|
---- Original
Message ----- |
| From |
Kathleen <kathleen.dickson@SNET.Net> |
| Date |
Thu, 13 Feb 2003 18:04:15
-0500 |
| To |
ajm@medicine.ucsf.edu,
gsbsnadm@umdnj.edu, gsbspisc@umdnj.edu |
| Subject |
[ILADS] LEONARD SIGAL |
COMPLAINT FORM FOR NEW JERSEY
MEDICAL EXAMINERS
http://www.state.nj.us/lps/ca/complaint/medcom.pdf
Greetings AJM and UMDNJ,
I am attaching the Connaught vaccine
trial results and Mr. Sigal's comments on the Lyme
vaccine for children.
Principal Investigator, Leonard
Sigal.
The following was published two
years later.
We were wondering if you can tell us
whether there was a problem with this?
You can see that the summary of the
results of infection status was performed with
the MarDx blot kits,
http://www.journals.uchicago.edu/CID/journal/issues/v31n1/991200/991200.html (Sigal, Persing, Molloy and Berardi)
"Since specimen quantities were
available, representative study
subjects were also tested by FDA-licensed
ELISA and WB kits for descriptive
and comparative purposes, ***making no
claim or attempt to formally
validate or invalidate these tests'
performances for vaccinated study subjects.***"
"Even when investigators are
familiar with this phenomenon,
problems with interpretation of test results
may arise in those situations when a vaccinated subject actually becomes
infected with B. burgdorferi (i.e., a vaccine failure)"
The manufacturer of the only
currently FDA-approved (and
released) recombinant OspA Lyme disease
vaccine has suggested that
vaccination does not interfere with serological
evaluation of Lyme disease in vaccine recipients [?] ***a
statement that is not supported by
the data presented here.*** Serum samples from 10 additional
study subjects that were obtained 30 days after dose 3 of a second
recombinant OspA Lyme disease
vaccine (Pasteur Meriéux Connaught,
Swiftwater, PA) were tested by the
same methodologies (data not shown).
Similar findings of multiple bands following vaccination were observed
when tests with use of conventional OspA-containing strains were done
but not when tests with use of OspA-free strains were done. This
particular vaccine is not currently licensed.
===================
I have another question, : Chronic Lyme Disease: Sigal and
Hassett's Response
Nowhere in our article (Sigal and
Hassett 2002) do we minimize or devalue the pain or suffering of
patients with chronic Lyme disease
nor do we state that such patients are
"crazy" or "delusional." Further, we do not dismiss the possibility that
some such patients actually have infection that persists despite
adequate prior antibiotic treatment. Nonetheless, we take this
opportunity to again issue a caution
against making the diagnosis of chronic Lyme
disease in the absence of objective clinical and microbiologic evidence
of infection.
Without demonstrable physical
findings and laboratory proof of the persistence of Borrelia burgdorferi
, the diagnosis should remain in significant doubt. Certainly, a few,
often poorly documented case reports claiming persistence (many
in Europe, where the organism, the vector, and the ambient human
immunogenetic types are different)
cannot be a basis for the widespread
diagnosis of chronic infection in
certain regions of the United States and in
certain practices.
We hope our article (Sigal and
Hassett 2002) will help educate physicians and assist them in being
more sensitive to their patients and to more correctly identify the true
underlying cause of their patients' symptoms in a compassionate manner.
However, many patients are misdiagnosed with chronic Lyme
disease, a diagnosis often made to provide an explanation for a
bewildering array of complaints
within an acceptable framework for both
patient and physician. Instead,
these patients deserve the truth.
Improvement and cure require
provision of a correct scientific and medical
explanation and properly directed therapies. For many of the patients
we see, chronic antibiotics, continuous reassurance, and yet
another antibiotic regimen when the current one fails have led to
frustration, anger, depression, and chronic suffering. Further, the
inappropriate use of broad spectrum antibiotics, often for long periods,
is not without personal (e.g., Clostridium dificile infection,
allergies, and other adverse
reactions) and societal (e.g., contribution to
the development of resistant strains such as methicillin- and
vancomycin-resistant Staphylococcus)
risks.
Leonard H. Sigal Afton L. Hassett UMDNJ-Robert Wood Johnson Medical
School New Brunswick,New Jersey E-mail: sigallh@umdnj.edu
Reference
But in Rahn and Evans' Lyme disease,
ACP Key Diseases Series, 1998, Mr Sigal writes: "With widespread anxiety about Lyme
disease has come Munchausen Syndrome and Munchausen
by proxy syndrome in those concerned about "chronic"
Lyme disease."-- page 149
I know that exactly says nothing,
which Mr. Sigal is an expert at (he was on the Debating
Team in College, he always mentions at conferences),
but one might think... Is he saying Lyme patients have
Munchausens?
Okay, he never said Lyme patients
were crazy or delusional.
I would argue that Munchausens could
be considered a version of "crazy".
-----------
And I was also wondering, since
Allen Steere
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3531237&dopt=Abstract and Dattwyler and Luft said changing
IgM bands was evidence of continuing infection (Schutzer- Lyme
Disease, Molecular and Immunologic Approaches- page 319), and then Mr. Sigal agrees: "Previous studies demonstrated that
specific antigen-antibody complexes in the sera of patients with LD
could be precipitated by
polyethylene glycol and could then be disrupted
with maintenance of the immunoreactivity of the released
antibodies, that specific anti-B. burgdorferi IgM was concentrated in
ICs, and that occasionally IgM to specific B. burgdorferi antigens was
found in the IC but not in unprocessed serum. EMIBA compared
favorably with commercial and CDC flagellin-enhanced enzyme-linked
immunosorbent assays and other
assays in confirming the diagnosis of LD.
EMIBA confirmed early B. burgdorferi infection more accurately than the
comparator assays. In addition,
EMIBA more accurately differentiated
seropositivity in patients with
active ongoing infection from
seroreactivity persisting long after
clinically successful antibiotic therapy; i.e.,
EMIBA identified seroreactivity indicating a clinical circumstance
requiring antibiotic therapy. Thus, EMIBA is a promising new assay for
accurate serologic confirmation of early and/or active LD."
IgM means persisting infection, and
patients can be seronegative, How can Mr. Sigal report results of
a vaccine trial, when he knows the CDC's standard is
inadequate?
========================
If Lyme disease becomes
Fibromyalgia,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12194894&dopt=Abstract
and as Mr. Sigal says, IgG
antibodies to Bb flagellin cross react with human heat shock protein
60 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11860186&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8096152&dopt=Abstract "As predicted, II-13 bound to
mitochondria, in a pattern of
cellular binding very different from H9724,
which bound in a scattered cytoplasmic, nonorganelle-related
pattern. ***H9724's effect is the first evidence that HSP60 may play a
role in peptide-hormone-receptor function and demonstrates the
modulatory potential of a monoclonal antibody on living cells."***
and as Mr Sigal says in Schutzer's
"Lyme disease" (page 208), IL-1 may be the cause of Fibromyalgia and
sleep disorder associated with and following "Lyme disease",
Does Mr Sigal test for these
objective signs before assigning the diagnosis of:
Environ Health Perspect 2002 Aug;110
Suppl 4:607-11 Related Articles, Links [Click here to read]
Contributions of
societal and geographical
environments to "chronic Lyme disease": the
psychopathogenesis and ***aporology***
of a new ***"medically unexplained
symptoms"*** syndrome. Sigal LH, Hassett AL.
New IgM, IgM Complexed, IgG
antibodies to Flagellin, IL-1 >>> all seemed to be diagnostic
clues of REAL ILLNESS, to Mr. Sigal, at one time.
Does Mr Sigal test for these before
he diagnoses UNEXPLAINED ILLNESS OR CONFUSION?
Is that required of a diagnostician?
Thanks, I hope you can help me out
with this.
I was just wondering if that was
what is meant by Insurance Fraud. Or Fraud, of any
kind.
I copied Mr. Sigal in. I know
he can help me out with this, because of the
Debating experience. First let's agree on the definitions
of Fraud.
Mr. Sigal, start your dictionary!!!
2 entries found for fraud. To select an entry, click on it. Main Entry: fraud <http://www.m-w.com/images/audio.jpg> Pronunciation: 'frod Function: noun Etymology: Middle English fraude,
from Middle French, from Latin
fraud-, fraus Date: 14th century 1 a : DECEIT, TRICKERY; specifically
: ***intentional perversion of truth in order to induce another to
part with something of value*** or to surrender a legal right b : an
act of deceiving or misrepresenting
: TRICK 2 a : a person who is not what he or
she pretends to be : IMPOSTOR; also : one who defrauds : CHEAT b : one
that is not what it seems or is represented to be synonym see DECEPTION, IMPOSTURE
------ One final consideration: THE SCIENTIFIC METHOD 1. Observation and description of a
phenomenon or group of phenomena.
2. Formulation of an hypothesis to
explain the phenomena. In physics, the hypothesis often takes the form
of a causal mechanism or a mathematical relation. 3. ***Use of the hypothesis to
predict the existence of other
phenomena, or to predict quantitatively the
results of new observations.*** 4. Performance of experimental tests
of the predictions by several independent experimenters and
properly performed experiments.
Does that mean, don't test for the
markers so you won't find them? Is
that what a Medical Scientist is? Do IgM, IgG to
flagellin, IL-1 predict a non-diagnosis?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11083273&dopt=Abstract
Did Mr. Sigal validate the use of
those psychometric tests in the presence
of these markers of pathophysiology he has found in
Lyme and post-Lyme Fibromyalgia?
Main Entry: im·pos·tor <http://www.m-w.com/images/audio.jpg> Variant(s): or im·pos·ter <http://www.m-w.com/images/audio.jpg> /im-'päs-t&r/ Function: noun Etymology: Late Latin impostor, from
Latin imponere Date: 1624 : one that assumes false identity or
title for the purpose of deception
Let me know if I should be asking
somewhere else for an explanation. My friends
hate being called crazy, or whatever is Mr. Sigal's
latest popular psychiatric diagnosis. It just
isn't compassionate at all, for a physici...
Person who graduated college and was on the debating
team.
Thanks,
Kathleen Dickson 23 Garden Street Pawcatuck, CT, 06379
|
----- Original
Message ----- |
| From |
Kathleen
<kathleen.dickson@SNET.Net> |
| Date |
Thu, 13 Feb 2003 20:02:47
-0500 |
| To |
acr@rheumatology.org,
iversen@simmons.edu,
cjhenderson@gsu.edu,
backman@interchange.ubc.ca |
| Subject |
[SpinLyme] Leonard Sigal |
UMDNJ-Robert Wood Johnson Medical
School New Brunswick,New Jersey E-mail: sigallh@umdnj.edu
Greetings ACR,
I was looking around the web for an
organization to report ths misconduct of Leonard Sigal,
UMDNJ. You must be it.
Sigal has a horrendous reputation as
an Insurance Company Reviewer, with tremendous bias
against a set of patients who do not even fall within his
bailiwick. The reason for the bias: That Lyme disease is
just an arthritis, is because he administered the Connaught
vaccine trial, and as you know, patients who bear the HLA-DR4 amd
DR2 haplotypes are essentially the arthritis-presenters.
The CDC set a conference in 1994 to
standardize the serodiagnosis of Lyme disease, and this was the IgG
criteria:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8380611&dopt=Abstract
In the field, it was actually
accurate 22% of the time.
Both vaccine trials were therefore
fraudulent, since one cannot throw out ~78% of one's
data and call it a study.
Would you please investigate the
concerns below. If his behavior is allowed to
persist, he will ruin the reputation of Rheumatology, as a
scientific practice.
Sigal insists on patients having
hard signs (lab) of illness, meanwhile, he routinely
assesses patients on behalf of Insurance Companies,
and reports without seeking these objective
determinations- ones he himself developed. That is what it is
looking like Rheumatology is being reduced to. I am
certain you will want to maintain your reputations as
practitioners, and discover whether or not this behavior is true
to the intended nature of the study and treatment of
connective tissue diseases.
I am also attaching the Tick-Borne
Diseases Management Plan. You will see that the
research included in that is largely that of those who
presented here:
http://rarediseases.info.nih.gov/news-reports/workshops/humanneuro20010909.html
Please investigate. This man
really has hurt a *lot* of people, and he just won't let up.
Thank You,
Kathlen Dickson 23 Garden Street Pawcatuck, CT 06379
Subject:
[SpinLyme] LEONARD SIGAL
Date:
Thu, 13 Feb 2003 18:04:15 -0500
From:
Kathleen <kathleen.dickson@SNET.Net> Reply-To:
SpinLyme@yahoogroups.com Organization:
member, ActionLyme
To:
ajm@medicine.ucsf.edu,
gsbsnadm@umdnj.edu, gsbspisc@umdnj.edu
CC:
njinsurancefraud@njdcj.org,
sigallh@umdnj.edu, spinlyme@yahoogroups.com,
ilads@yahoogroups.com
COMPLAINT FORM FOR NEW JERSEY
MEDICAL EXAMINERS
http://www.state.nj.us/lps/ca/complaint/medcom.pdf
Greetings AJM and UMDNJ,
I am attaching the Connaught vaccine
trial results and Mr. Sigal's comments on the Lyme
vaccine for children.
Principal Investigator, Leonard
Sigal.
The following was published two
years later.
We were wondering if you can tell us
whether there was a problem with this?
You can see that the summary of the
results of infection status was performed with
the MarDx blot kits,
http://www.journals.uchicago.edu/CID/journal/issues/v31n1/991200/991200.html (Sigal, Persing, Molloy and Berardi)
"Since specimen quantities were
available, representative study
subjects were also tested by FDA-licensed
ELISA and WB kits for descriptive
and comparative purposes, ***making no
claim or attempt to formally
validate or invalidate these tests'
performances for vaccinated study subjects.***"
"Even when investigators are
familiar with this phenomenon,
problems with interpretation of test results
may arise in those situations when a vaccinated subject actually becomes
infected with B. burgdorferi (i.e., a vaccine failure)"
The manufacturer of the only
currently FDA-approved (and
released) recombinant OspA Lyme disease
vaccine has suggested that
vaccination does not interfere with serological
evaluation of Lyme disease in vaccine recipients [?] ***a
statement that is not supported by
the data presented here.*** Serum samples from 10 additional
study subjects that were obtained 30 days after dose 3 of a second
recombinant OspA Lyme disease
vaccine (Pasteur Meriéux Connaught,
Swiftwater, PA) were tested by the
same methodologies (data not shown).
Similar findings of multiple bands following vaccination were observed
when tests with use of conventional OspA-containing strains were done
but not when tests with use of OspA-free strains were done. This
particular vaccine is not currently licensed.
===================
I have another question, : Chronic Lyme Disease: Sigal and
Hassett's Response
Nowhere in our article (Sigal and
Hassett 2002) do we minimize or devalue the pain or suffering of
patients with chronic Lyme disease
nor do we state that such patients are
"crazy" or "delusional." Further, we do not dismiss the possibility that
some such patients actually have infection that persists despite
adequate prior antibiotic treatment. Nonetheless, we take this
opportunity to again issue a caution
against making the diagnosis of chronic Lyme
disease in the absence of objective clinical and microbiologic evidence
of infection.
Without demonstrable physical
findings and laboratory proof of the persistence of Borrelia burgdorferi
, the diagnosis should remain in significant doubt. Certainly, a few,
often poorly documented case reports claiming persistence (many
in Europe, where the organism, the vector, and the ambient human
immunogenetic types are different)
cannot be a basis for the widespread
diagnosis of chronic infection in
certain regions of the United States and in
certain practices.
We hope our article (Sigal and
Hassett 2002) will help educate physicians and assist them in being
more sensitive to their patients and to more correctly identify the true
underlying cause of their patients' symptoms in a compassionate manner.
However, many patients are misdiagnosed with chronic Lyme
disease, a diagnosis often made to provide an explanation for a
bewildering array of complaints
within an acceptable framework for both
patient and physician. Instead,
these patients deserve the truth.
Improvement and cure require
provision of a correct scientific and medical
explanation and properly directed therapies. For many of the patients
we see, chronic antibiotics, continuous reassurance, and yet
another antibiotic regimen when the current one fails have led to
frustration, anger, depression, and chronic suffering. Further, the
inappropriate use of broad spectrum antibiotics, often for long periods,
is not without personal (e.g., Clostridium dificile infection,
allergies, and other adverse
reactions) and societal (e.g., contribution to
the development of resistant strains such as methicillin- and
vancomycin-resistant Staphylococcus)
risks.
Leonard H. Sigal Afton L. Hassett UMDNJ-Robert Wood Johnson Medical
School New Brunswick,New Jersey E-mail: sigallh@umdnj.edu
Reference
But in Rahn and Evans' Lyme disease,
ACP Key Diseases Series, 1998, Mr Sigal writes: "With widespread anxiety about Lyme
disease has come Munchausen Syndrome and Munchausen
by proxy syndrome in those concerned about "chronic"
Lyme disease."-- page 149
I know that exactly says nothing,
which Mr. Sigal is an expert at (he was on the Debating
Team in College, he always mentions at conferences),
but one might think... Is he saying Lyme patients have
Munchausens?
Okay, he never said Lyme patients
were crazy or delusional.
I would argue that Munchausens could
be considered a version of "crazy".
-----------
And I was also wondering, since
Allen Steere
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3531237&dopt=Abstract and Dattwyler and Luft said changing
IgM bands was evidence of continuing infection (Schutzer- Lyme
Disease, Molecular and Immunologic Approaches- page 319), and then Mr. Sigal agrees: "Previous studies demonstrated that
specific antigen-antibody complexes in the sera of patients with LD
could be precipitated by
polyethylene glycol and could then be disrupted
with maintenance of the immunoreactivity of the released
antibodies, that specific anti-B. burgdorferi IgM was concentrated in
ICs, and that occasionally IgM to specific B. burgdorferi antigens was
found in the IC but not in unprocessed serum. EMIBA compared
favorably with commercial and CDC flagellin-enhanced enzyme-linked
immunosorbent assays and other
assays in confirming the diagnosis of LD.
EMIBA confirmed early B. burgdorferi infection more accurately than the
comparator assays. In addition,
EMIBA more accurately differentiated
seropositivity in patients with
active ongoing infection from
seroreactivity persisting long after
clinically successful antibiotic therapy; i.e.,
EMIBA identified seroreactivity indicating a clinical circumstance
requiring antibiotic therapy. Thus, EMIBA is a promising new assay for
accurate serologic confirmation of early and/or active LD."
IgM means persisting infection, and
patients can be seronegative, How can Mr. Sigal report results of
a vaccine trial, when he knows the CDC's standard is
inadequate?
========================
If Lyme disease becomes
Fibromyalgia,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12194894&dopt=Abstract
and as Mr. Sigal says, IgG
antibodies to Bb flagellin cross react with human heat shock protein
60
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11860186&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8096152&dopt=Abstract "As predicted, II-13 bound to
mitochondria, in a pattern of
cellular binding very different from H9724,
which bound in a scattered cytoplasmic, nonorganelle-related
pattern. ***H9724's effect is the first evidence that HSP60 may play a
role in peptide-hormone-receptor function and demonstrates the
modulatory potential of a monoclonal antibody on living cells."***
and as Mr Sigal says in Schutzer's
"Lyme disease" (page 208), IL-1 may be the cause of Fibromyalgia and
sleep disorder associated with and following "Lyme disease",
Does Mr Sigal test for these
objective signs before assigning the diagnosis of:
Environ Health Perspect 2002 Aug;110
Suppl 4:607-11 Related Articles, Links [Click here to read]
Contributions of
societal and geographical
environments to "chronic Lyme disease": the
psychopathogenesis and
***aporology*** of a new ***"medically unexplained
symptoms"*** syndrome. Sigal LH, Hassett AL.
New IgM, IgM Complexed, IgG
antibodies to Flagellin, IL-1 >>> all seemed to be diagnostic
clues of REAL ILLNESS, to Mr. Sigal, at one time.
Does Mr Sigal test for these before
he diagnoses UNEXPLAINED ILLNESS OR CONFUSION?
Is that required of a diagnostician?
Thanks, I hope you can help me out
with this.
I was just wondering if that was
what is meant by Insurance Fraud. Or Fraud, of any
kind.
I copied Mr. Sigal in. I know
he can help me out with this, because of the
Debating experience. First let's agree on the definitions
of Fraud.
Mr. Sigal, start your dictionary!!!
2 entries found for fraud. To select an entry, click on it. Main Entry: fraud <http://www.m-w.com/images/audio.jpg> Pronunciation: 'frod Function: noun Etymology: Middle English fraude,
from Middle French, from Latin
fraud-, fraus Date: 14th century 1 a : DECEIT, TRICKERY; specifically
: ***intentional perversion of truth in order to induce another to
part with something of value*** or to surrender a legal right b : an
act of deceiving or misrepresenting
: TRICK 2 a : a person who is not what he or
she pretends to be : IMPOSTOR; also : one who defrauds : CHEAT b : one
that is not what it seems or is represented to be synonym see DECEPTION, IMPOSTURE
------ One final consideration: THE SCIENTIFIC METHOD 1. Observation and description of a
phenomenon or group of phenomena.
2. Formulation of an hypothesis to
explain the phenomena. In physics, the hypothesis often takes the form
of a causal mechanism or a mathematical relation. 3. ***Use of the hypothesis to
predict the existence of other
phenomena, or to predict quantitatively the
results of new observations.*** 4. Performance of experimental tests
of the predictions by several independent experimenters and
properly performed experiments.
Does that mean, don't test for the
markers so you won't find them? Is
that what a Medical Scientist is? Do IgM, IgG to
flagellin, IL-1 predict a non-diagnosis?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11083273&dopt=Abstract
Did Mr. Sigal validate the use of
those psychometric tests in the presence
of these markers of pathophysiology he has found in
Lyme and post-Lyme Fibromyalgia?
Main Entry: im·pos·tor <http://www.m-w.com/images/audio.jpg> Variant(s): or im·pos·ter <http://www.m-w.com/images/audio.jpg> /im-'päs-t&r/ Function: noun Etymology: Late Latin impostor, from
Latin imponere Date: 1624 : one that assumes false identity or
title for the purpose of deception
Let me know if I should be asking
somewhere else for an explanation. My friends
hate being called crazy, or whatever is Mr. Sigal's
latest popular psychiatric diagnosis. It just
isn't compassionate at all, for a physici...
Person who graduated college and was on the debating
team.
Thanks,
Kathleen Dickson 23 Garden Street Pawcatuck, CT, 06379
|
----- Original
Message ----- |
| From |
Kathleen
<kathleen.dickson@SNET.Net> |
| Date |
Fri, 14 Feb 2003 04:51:23
-0500 |
| To |
acr@rheumatology.org,
iversen@simmons.edu,
cjhenderson@gsu.edu,
backman@interchange.ubc.ca |
| Subject |
[scilyme] Leonard Sigal 2 |
Part 2 of the complaint regarding
Sigal's "authority" in "Lyme disease".
SIGAL:
"At the December 1994 National
Clinical Conference on Lyme Disease,
10 experts presented the clinical state
of the art on the infection. Panel discussions followed, allowing for
interchange with clinicians. The conference was sponsored by the
UMDNJ Center for Continuing
Education and the American Lyme Disease
Foundation, Inc.; it was
underwritten by Connaught Laboratories, Inc."
http://www.umdnj.edu/umcweb/hstate/aut96/aug96lym.html
Do you think this is a conflict,
since Sigal then went on to be the Connaught trial
administrator?
IS THIS TRUE?
"The serologic and molecular
biologic diagnostic tests are as
accurate as most such tests for infectious
disease, but they should be used
only with a full understanding of their
limitations."
Or, rather, does it make sense?
The conceptual framework of Sigal,
to put it nicely, is that only 1) one spirochete, one
with lipoprotein-code-bearing plasmids that are similar to those
found in B burgdoferi (as defined by the presence of the OspA
plasmid) can produce disease, 2) that disease manifests
as a reactive arthritis, and 3) it only lasts one month,
since antibiotics "kill" spirochetes in vitro.
http://www.geocities.com/kmdickson0308/1-4.txt
"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."
Nobody in the professional Lyme
disease arena ever said anything
about a super bug. As you will see
below, in vitro, is not the same
thing as in vivo (Klempner). The
argument is, that spirochetes behave
like spirochetes. The argument is that they sequester
(latency, asymptomatic, starvation forms, spheroplasts, stringent forms,
"cysts", "morphometrics") in
antibiotic and immune privileged sites, and
that patients need to be retreated
when they are symptomatic.
If it is not true, as Sigal says in
the article above, that Lyme is a Great Imitator, "Lyme disease
was incorrectly called "The Great Imitator" because of its apparent ability to
mimic other diseases, one wonders what other disease syndromes are
possibly left out here of the representations are left out of the multitissue
tropism and immune dysregulation discussed below?
1) Zentralbl Bakteriol Mikrobiol Hyg
[A] 1986 Dec;263(1-2):201-5 Clinical
manifestations of Lyme disease.
Steere AC, Bartenhagen NH,
Craft JE, Hutchinson GJ, Newman JH, Pachner AR, Rahn DW, ***Sigal LH***, Taylor E, Malawista
SE.
Lyme disease
typically begins with a unique skin
lesion, erythema chronicum migrans (ECM) (stage 1).
Patients with this lesion may also have headache, meningeal irritation,
mild encephalopathy, multiple annular secondary lesions, malar or
urticarial rash, generalized lymphadenopathy and splenomegaly,
migratory musculoskeletal pain, hepatitis, sore throat,
non-productive cough,
conjunctivitis, periorbital edema, or testicular
swelling. After a few weeks to
months (stage 2), about 15% of patients
develop frank neurologic
abnormalities, including meningitis, encephalitis,
cranial neuritis (including bilateral facial palsy), motor or
sensory radiculoneuritis,
mononeuritis multiplex, or myelitis. At this
time, about 8% of patients develop cardiac involvement--AV block, acute
myopericarditis, cardiomegaly, or pancarditis. Throughout this stage,
many patients continue to experience migratory musculoskeletal pain in
joints, tendons, bursae, muscle, or bone. Months to years after disease
onset (stage 3), about 60% of patients develop frank arthritis,
which may be intermittent or
chronic. Recently evidence suggests that Lyme
disease may also be associated with chronic neurologic or skin
involvement. Thus, Lyme disease
occurs in stages with different clinical
manifestations at each stage, but
the course of the illness in each
patient is highly variable. PMID: 3554839 [PubMed - indexed for
MEDLINE]
2) Semin Neurol 1997 Mar;17(1):63-8
Related Articles, Links
Immunologic
mechanisms in Lyme neuroborreliosis:
the potential role of autoimmunity and molecular
mimicry.
***Sigal LH.***
Department of
Medicine and Disease Center,
University of Medicine and Dentistry of New Jersey-Robert
Wood Johnson Medical School, New Brunswick 08903-0019, USA.
Most of the clinical
manifestations of Lyme disease are
due to the local presence of the causative
agent, Borrelia burgdorferi, in the affected tissues. However, the
precise means of tissue damage are
not well understood and there is no
proof that the organism, live or
dead, is always present. An understanding
of the complex interaction between the organism, the immune response
elicited by the organism, and the
host can explain manifestations of the
disease and persistence of symptoms and signs after the
antibiotic-induced death of the
organism. It is possible that dead spirochetes, or
fragments thereof may persist and
act as a focus of ongoing inflammation.
Different immunogenetic types may predispose to different immunologic
responses, with distinct clinical outcomes. Vascular changes induced
by the infection, either by local infection or the effects of
cytokines on the vessel wall, may
underlie tissue pathology. Finally, the
immune response to B. burgdorferi
may elicit the production of antibodies
capable of recognizing and damaging or modifying normal host tissues.
***Only by establishing the
mechanisms causing tissue damage in Lyme
disease can rational therapeutic strategies be developed.*** Only by
understanding these mechanisms can physicians and patients interpret
clinical responses to therapy and accurately appreciate the clinical
prognosis.PMID: 9166962 [PubMed - indexed for MEDLINE]
I think that means, there are still
unknowns. I think that means Sigal knew this was the case, before
the start of the Connaught trials, and his statements regarding the
completed framework of all outcomes of "Lyme disease" are false,
particularly since it is yet
unknown, what are the clinical syndromes
associated with antibodies which "cross-react" with host antigens (antiflagellin
antibodies and Human Heat Shock Protein 60- Sigal's work), and what is the
result of persisting dysregulated cytokines.
======== PERSISTENCE PAST TREATMENT (latency,
asymptomatic, etc):
http://www.acponline.org/journals/annals/15mar94/acids.htm
http://www.acponline.org/journals/annals/15oct94/lyme.htm
STEERE:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8272083&dopt=Abstract
(You have to get the full text of
that. Figure 1 shows 10 patients had persisting DNA after
treatment--and only via these primers; 'will get back to
primers later-- up to 7 years, which was the upper time limit of
the study)
LOBET at the FDA's Vaccine meeting:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2.htm
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_02_lobet.pdf
KLEMPNER:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1634816&dopt=Abstract
STRAUBINGER (ANTIBIOTIC- TREATED
DOGS):
http://jcm.asm.org/cgi/reprint/35/1/111.pdf
COYLE (Relapsing Neuroborreliosis-
Seronegative):
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7796837&dopt=Abstract
SYPHILITIC LATENCY:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10780185&dopt=Abstract
LYMErix vaccine trial results:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf or
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9673298&dopt=Abstract see the charts, the data. Few
"asymptomatics" in the vaccine
groups, while increasing "Unconfirmed Lyme"--
raises a red flag. Such
tabulation of results was not published for
Connaughts trial.)
"SEEDING"
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7501150&dopt=Abstract
Starvation Forms, Morphometrics:
BURGDORFER:
http://www.radio.cbc.ca/programs/ideas/shows/bacteria/willy.html ('references the Brorsons)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9266264&dopt=Abstract
NELSON:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12511489&dopt=Abstract
BARBOUR:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7103461&dopt=Abstract
MARGULIS ("morphometrics"):
http://www.pnas.org/cgi/reprint/90/15/6966.pdf
US ARMY (aerosolized leptospira):
http://www.afpmb.org/pubs/dveps/haiti.pdf
Lastly, spirochetes are parasites.
There apparently limitless variations in surface antigens of the Borreliae,
and the evidence does not all
support the notion that the B. burgdorferi is
stable, predictably generates invariable antigen (and thus inflammatory
effects - in fact, it is
characterized by just the opposite), that B.
burgdorferi is even a distinct
species, or that it is the only one which
produces disease in humans and is
vectored only by Ixodes.
http://coproweb.free.fr/pagbac/borrelia.htm
see
http://www.pasteur.fr/recherche/borrelia/Group_DN127.html
STARI-- Texas to NJ
http://www.cdc.gov/ncidod/eid/vol7no3/burkot.htm
http://www.cdc.gov/ncidod/dvbid/stari/
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8573491&dopt=Abstract
Int J Syst Bacteriol 1996
Jan;46(1):167-72
Analysis of the
genetic polymorphism of Borrelia
burgdorferi sensu lato by multilocus enzyme
electrophoresis.
Balmelli T,
Piffaretti JC.
Istituto Cantonale
Batteriosierologico, Lugano,
Switzerland.
***The relapsing fever spirochetes
were were not clearly separated from the
spirochetes associated with Lyme disease.*** In conclusion, we
believe that ***the previously
proposed subdivision of B. burgdorferi sensu
lato into only four species should be reconsidered.*** PMID:
8573491 [PubMed - indexed for
MEDLINE]
Related:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=8573491
phylogenetic analysis of rRNA genes
http://jcm.asm.org/cgi/reprint/33/9/2427.pdf
Int J Syst Bacteriol 1996
Oct;46(4):898-905
Phylogenetic analysis
of Borrelia species based on
flagellin gene sequences and its application for
molecular typing of Lyme disease borreliae.
Fukunaga M, Okada K,
Nakao M, Konishi T, Sato Y.
Faculty of Pharmacy
and Pharmaceutical Sciences,
Fukuyama University, Hiroshima, Japan.
mfukunag@supernig.nig.ac.jp
We determined almost
complete flagellin gene sequences of
various Borrelia species and aligned them
with previously published sequences.
A neighbor-joining phylogenetic
analysis showed that the genus
Borrelia was divided into the following three
major clusters: New World relapsing fever borreliae (Borrelia turicatae,
Borrelia parkeri, and Borrelia hermsii), Old World relapsing fever
borreliae (Borrelia crocidurae, Borrelia duttonii, and Borrelia
hispanica), and Lyme disease
borreliae (Borrelia burgdorferi sensu stricto,
Borrelia garinii, and Borrelia afzelii). Agents of animal
spirochetosis (Borrelia coriaceae
and Borrelia anserina) and species of
unknown pathogenicity (Borrelia miyamotoi and Borrelia lonestari)
were related to relapsing fever borreliae. Although the Lyme disease
borreliae, two related species (Borrelia japonica and Borrelia
andersonii), and some newly
described genomic groups (groups PotiB2,
VS116, DN127, Hk501, and Ya501) were closely related to each other, each
taxon formed an independent branch on the phylogenetic tree. The data
obtained in this study indicate that the flagellin genes are useful in
Borrelia taxonomy. To distinguish
the Lyme disease borreliae from related
organisms easily, we designed an oligonucleotide primer set for the
flagellin gene and performed a PCR-restriction fragment length
polymorphism (PCR-RFLP) analysis.
The primer set amplified an
approximately 580-bp DNA fragment
that included species-specific restriction sites,
and HapII, HhaI, CelII, HincII, or DdeI digestion of the product
resulted in distinctively different PCR-RFLP patterns. The PCR-RFLP
typing method which we developed
should facilitate rapid identification of
Lyme disease borreliae and related organisms obtained from biological
and clinical specimens. PMID: 8863416 [PubMed - indexed for
MEDLINE]
DURLAND FISH:
http://www.yale.edu/opa/v29.n29/story8.html "It is completely cryptic, which
means there is no way to diagnose
it," Fish says. "None of the Lyme disease
tests would detect an infection by this organism.
UNKNOWNS/COINFECTIONS (in addition
to viral, bacterial knowns)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12459246&dopt=Abstract J Microbiol Methods 2003
Feb;52(2):251-60
Application of
broad-range 16S rRNA PCR
amplification and DGGE fingerprinting for detection of
tick-infecting bacteria.
"Two sequences were related to the
yet to be cultivated
Haemobartonella. To our knowledge, Haemobartonella
has never been directly detected in
I. ricinus.
"In addition, members of the genera
Staphylococcus, Rhodococcus, Pseudomonas, and Moraxella were
detected, which have not been
identified in ticks so far.
"Two bacteria were most closely
related to a rickettsial
endosymbiont of an Acanthamoeba sp., and to an
endosymbiont (Legionellaceae,
Coxiella group) of the microarthropod
Folsomia candida.
MEDIA: Does BSK represent
reality?
http://peer1.nasaprs.com/peer_review/taskbook/micro/mg00/agreement.html Progress Report: We have conducted
multiple trials to explore the feasibility of cultivating the
Borrelia burgdorferi, under ex-vivo conditions in the RWV utilizing
human tissue substrates. We have
shown that RWV cultures: a) allow
maintained growth of low passage
Borrelia burgdorferi spirochetes in RWVs
(manuscript in preparation), b)
permit the colonization of human tissue
samples co-cultivated with the microorganisms (Figures 6 & 7) and
c) allow exponential increases in
the numbers of spirochetes in far
greater numbers compared to current methods existing in the literature.
Numerous experiments were done utilizing controls, inhibition
steps, and culture medium trials
with and without the RWV, with the best
results obtained using human
tonsillar tissue substrates and RPMI medium
for growth up to 28-30 days. Tissue biopsies from patients with Lyme
disease have been cultured in RWVs
to look for proliferation of
spirochetes in primary infected
tissue. The RWV has also been used to culture
normal human tissues with Borrelia,
to study the infection process.
======
It's quite simple: Borrelial
infections in humans can't be fully described, regardless of one's need
to be an Insurance Company Reviewer, or Prinicipal Investigator of a
lipoprotein vaccine for one strain
of B. burgdorferi. Host selection
pressures, coinfections, the
inherent "instability" of the genus, unknown
coinfections, phage-vectored plasmid exchange, resistence, morphological
forms, incompletely descibed vector-ranges and vector competence,
global warming, and the inherently unpredictable response in any human
individual, don't support the notion:
http://www.umdnj.edu/umcweb/hstate/aut96/aug96lym.html
"The clinical manifestations of Lyme
disease are now well described. It is not, and has never been, a mimic
of all syndromes and diseases."
Silliness.
Kathleen M. Dickson 23 Garden Street Pawcatuck, CT 06379
|
----- Original
Message ----- |
| From |
Kathleen
<kathleen.dickson@SNET.Net> |
| Date |
Fri, 14 Feb 2003 09:34:20
-0500 |
| To |
Arthur.Weinstein@Medstar.net |
| Subject |
[ILADS] Re: Leonard Sigal 2 |
Arthur.Weinstein@Medstar.net
wrote: > > Kathleen > > Without entering into polemics and
personalities, the only issue I
would > make is that one cannot always
infer that persistent or recurrent
symptoms > are caused by persistent or
recurrent infection. There are
many examples > in medical illness, including
other infectious diseases, where a
percentage > of patients develop chronic
symptoms and yet the original
trigger, be it an > organism or other, has been
eradicated from the body. The
mechanism of > this clinical phenomenon is in
many cases ill understood and
efforts should > be made to study it so that
rational, scientifically-based
treatment can be > administered. > > Arthur Weinstein, MD > Professor of Medicine > Georgetown University Medical
Center > Director, Section of Rheumatology,
#2A-66 > Washington Hospital Center > 110 Irving St, NW > Washington, DC 20010 > Tel: 202-877-6274 > Fax: 202-877-6130 > Pager #5412
My statement on the state of the
illness is attached.
