme of Lyme
Disease."
http://www.actionlyme.org/CRYME_DISEASE.htm
The b-stards insist "Lyme Disease" belongs to the
autoimmune/hypersensitivity class, when the
opposite is more true in the sickest patients.
*WE,* the Chronic Lyme/Relapsing Fever/Lyme
Borreliosis/Pam3Cys Immune Dysregegulation
patients, do not have Steere's Knees Disease.
See what Klempner and Wormser say about the
difference, here:
http://www.journals.uchicago.edu/doi/pdf/10.1086/432733
"Lyme disease is caused by infection with the tickborne bacterium
Borrelia burgdorferi. Antibiotic treatment is highly effective
for the acute symptoms of Lyme disease and is also effective
for late septic manifestations [1]. After standard treatment with
antibiotics, some patients have persistent symptoms. There appear
to be at least 2 distinct syndromes in patients with persistent
symptoms after antibiotic treatment. One syndrome has
localized symptoms that are similar to pretreatment symptoms.
Patients with this syndrome often have recurrent episodes of
arthritis/synovitis. Results of synovial fluid cultures and polymerase
chain reaction (PCR) for B. burgdorferi are negative [2].
****Patients generally feel well aside from their arthritis
symptoms.****
"Patients generally feel well, except
for bad-knee, when they have 'Lyme
Disease,'" or Steere's Autoimmune Knees.
Steere's Autoimmune Knees is the Dearborn,
1995, CDC "case definition."
If you don't have an autoimmune knee
and *only* an autoimmune bad knee, you
do not know "Lyme Disease."
Kapisch?
Get the game now?
No one cares about "Lyme Disease." The
lady at the bank I use - a teller - has
Steere's Bad Knees, which is why she
can still be a bank teller. No one with
the dementia syndrome of Neuroborreliosis
(note that Neuroborreliosis has no CDC "case
definition," no blood testing standard,
is known to not test positive to "Lyme
Disease," and has no "IDSA Guidelines on
the Non-Treatment of________") could possibly
be a bank teller.
Note my brain SPECT scans:
http://www.actionlyme.org/PHILLIPS_JE_PERVERT.htm
That's known as a DSM-IV "DELIRIUM."
Note my Western Blot:
http://www.actionlyme.org/Schoen.htm
Those ^^ are antibodies against Heat Shock
Proteins, which is a sign of Multiple
Sclerosis.
The only arthritis I have is in my
hands (hereditary) and my neck, from
the chronic meningitis and the latter
you can see from the EMGs:
http://www.actionlyme.org/PHILLIPS_JE_PERVERT.htm
Every ^^^ single nerve coming out of my
cervical spine is damaged,... which we
all know to be caused by DSM IV Not-
Enough-Penis Disease.
Stop worrying about what these idiots
say. They persist in reporting nonsense
about a disease that needs aspirin. What
these crooks are saying about the VlsE below
is that people with bad-knees HLA are also
*allergic* to the VlsE antigen.
Great.
Fabulous.
Such patients can still work at a bank.
Kathleen M. Dickson
http://www.actionlyme.org
http://www.relapsingfever.org
-----------------------
To: Lyme...@yahoogroups.com
Sent: Wed, Dec 2, 2009 1:28 pm
Subject: [LymeInfo] [sci] 2-Tiered Antibody Testing for Early and Late
Lyme Disease Using Only an IgG Blot with a VlsE Band as the 2nd Tier
Test
2-Tiered Antibody Testing for Early and Late Lyme Disease Using Only
an
Immunoglobulin G Blot with the Addition of a VlsE Band as the
Second-Tier Test
John A. Branda, Maria E. Aguero-Rosenfeld, Mary Jane Ferraro, Barbara
J.
B. Johnson, Gary P. Wormser, and Allen C. Steere
Clinical Infectious Diseases, electronically published 30 November
2009.
http://dx.doi.org/10.1086/648674
MAJOR ARTICLE
Background
Standard 2-tiered immunoglobulin G (IgG) testing has performed well in
late Lyme disease (LD), but IgM testing early in the illness has been
problematic. IgG VlsE antibody testing, by itself, improves early
sensitivity, but may lower specificity. We studied whether elements of
the 2 approaches could be combined to produce a second-tier IgG blot
that performs well throughout the infection.
Methods
Separate serum sets from LD patients and control subjects were tested
independently at 2 medical centers using whole-cell enzyme
immunoassays
and IgM and IgG immunoblots, with recombinant VlsE added to the IgG
blots. The results from both centers were combined, and a new
second-tier IgG algorithm was developed.
Results
With standard 2-tiered IgM and IgG testing, 31% of patients with
active
erythema migrans (stage 1), 63% of those with acute neuroborreliosis
or
carditis (stage 2), and 100% of those with arthritis or late
neurologic
involvement (stage 3) had positive results. Using new IgG criteria, in
which only the VlsE band was scored as a second-tier test among
patients
with early LD (stage 1 or 2) and 5 of 11 IgG bands were required in
those with stage 3 LD, 34% of patients with stage 1, 96% of those with
stage 2, and 100% of those with stage 3 infection had positive
responses. Both new and standard testing achieved 100% specificity.
Conclusions
Compared with standard IgM and IgG testing, the new IgG algorithm
(with
VlsE band) eliminates the need for IgM testing; it provides comparable
or better sensitivity, and it maintains high specificity.
http://dx.doi.org/10.1086/648674
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci