"Inflammation as Disease" in the AL (WayBack Machine) in the Pre-Weintraub Era- before I trained her and the Under-Our-Skin team
Mort Zuckerman
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Subject: "Inflammation as Disease" in the AL (WayBack Machine) in the
Pre-Weintraub Era- before I trained her and the Under-Our-Skin team
Date: May 28, 2010 12:30 PM
"INFLAMMATION" as the only way
a person could have a "disease."
Quote in the PBS Series, Life On Earth,
Below
========================================
The crooks changed the definition of
the "disease" from "Lyme Relapsing
Fever" to "Lyme 'disease'" or "Just-an
Allen-Steere-HLA-linked-Bad-Knee" at Dearborn,
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
so these crooks think they're not lying when
they say "disease." This is how and what
they meant. You will find testimony online
where Lenny Sigal perjures himself by
calling neurological Lyme or Relapsing
Fever or Borreliosis, "Not 'Lyme Disease,'"
thinking he is being clever.
People, humans - let's be clear about
whom I speak when I say "people"; I refer
only to Lyme victims or humans, not any
of the Homo sapiens associated with Yale
or UConn - don't know these crooks are only
talking about "The Knee," when they say,
"Lyme Disease," as redefined at Dearborn as
shown in the main graphic here:
http://www.relapsingfever.org
Steere has now debunked the crooks'
own position on "inflammation":
http://www.ncbi.nlm.nih.gov/pubmed/20506317
[The whole thing seems to be too too
scientifical to ever be published in
the LameStream, even though, as I said,
all you need to do is *look* at what Allen
Steere did with the various forms of
Borreliosis in his comparative ELISAs
here:
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
And now Steere is backtracking in his own
position, or the Dearborn Diagnostic
Standard, by saying, "People with chronic
Lyme knees have an incompetent, suppressed
immune response":
http://www.ncbi.nlm.nih.gov/pubmed/20506317
The NYTimes is too afraid to run the story
because they can't speak to "it," without
saying "it." They did incompetent investigative
work and they paid off their only writer who
performed competent investigation, Holc Noble,
to keep his mouth shut:
http://www.actionlyme.org/100513.htm
The AMA says it, Allen Steere says it, the
FDA says it, the WHO and the EU say it... but
the NYTimes will never run this story of the Lyme Crymes...
KMDickson
=====================================
http://www.actionlyme.org/Actionlyme_History.htm
Published in November 2000:
http://web.archive.org/web/20010429213719/http://www.geocities.com/kmdickson0308/lyme-dilemma.html
http://web.archive.org/web/20030620031132/www.geocities.com/kmdickson0308/1-4.txt
4. Sigal and Shapiro Spinning Lyme for the Press
From the Life on Earth Series: 9/15/00
(Linked or enclosed)
SHAPIRO: What some people would have you believe is that there are two
different diseases.
SHAPIRO: Somehow, for that form of the disease, antibiotics are
effective. They do fine. But then there's some other form of the
disease which is, you can't put your hand around it. They don't have
objective findings of inflammation, which is the way bacteria cause
disease.
TOOMEY: What these patients do have are symptoms that doctors call
nonspecific. They span a broad spectrum. Emotional problems, as in the
case of Lisa's daughter; or fatigue, muscle pains, depression. Doctor
Shapiro helped write the Lyme treatment guidelines put out by the
Infectious Diseases Society of America. Guidelines that state even the
most advanced cases of infection can be eradicated with two months of
oral or intravenous antibiotics. But for the patients with these
ongoing, nonspecific symptoms, the maximum treatment didn't seem to
work.
SHAPIRO: They would have you believe that form of the disease, somehow
this is, the bacteria knows to act differently and it doesn't respond
to
antibiotics in this sense. It really doesn't make any sense.
SIGAL: Nobody has ever found a Borrelia Burgdorfer that is resistant
to
the standard antibiotics that are used in the treatment of Lyme
Disease.
Which I think really
pokes a major league hole in the theory that what you've got is you
need
more antibiotics because you've made a super-bug.
[notice he did not qualify that by saying in vitro]
5 abstracts published in the US showing antibiotic resistence and
intracellularity of Bb
as a mechanism of antibiotic evasion.
Below: The patient was treated for 6 weeks with oral doxy 200 mgs/day
and then 2 weeks
IV ceftriaxone, and then 3 weeks of roxithromycin, sulfatmethoxazole
and
trimethoprim, and then surgery was performed.
1) Persistence of Borrelia burgdorferi in ligamentous tissue from a
patient with chronic Lyme borreliosis.
AUTHORS: Haupl T; Hahn G; Rittig M; Krause A; Schoerner C; Schonherr
U;
Kalden JR; Burmester GR
Department of Medicine III, University of Erlangen-Nuremberg, Germany.
Arthritis Rheum 1993 Nov;36(11):1621-6
OBJECTIVE. To document the persistence of **Borrelia burgdorferi**
in ligamentous tissue samples obtained from a woman with chronic Lyme
borreliosis. METHODS. Spirochetes were isolated from samples of
ligamentous tissue, and the spirochetes were characterized
antigenetically and by molecular biology techniques. The ligamentous
tissue was examined by electron microscopy. Humoral and cellular
immune
responses were analyzed.
RESULTS. Choroiditis was the first recognized manifestation of Lyme
disease in this patient. Despite antibiotic therapy, there was
progression to a chronic stage, with multisystem manifestations. The
initially significant immune system activation was followed by a loss
of
the specific humoral immune response and a decrease in the cellular
immune response to B burgdorferi over the course of the disease.
"Trigger finger"
developed, and a portion of the flexor retinaculum obtained at surgery
was cultured. Viable spirochetes were identified.
Ultramorphologically, the spirochetes were situated
between collagen fibers and along fibroblasts, some of which were
deeply
invaginated by these organisms. The cultured bacteria were identified
as
B burgdorferi by reactions with
specific immune sera and monoclonal antibodies, and by polymerase
chain
reaction amplification and Southern blot hybridization techniques.
CONCLUSION. To our knowledge, this is the first report of the
isolation
of B burgdorferi from ligamentous tissue. This suggests that tendon
tissues serve as a specific site of spirochete residence in human
hosts.
2) TITLE: Seronegative chronic relapsing neuroborreliosis [see
comments]
AUTHORS: Lawrence C; Lipton RB; Lowy FD; Coyle PK
AUTHOR AFFILIATION: Department of Medicine, Albert Einstein College
of Medicine, New York, N.Y., USA.
SOURCE: Eur Neurol 1995;35(2):113-7
CITATION IDS: PMID: 7796837 UI: 95317331
COMMENT: Comment in: Eur Neurol 1996;36(6):394-5
ABSTRACT: We report an unusual patient with evidence of Borrelia
burgdorferi infection who experienced repeated neurologic relapses
despite aggressive antibiotic therapy. Each course of therapy was
associated with a Jarisch-Herxheimer-like reaction. Although the
patient
never had detectable free antibodies to B. burgdorferi in serum or
spinal fluid, the CSF was positive on multiple occasions for complexed
anti-B. burgdorferi antibodies, B. burgdorferi nucleic acids and free
antigen.
3) TITLE: Ultrastructural demonstration of spirochetal antigens in
synovial fluid and synovial membrane in chronic Lyme disease: possible
factors contributing to persistence of organisms.
AUTHORS: Nanagara R; Duray PH; Schumacher HR Jr
AUTHOR AFFILIATION: Allergy-Immunology-Rheumatology Division,
Department of Medicine, Faculty of Medicine, KhonKaen University,
Thailand.
SOURCE: Hum Pathol 1996 Oct;27(10):1025-34
CITATION IDS: PMID: 8892586 UI: 97047745
ABSTRACT: To perform the first systematic electronmicroscopic (EM)
and
immunoelectron microscopy (IEM) study of the pathological changes and
the evidence
of spirochete presence in synovial membranes and synovial fluid (SF)
cells of patients with chronic Lyme arthritis. EM examination was
performed on four synovial membrane and eight SF cell samples from
eight
patients with chronic Lyme disease. Spirochetal antigens in the
samples
were sought by IEM using monoclonal antibody to Borrelia burgdorferi
outer surface protein A (OspA) as the immunoprobe. Prominent
ltrastructural findings were surface fibrin-like material, thickened
synovial lining cell layer and signs of vascular injury. Borrelia-like
structures were identified in all four synovial membranes and in two
of
eight SF cell samples. The presence of spirochetal antigens was
confirmed by IEM in all four samples studied (one synovial membrane
and
three SF cell samples). OspA labelling was in perivascular areas, deep
synovial stroma among collagen bundles, and in vacuoles of fibroblasts
in synovial membranes; and in cytophagosomes of mononuclear cells in
SF
cell samples. Electron microscopy adds further evidence for
persistence
of spirochetal antigens in the joint in chronic Lyme disease.
Locations
of spirochetes or spirochetal antigens both intracellulary and
extracellulary in deep synovial connective tissue as reported here
suggest sites at which spirochaetes may elude host immune response and
antibiotic treatment.
4) TITLE: Invasion of human skin fibroblasts by the Lyme disease
spirochete, Borrelia burgdorferi.
AUTHORS: Klempner MS; Noring R; Rogers RA
AUTHOR AFFILIATION: Division of Geographic Medicine and Infectious
Diseases,
New England Medical Center, Tufts University School of Medicine,
Boston,
Massachusetts 02111.
SOURCE: J Infect Dis 1993 May;167(5):1074-81
CITATION IDS: PMID: 8486939 UI: 93253286
ABSTRACT: The ability of Borrelia burgdorferi to attach to and invade
human fibroblasts was investigated by scanning electron and confocal
microscopy. By scanning electron microscopy, B. burgdorferi were
tightly
adherent to fibroblast monolayers after 24-48 h but were eliminated
from
the cell surface by treatment with ceftriaxone (1 microgram/mL) for 5
days. Despite the absence of visible spirochetes on the cell surface
after antibiotic treatment, viable B. burgdorferi were isolated from
lysates of the fibroblast monolayers. B. burgdorferi were observed in
the perinuclear region within
human fibroblasts by laser scanning confocal microscopy. Intracellular
spirochetes specifically labeled with monoclonal anti-flagellin
antibody
were also identified by fluorescent laser scanning confocal
microscopy.
These observations suggest that B. burgdorferi can adhere to,
penetrate,
and invade human fibroblasts in organisms that remain viable.
5) TITLE: Fibroblasts protect the Lyme disease spirochete,
Borrelia burgdorferi, from ceftriaxone in vitro.
AUTHORS: Georgilis K; Peacocke M; Klempner MS
AUTHOR AFFILIATION: Department of Medicine, New England
Medical Center, Boston, Massachusetts.
SOURCE: J Infect Dis 1992 Aug;166(2):440-4
CITATION IDS: PMID: 1634816 UI: 92340959
ABSTRACT: The Lyme disease spirochete, Borrelia burgdorferi, can be
recovered long after initial infection, even from antibiotic-treated
patients, indicating that it resists eradication by host defense
mechanisms and antibiotics. Since B. burgdorferi first infects skin,
the
possible protective effect of skin fibroblasts from an antibiotic
commonly used to treat Lyme disease, ceftriaxone, was examined. Human
foreskin fibroblasts protected B. burgdorferi from the lethal action
of
a 2-day exposure to ceftriaxone at 1 microgram/mL, 10-20 x MBC. In the
absence of fibroblasts, organisms did not survive. Spirochetes were
not
protected from ceftriaxone by glutaraldehyde-fixed fibroblasts or
fibroblast lysate, suggesting that a living cell was required. The
ability of the organism to survive in the presence of fibroblasts was
not related to its infectivity. Fibroblasts protected B. burgdorferi
for
at least 14 days of exposure to ceftriaxone. Mouse keratinocytes,
HEp-2
cells, and Vero cells but not Caco-2 cells showed the same protective
effect. Thus, several eukaryotic cell types provide the Lyme disease
spirochete with a protective environment contributing to its long-term
survival.
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