You will find I agree with you that
infection alone is not a/the primary disorder.
The fact is Lenny has used the
following statements to characterize us: "Lyme Anxiety", "Munchausens's",
"Antibiotics are Poison", "Aporology", "Unexplained
Medical Illness", "Catatrophizing", "Women and girls
should not be told they have Lyme disease"...
Another important fact is that you
"validated" the Fibromyalgia Impact Questionaire
to be used by Klempner in his NIH "study"; this
was performed/reported AFTER the study was started, and it
showed the etiologies were different. So that is not
a validation.
We also know that you thought you
had to come down to Valhalla and teach people about
seroassay for Lyme antibodies, and that you said
Dressler/Steere (Dearborn IgG) was valid, because
loud blots are loud.
People in their right minds want
their disease to be detected and treated. That
would *mean* increase sensitivity. That would *mean*
loud blots being loud is... not thinking of the best
interest of the patients.
We know you were on the Dearborn
Committee to approve Dressler, and we know this was not a
consensus, although participants who were invited, were
led to believe it would be a consensus meeting.
This is not hearsay.
If you want to talk about other
illnesses that are similar to Lyme, I am sure you
always execute the validated clinical analyses, some of
which are listed in the attached management
plan, to determine objectively, pathophysiology.
The point is exactly, to do
otherwise, to pretend your expertise in clinical exam
gives you license to transcends into the domain of
unsubtantiated, pathophysiologically, psychiatric
syndromes, and that people can't detect the fallacy
in this, means your Rheumatology Mates have a
harder row to hoe, in terms of re-establishing any
respect for your genre.
We patients have done more good,
have helped more Fibromyalgia/CFIDS patients, than
any Rheumatologist in CT, and that may be true for New
York as well.
It's not that tough. We just
help. We care. I think that may give you some
consideration over whether or not were are somatizing,
preoccupied with symptoms, ... or whatever other
characterizations Rheumatologists seem to have in mind
for a therapeutic strategy.
I agree with what you say above:
"Lyme disease" is not simply a spirochetal
infection. It's not like, a "septic arthritis in the
knee", as Klempner says. *You* may believe it is
so, because your mates, and Steere, defined it that way in
order to sell a few vaccines, and to bring business to
L2 Diagnostics and Imugen. If you want to
maintain that Lyme disease is a simple as a boo-boo, why does the
ALDF have such well-positioned (on Wall Street) individuals on its
Board of Directors? Why is Ray Dattwyler's
office/Company/Biotaech Incubator in the same place as NYBA.org
Administrative Offices? Why is Kemp Hannon against OPMC
reform?
Because Borreliosis and related Gold
Mines of Biotechnology truely cannot be defined. In
the case of Lyme disease, a spirochetal infection became 5 of
10 bands and a knee. Field studies showed 22-25% accuracy
of Dressler. The vaccine was 76% "safe" and
"effective". Because 100- (22-25) of the data was
thrown out. ("Unconfirmed Lyme")
Politically. Only. Falsely. To suit the intended outcome of the
biocommercial product. And Lenny is the
MouthPiece. And it is no surprise to us, that you might
try to defend him.
First, Do No Harm.
When you start demonstrating a
respect for patients, humans, you may gain some self
respect.
Perhaps you can start with "What
does OspA do in an Asymptomatic infection?"
And answer that honestly.
Kathleen Dickson
|
----- Original
Message ----- |
| From |
Kathleen
<kathleen.dickson@SNET.Net> |
| Date |
Fri, 14 Feb 2003 09:44:52
-0500 |
| To |
Arthur.Weinstein@Medstar.net |
| Subject |
[ILADS] I forgot... This is
Sigal_1... was...Re: Leonard
Sigal 2 |
Since you are a blot expert, what
happened here, and why did the trials go forward?
http://www.journals.uchicago.edu/CID/journal/issues/v31n1/991200/991200.html (Sigal, Persing, Molloy and Berardi)
"Since specimen quantities were
available, representative study
subjects were also tested by FDA-licensed
ELISA and WB kits for descriptive
and comparative purposes, ***making no
claim or attempt to formally
validate or invalidate these tests'
performances for vaccinated study subjects.***"
"Even when investigators are
familiar with this phenomenon,
problems with interpretation of test results
may arise in those situations when a vaccinated subject actually becomes
infected with B. burgdorferi (i.e., a vaccine failure)"
The manufacturer of the only
currently FDA-approved (and
released) recombinant OspA Lyme disease
vaccine has suggested that
vaccination does not interfere with serological
evaluation of Lyme disease in vaccine recipients [?] ***a
statement that is not supported by
the data presented here.***
Arthur.Weinstein@Medstar.net wrote: >
> Kathleen > > Without entering into polemics and
personalities, the only issue I
would > make is that one cannot always
infer that persistent or recurrent
symptoms > are caused by persistent or
recurrent infection. There are
many examples > in medical illness, including
other infectious diseases, where a
percentage > of patients develop chronic
symptoms and yet the original
trigger, be it an > organism or other, has been
eradicated from the body. The
mechanism of > this clinical phenomenon is in
many cases ill understood and
efforts should > be made to study it so that
rational, scientifically-based
treatment can be > administered. > > Arthur Weinstein, MD > Professor of Medicine > Georgetown University Medical
Center > Director, Section of Rheumatology,
#2A-66 > Washington Hospital Center > 110 Irving St, NW > Washington, DC 20010 > Tel: 202-877-6274 > Fax: 202-877-6130 > Pager #5412
|
----- Original
Message ----- |
| From |
Kathleen
<kathleen.dickson@SNET.Net> |
| Date |
Fri, 14 Feb 2003 17:55:29
-0500 |
| To |
ILADS@yahoogroups.com |
| Subject |
[EuroLyme] Leonard Sigal 3 |
"Aporia. No way out, nothingness,
or the impenetrable. It is something which is not porous which cannot
leak. The interlocutors in the early Platonic dialogues cannot get out of
the dead-ends into which Socrates leads them. They are in aporia;
hence, the locution "aporetic" dialogues, the early dialogues where
there seems to be no positive result."
