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What I told the Albany New York Legislators in Nov 2001

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Peenies, Peenies, Peenies, My Name is Chuck and I love McSweenies'

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Subject:
What I told the Albany New York Legislators in Nov 2001
Date:
Wednesday, December 27, 2006 11:09:50 AM

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Public Servants? Human Rights Activism is insanity, says AAG Jessica
Gauvin. But you should see the way she dresses. She must belong to
the
New-Hair-Color-a-Month Club, too. 'A classic floozy and very bizarre
creature,
but then we learned DCF Floozies is not an extraordinary phenomenon:
http://www.actionlyme.org/SOCIAL_WORKER_WHORING_STARTS_IN_COLLEGE.htm
The guys on UseNet remark about college days and the Schools of "Social
Work."
One of them writes:

"Overheard at one party:

"Brother A - surveying the crowd - "Man, what a herd of porkers"

"Brother B - "But they <blank>, man, they <blank> !"

http://www.actionlyme.org/RAGAGLIA_GRANDJURY_DETAILS.htm
Ho ho ho...

(Oh, and I was right the first time, it should be Phylum and not Order)
====================================================================
*** ALBANY, November, 2001
ASSEMBLY COMMITTEE ON HEALTH
CORRECTED VERSION 7/14/02 Replaced Phylum with Order (see Lynn
Margulis' work)
Richard N. Gottfried Chair
Lara Kassel
Legislative Associate
Assembly Member Gottfried's office
822 Legislative Office Building
Albany, NY 12248

From: ActionLyme, International Patient Advocacy Group, by K. M.
Dickson
ActionLyme Mission: To influence planning and policy in Vector Borne
Diseases
founded upon a complete presentation of the dynamic and extensive
evidence of
both spirochetal diseases, in general, and Borreliosis, more
specifically, in
humans.
Introduction:
"Lyme disease" is infectious arthritis in a joint, with a high antibody
response
(i.e, 5 of 10 bands on a Western Blot), according to the CDC. It is
culturable
Borrelia burgdorferi organisms from joint fluid.
Neuroborreliosis, or Lyme borreliosis is the chronic neurologic illness
that is
more commonly, and historically, (i.e., before Lyme, CT's Polly Murray
discovered a cluster of juvenile arthritis) associated with spirochetal

infections of mammals. The simplest analogy is tertiary syphilis, a
late
neurologic spirochetal illness.
It is extremely uncommon for there to be a spirochetal infection that
results in
joint inflammation alone. "Lyme
disease" may be unique among spirochetal infections, in that respect.
Part I.
VALIDATION OF THE SCIENCE
In answer to the question, "Do the NY OMPC investigated Lyme treating
physicians
have valid reason to believe Lyme borreliosis is a persisting
infection, such
that they treat and retreat Lyme Borreliosis according to methods that
match the
extensive evidence of how spirochetal microbes in general, and Borrelia

burgdorferi, in particular, behave," ActionLyme has provided a
summary of
scientific articles which support not only the Borreliae as persisting
organisms, but support the ruggedness and persistence of the
representatives of
the entire Order Spirochaetales against environmental extremes,
including
chemical or antibiotics.
Part I of this ActionLyme response, examples of persistence from
Nature, are
only part of the picture of persistence across the Order. The greater
bulk of
confirming scientific publications are available to be read on the
ActionLyme website:
http://actionlyme.50megs.com/OPMC.htm

In summary, Spirochetes are capable of:
-Morphological changes- spheroplast or "cyst" form, which is
infectious/regenerates to intact form
-Dessication or near-Dessication
-Antimicrobial resistance-gene sharing, via plasmid
-Lateral gene transfer
-Intracellular persistence resulting in immune and antibiotic evasion
(Klempner)
-Antigenic variation resulting in immune evasion
-Freezing. Lyme patients cannot donate blood, per the Red Cross
-Porins- >> Confer resistance to antimicrobials, are possibly
superantigens

Spirochetes do not behave like other bacteria. They are their own
Order, the
next degree of taxonomic classification under the Animal Kingdom is
Class
considerable uniqueness from other bacteria (Linnaean System: Kingdom,
Phylum,
Class, Order, Family Genus, Species)..

Part II is a summary of publications and testimony on "Autoimmunity" in

Neuroborreliosis. The argument that treatment-resistant Lyme arthritis
is an autoimmune
disorder is commonly known, although still a
hypothesis; there is a known association to T cell haplotypes, or the
genetic
code for Major Histocompatibility Complex class II "antigens", or
antigen-presenting molecules in autoimmune disease and in autoimmune
Lyme
arthritis. Simply put, people with HLA-DR4 or -DR2, the
arthritis-prone
individuals, tend to have a high antibody response and prolonged and
extensive
joint inflammation from B. burgdorferi, or, they have "Lyme disease".

There are now 2 known associations with persistent Neuroborreliosis as
an
autoimmune disorder, HLA-DR1*1501 and HLA-DQB1*0602, which are the two
primary
class II haplotypes associated with Multiple Sclerosis. Klempner found
that
Chronic Lyme patients tend to have this *0602 haplotype much more than
would be
expected, and therefore, believes may be a correlate in this illness.
This
discovery was not reported in the New England Journal last summer. It
is still
a hypothesis, that these antigen-presenting molecules have "molecular
mimicry"
or similarity to, and attack self, but there
is an increased prevalence of at least one of these two haplotypes
expressed in
Multiple Sclerosis/Lyme and is therefore, now a current area of
discovery.

Multiple Sclerosis is a Central Nervous System disease. Lyme
borreliosis
patients have been accused of exhibiting behavior that is not rational
(Steere),
neurotic (Weld), may be Munchausen and Munchausen-by-Proxy (Sigal),
paranoid
(Schoen), anxious (Shapiro), ignorant (Benach), neuropsychiatric
illness without
objective evidence (Klempner), etc.,...

Rather than publicly stating that Lyme borreliosis patients have a CNS
disorder,
rather than providing the evidence of the association in MS haplotypes,
rather
than providing the evidence in the pathophysiology that these
researchers have
found, this data is withheld, and instead, it is publicly suggested
that
Neuroborreliosis patients exhibit severely psychopathology.

It is said, by these researchers, that Neuroborreliosis symptoms are
"vague", but
actually, they are only "vague" when the physician
doesn't look at symptoms with the available objective tools.

"Lyme disease" is not vague. A swollen, red knee does not require
anything more
than human eyes to detect. It is Lyme borreliosis, that requires more
sophisticated perceptive abilities and analytical equipment.

The medical and social respect, care, and deference given to MS, Lupus,

Narcolepsy, HIV and other neurological patients are being denied Lyme
borreliosis patients. Instead, these researchers invoke the stigma of
mental
illness as a deliberate means to deny the validity of our complaints
and our
access to treatment for a medical condition. This denial of 1) our
basic human
dignity and 2) access to medical care for a medical condition, are
Human Rights
Abuses.

Whether Lyme borreliosis becomes a form of Multiple Sclerosis, or Lyme
borreliosis is a cause of multiple sclerosis in the absence of
persisting
organism, or that any infectious cause of Multiple Sclerosis is either
persisting
infection or is true autoimmunity, are subjects of
current scientific debate.

The evidence in Neuroborreliosis is that spirochetes persist past
antibiotic
treatment. The evidence is that patients have one of three outcomes:
1) Lyme
arthritis and high antibody response, 2) signs of infection resolve and
the
patient becomes asymptomatic, 3) patients develop a chronic neurologic
syndrome
clinically indistinguishable from Multiple Sclerosis.

It is scenario 3 that Lyme treating physicians treat, primarily; the
chronic
fatigue/ chronic musculoskeletal/ chronic neurocognitive disorder. That
they
treat with longer antimicrobial therapies than would meet with the
intentions of
Managed Care bottom line, is because the evidence from the Order is
that
spirochetes do not behave like other bacteria- they undergo physical
changes
which protect them from enviromental extremes.

We have no data that says spirochetal infections are not persistent.
There is
no specific antibiotic cure for Borreliosis, nor are there any specific
antibiotic
cures for Syphilis,
Leptospirosis, or Brachyspirosis. That is the state of the science:
There is
no specific, targeted, antibiotic known to kill all these organisms in
any
mammal.
ActionLyme will provide evidence from the scientific research that,
indeed,
Neuroborreliosis results in a CNS disease with similarities to Multiple

Sclerosis, and is the presence of real pathology, rather than is a
psychogenic/hypochondriacal syndrome.

Table of Contents: (HARD COPY of these will be hand-delivered Tuesday
Nov 27 to
Assembly)
Part I. THE CAUSE OF CHRONIC NEUROBORRELIOSIS, Evidence from Nature.
The Order,
on persistence.
1) "Composite, large spirochetes from microbial mats: spirochete
structure
review."
Morphological changes may be responsible for relapsing, persisting
illness.
http://www.pnas.org/cgi/reprint/90/15/6966.pdf
2) "Conversion of Borrelia garinii cystic forms to motile spirochetes
in vivo."
Transfer of the spheroplast results in infection.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11478686&dopt=Abstract
3) "Effects of Penicillin, Ceftriaxone, and Doxycycline on Morphology
of
Borrelia burgdroferi"
Conversion to spheroplast may not be the end stage.
http://aac.asm.org/cgi/reprint/39/5/1127.pdf
4) - "The Complexity of Vector-borne Spirochetes (Borrelia spp)"
Willy Burgdorfer 12th International Conference on Lyme Disease and
Other
Spirochetal and Tick-Borne Disorders April 9, 1999 Keynote Address
Dr. Burgdorferi recognizes the older data on morphological variants.
http://www.medscape.com/medscape/cno/1999/lyme/Story.cfm?story_id=534
5) "Detection of Borrelia burgdorferi DNA by polymerase chain reaction
in
synovial fluid from patients with Lyme arthritis."- Steere
Standard antimicrobial therapy does not kill all spirochetes. The
longer the
therapy, the lower the DNA concentration in Lyme arthritis.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8272083&dopt=Abstract
6) "Fibroblasts protect the Lyme disease spirochete, Borrelia
burgdorferi, from
Ceftriaxone in vitro."-- Klempner
14 days exposure to ceftriaxone does not kill all B. burgdorferi due to

intracellularity of the organism.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1634816&dopt=Abstract
7) "Relapsing Fever-Treatment and Control" Chapter by Jay P.
Sanford, from
Biology of Parasitic Spirochetes, Academic Press, 1976, edited by
Russell C.
Johnson Jay P. Sanford, Uniformed Services University School of
Medicine,
Bethesda, Maryland p. 390
"There are aspects of the treatment of relapsing fever, syphilis,
leptospirosis
that illustrate similarities and from which therapeutic principles may
be
developed. The ability of borrelia, especially tick-borne strains, to
persist
in the brain and in the eye during remission after treatment with
arsenic or
with penicillin or even after apparent cure is well known (1). The
persistence
of treponemes after
treatment of syphilis is a major area which currently requires
additional study
(3,5,10,11)."
8) "Central nervous system manifestations of Lyme disease." -Duray,
Steere,
Pachner
Brain biopsy from patient with subacute Lyme encephalitis produced an
organism
morphologically compatible with B. burgdorferi. It appears spirochetes
infect
human brain tissue.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2742551&dopt=Abstract
9) "In vivo activities of Ceftriaxone and Vancomycin against Borrelia
spp. in
the mouse brain and other sites." - Barbour
After 7 days delay, vancomycin treatment failed to eradicate Borrelia
from the
brains of immune compromised mice.
http://aac.asm.org/cgi/reprint/40/11/2632.pdf

Part II. THE EFFECT OF NEUROBORRELIOSIS
Multiple Sclerosis and Persisting Infection? Evidence from the
laboratory.
(More, again, on the ActionLyme website.)
1) Martin (NIH) and T cells and HLA-DR1*1501:
"Identification of candidate T-cell epitopes and molecular mimics in
chronic
Lyme disease"
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v5/n12/full/nm1299_1375.html
2) Klempner (Tufts) quoting Martin (NIH), "Is it thee or
me?-autoimmunity in
Lyme disease"
Autoreactive T cells to human nerves.
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nm/journal/v5/n12/full/nm1299_1346.html
3) Klempner to Rhode Island Doctors and HLA-DQB1*0602
South County Hospital, "Diseases of Summer Conference", July, 2001
What was discovered, but not published in NEJM
The validity of the Fibromyalgia Impact Questionnaire or SF-36 as
assessment
tools for outcomes of standard treatment, over re-examining and
re-reporting
cerebrospinal fluid Matrix- Metalloproteinases- enzymes seen in the
pathophysiology of Multiple Sclerosis, and previously reported by
Klempner in
Neuroborreliosis patients.
See separate pages ___;Bransfield/Brand Rebuttal to Klempner, July 12,
NEJM.
4) "Matrix metalloproteinases in the cerebrospinal fluid of patients
with Lyme neuroborreliosis."
Klempner reports MMPs- enzymes found in the CSF of Multiple Sclerosis
patients,
as well as Borreliosis patients.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9466528&dopt=Abstract
5) "Clonal expansion is a characteristic feature of the B-cell
repertoire of
patients with rheumatoid arthritis"
B cells and "Autoimmunity"- The picture involves more than T cells.
It could
be there is continually presented antigen- from somewhere.
http://arthritis-research.com/content/2/1/50
6) "Lyme Disease and the Clinical Spectrum of Antibiotic Responsive
Chronic
Meningoencephalomyelitides"
Ken Liegner's autopsy results. Many sad stories. Probably not
psychogenic.
http://www.medscape.com/SLACK/JSTD/1997/v04.n03/jst0403.04.lieg/jst0403.04.lieg-01.html
7) THE EARLY HISTORY OF LYME TREATMENT:
At one time, all of the Authors of the IDSA Guidelines, except Durland
Fish who
is an entomologist, believed there was evidence to provide longer
treatment. See
"Early Treatment History Data" set.
Page___
8) So where are we? Some researchers are still dedicated, despite the

harassment by the OPMC and similar controlling entities elsewhere in
the US, and
the frustrations of dealing with Managed Care, to figuring out how to
help
patients with borreliosis. There were two studies completed in the
United
States that have shown improvement with longer term therapy; outside
imaginary,
and as yet, un-validated, standards of care. One is an ongoing study
by Dr.
Brian Fallon of Columbia, See: http://www.columbia-lyme.org/
a) "Repeated Antibiotic Treatment in Chronic Lyme Disease"- Fallon, et
al.
http://www.medscape.com/SLACK/JSTD/1999/v06.n04/std0604.02.fall/std0604.02.fall-01.html
b) "Tetracycline therapy for chronic Lyme disease." Sam T. Donta,
Boston
University School of Medicine, Infectious Diseases Faculty.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9233665&dopt=Abstract

Mark Klempner, Tufts, to Rhode Island Doctors: South County Hospital,
"Diseases of Summer
Conference", July, 2001
What was discovered, but not published in NEJM. An audio transcript.

"Um, There, these patients obviously, are very, very much interested in
that
question, as we are, and I just want to highlight a preliminary piece
of data of
where we think we're going from here, unpublished*, and not for large,
uh,
dissemination, but here is the preliminary data.

And, that is, that when you look for the possibility of an autoimmune
disease,
the best way to look is to see if there is any genetic clustering in
HLA
haplotypes. The reason for that is the way antigens get presented in
the context
of who you are, that is, your HLA haplotype. And we can talk in some
detail
about that. Those diseases that I think everybody would agree are so
called
Autoimmune: lupus, rheumatoid arthritis, type 1 diabetes, and perhaps
MS, have
some clear genetic clustering that leads us to believe that these are
indeed
autoimmune diseases, although we do not satisfy so-called co-postulates
of
autoimmune disease that
we've written about. And the odds ratio for your having that
particular HLA
type, in the case of Rheumatoid arthritis, a DR4. Or a DQB0602 to
protect you
from type 1 diabetes, are on the order of 3 to 6. One of the ones
that is
probably highest, of course, is B27, in patients with alkyloiding
spondolytis
and the like. It turns out that if you lo
ok at the first 51 patients with post- treatment chronic Lyme disease,
the
patient population that participated in our study, there was a very
high
incidence of DQB0602 with an odds ratio of 770%. So it may well be
that
exposure to THAT organism with THAT background of HLA haplotype may
lead you to
develop chronic symptoms. That is a hypothesis that needs to be
tested. It
would obviously lead to an entirely new form and approach to therapy."

"There were also many outcomes that were done in the laboratory. I
won't focus
that much on them. They are still a focus of great interest for us.
And that is
these serial plasma samples for PCR, at the dates that
I mentioned here to try to determine if we could pick up sequestered
infectious
organisms. Urine samples on multiple days for antigen testing and I'll
comment
on perhaps at the end of there's time, about the Lyme Urine Antigen
Test- what
we found in that regard. Um, a new test that we're still working on,
looking in
the spinal fluid for a particular matrix-metalloproteinase, a CSF
gelatinase,
which I won't have time to comment on. We published on this before,
we're still
looking at it, and it may be an interesting marker in these patients."


Early Treatment History Data set

TITLE: Treatment of Lyme disease., Schoen RT, Conn Med 1989
Jun;53(6):335-7
ABSTRACT: Lyme disease, a tick-transmitted spirochetal infection, can
be divided
into three stages that can overlap or occur alone. The goals of
antibiotic
therapy in stage one are to shorten the duration of early disease and
to prevent
the development of later stages of the illness. This can usually be
accomplished
with oral antibiotic therapy.
Later stages of the illness are frequently more difficult to treat,
requiring
prolonged oral or intravenous antibiotic therapy.

Dattwyler and Luft
TITLE: A perspective on the treatment of Lyme borreliosis., Luft BJ;
Gorevic PD;
Halperin JJ; Volkman DJ; Dattwyler RJ, Department of Medicine,
University of
New York, Stony Brook 11794-8153. SOURCE: Rev Infect Dis 1989
Sep-Oct;11 Suppl
6:S1518-25
ABSTRACT: Lyme borreliosis has become the most common tick-borne
infection in
the United States. Although both beta-lactam and tetracycline
antibiotics have
been shown to be effective in the treatment of this spirochetosis, the
development of optimal therapeutic modalities has been hampered by the
lack of
reliable microbiologic or immunologic criteria for the diagnosis or
cure of this
infection. In vitro sensitivity studies have been performed by several
laboratories, but there has been no standardization of the methodology
for
measuring either inhibitory or bactericidal levels. Clinical studies
have documented the
efficacy of antibiotics, but therapy has failed in as many as 50% of
cases of
chronic infection. Although new antibiotic regimens appear promising,
the
optimal treatment of this infectious disease remains to be determined.
In this
report we review the clinical and experimental rationale for the
antibiotic
regimens that we currently use and the need for a more standar
dized approach to treatment trials.

CONTRAST quote to New York Times by Dattwyler:
"In contrast, antibiotics have been shown to work extraordinarily
well when, for
instance, the Lyme organism has demonstrably infected the brain, Dr.
Dattwyler
said."