We *definitely* know who's stuck in
a loop around here, and it isn't the
patients:
SIGAL:
http://ehpnet1.niehs.nih.gov/docs/2002/suppl-4/607-611sigal/abstract.html
Lyme disease is a relatively
well-described infectious disease
with multisystem manifestations. Because
of confusion over conflicting reports, anxiety related to
vulnerability to disease, and sensationalized and inaccurate lay
media coverage, a new syndrome, "chronic Lyme disease," has become
established. Chronic Lyme disease is the most recent in a continuing
series of "medically unexplained symptoms" syndromes. These
syndromes, such as fibromyalgia,
chronic fatigue syndrome, and multiple
chemical sensitivity, meet the need
for a societally and morally acceptable
explanation for ill-defined symptoms in the absence of objective physical
and laboratory findings. We describe factors involved in the
psychopathogenesis of chronic Lyme disease and focus on the confusion
and insecurity these patients feel, which gives rise to an inability to
adequately formulate and articulate their health concerns and to deal
adequately with their medical needs,
a state of disorganization termed
***aporia***. Key words: aporology, chronic Lyme disease, Lyme disease,
medically unexplained symptoms, misdiagnosis, psychological,
psychopathogenesis. Environ Health
Perspect 110(suppl 4):607-611 (2002).--
We all are aware of the motive for
shifting borreliosis into the catagory
"Medically Unexplained"- Declare "Chronic Lyme Disease" to be
an entity with no markers, no evidence, such that no
discovery is attempted, and therefore no medical treatment
or cost to Managed Care.
It's already been established that
Sigal has drawn in terms like Munchausens and
so forth, but a short history of the confusion
Sigal has spun, and why his problems have been
apparently projected into patients:
"It could be the fibromyalgia, but
you cannot assume it is Lyme disease. Or it could be Lyme disease, but you should not
assume it is the fibromyalgia": -Leonard H. Sigal, MD, in American
Journal of Medicine, vol. 98, suppl. 4A "Tertiary neuroborreliosis can be
differentiated from the early disseminated neurological disease by the fact
that it is later, very frequently in association with inflammatory joint disease, but
quite frequently it will be on its
own, and sometimes it will be the very first
manifestation of Lyme disease": -Leonard H. Sigal, MD, Chief,
Division of Rheumatology, Robert
Wood Johnson Medical School, New Brunswick, N.J., in his
paper read at Yale's 6th Annual Lyme Disease Symposium, June 16, 1993
"Lyme disease, although a problem,
is not nearly as big a problem as most people think." The bigger epidemic," Dr.
Sigal said, "is Lyme anxiety." And,
he said, "even if you get the disease, it is easily
treatable and it is curable."
- Leonard H. Sigal, MD, Quoted by
Gina Kolata in New York Times, June 13, 2001
NEW YORK TIMES QUOTE OF THE DAY:
"Antibiotics are Poison"-- Lenny
Sigal (6-13-01)
======= "In practicing medicine we must
demand objective findings to
diagnose patients; we must develop and
use diagnostic criteria; and we must include the possibility of
intercurrent disease or evolution of
the process in our ongoing analysis of
patients. ...
...A new diagnosis has emerged,
"pseudo-LD", to coin a term.
It describes the certainty that LD is present
when there is no verifiable evidence
of disease."
-- From "Bulletin on the Rheumatic
Diseases"; a Publication of the ARTHRITIS FOUNDATION; Vol.44, No.8, December
1995---- SIGAL
As Sigal was an author of this
http://www.acponline.org/lyme/calculator/
we wonder how helpful it is to use
this analytical method to discover the
objective source of the medical disorder for
which the patient seeks treatment?
Sigal has produced several articles
on the immunological effects of borreliosis, and these
were mentioned previously (anti-41, IL-1, etc)
Annu Rev Immunol 1997;15:63-92
Lyme disease: a
review of aspects of its immunology
and immunopathogenesis. Sigal LH.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9143682&dopt=Abstract
CYTOKINES AND THE BRAIN:
http://www.life.uiuc.edu/neuroscience/343/PDF/cytokines.pdf
http://bioinformatics.weizmann.ac.il/cytokine/news1_01/brain.html
The markers of illness, the markers
identified in borreliosis, the markers
discussed by Lenny Sigal do have an effect on affect and
consciousness.
It's just not acceptable any more,
to declare an emerging clinical syndrome an
emotional disorder.
In a time of bioweapons threats, is
not sane health policy.
This is what the respectable
researchers in the field of mental disorders are doing:
http://www.scripps.edu/newsandviews/e_20021216/bloom2.html
It's real research. It's not
lay media attention-seeking, sensationalizing behavior ("Antibiotics are Poison").
These people do not serve the insurance industry.
=========== The Lyme vaccines were not qualified
with a valid standard. CDC Dearborn criteria are
inaccurate, and the Dearborn meeting was not a consensus meeting.
"Lyme disease" is 5 of 10 band on a Western blot because this
allowed the false "qualification" of vaccines, and
allowed allows for denial of care, routinely, by those
performing reviews for insurance companies and in legal
testimony:
http://www.geocities.com/HotSprings/Oasis/6455/conrail.txt
http://ourworld.compuserve.com/homepages/frankd/Sigal2.htm
We're tired of it. We would
like him assessed for his abilities to perform a valuable
service in the role of a "Healing Profession".
The final insult had had to be that he denies calling us
"crazy".
http://ehpnet1.niehs.nih.gov/docs/2003/111-2/correspondence.html
"Nowhere in our article (Sigal and
Hassett 2002) do we minimize or devalue the pain or suffering of
patients with chronic Lyme disease
nor do we state that such patients are
"crazy" or "delusional." "
That's all he's ever done.
"Aporia. No way out, nothingness, or
the impenetrable. It is something which is not porous which cannot
leak. The interlocutors in the early Platonic dialogues cannot get out of
the dead-ends into which Socrates leads them. They are in aporia;
hence, the locution "aporetic" dialogues, the early dialogues where
there seems to be no positive result."
Kathleen Dickson |