Coyle

TITLE: Seronegative chronic relapsing neuroborreliosis [see comments],
Lawrence
C; Lipton RB; Lowy FD; Coyle PK, Department of Medicine, Albert
Einstein
College of Medicine, New York, N.Y., USA. Eur Neurol 1995;35(2):113-7
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.

Coyle on long term effects

TITLE: Cognitive functioning in late Lyme borreliosis [see comments],
Krupp LB;
Masur D; Schwartz J; Coyle PK; Langenbach LJ; Fernquist SK; Jandorf L;
Halperin
JJ, Department of Neurology, State University of New York, Stony Brook
11794.,
Arch Neurol 1991 Nov;48(11):1125-9
ABSTRACT: Lyme borreliosis, a tick-borne multisystem disease, may cause
a
variety of neurologic complications, including meningoencephalitis and
encephalopathy. To evaluate neurobehavioral function following treated
Lyme
borreliosis, 15 patients with Lyme disease and complaints of persistent
cognitive
difficulty a mean of 6.7 months following antibiotic treatment
underwent
neuropsychological evaluation and were compared with 10 healthy
controls,
matched in aggregate for age and education, who underwent the identical

neuropsychological assessment. Compared with controls, patients with
Lyme
disease exhibited marked impairment on memory tests and particularly on

selective reminding measures of memory retrieval. The memory impairment
did not
correlate with serum or cerebrospinal fluid anti-Borrelia burgdorferi
antibody
titers and was not explained by magnetic resonance imaging findings or
depression. The cause of this encephalopathy is currently unknown;
however,
indirect effects of s
ystemic infection or other toxic-metabolic factors may be partly
responsible.


Wormser and Nadelman

TITLE: Isolation of Borrelia burgdorferi from the blood of seven
patients with
Lyme disease., Nadelman RB; Pavia CS; Magnarelli LA; Wormser GP:
Department of
Medicine, New York Medical College, Valhalia., Am J Med 1990
Jan;88(1):21-6
ABSTRACT: PURPOSE: Borrelia burgdorferi, the etiologic agent of Lyme
disease,
has rarely been successfully cultured from blood. We report on seven
patients
from Westchester County, New York, with B. burgdorferi bacteremia
diagnosed
between April 1987 and August 1987. PATIENTS AND METHODS: One hundred
thirty-two
attempts to isolate spirochetes were made on blood specimens obtained
from 104
patients. Twenty-two of these specimens were obtained from nine
patients who had
recently been bitten by Ixodes ticks but who were asymptomatic.
Heparinized
blood or serum specimens (0.2 to 0.4 mL) were inoculated onto 6 mL of
modified
Barbour-Stoenner-Kelly medium. Lyme serology was performed by
enzyme-linked
immunosorbent polyvalent, IgM, and IgG assays, fluorescent immunoassay,
and
microhemagglutination. RESULTS: Four of the seven patients had
erythema
migrans, two had facial nerve palsy, and one had a flu-like syndrome
without
rash. These patients represented 21% (four of 19) of all patients
with the characteristic skin lesion who had blood cultures for B.
burgdorferi, and 40%
(two of five) of all those with facial nerve palsy. Serologic testing
was
frequently nonreactive; two patients had no detectable antibody on
multiple sera
by five different assays. All patients improved with antibiotic
treatment, and
had negative subsequent blood cultures, but five of seven had
persistent
complaints after completion of therapy. CONCLUSION: Culturing blood
for B.
burgdorferi may be useful in confirming the diagnosis of Lyme disease
in
selected patients. Use of spirochete blood cultures may facilitate a
better
understanding of the pathogenesis and natural history of Lyme disease.

Wormser and Nadelman

TITLE: A clinical approach to Lyme disease., Nadelman RB; Wormser GP,
Department
of Medicine, New York Medical College, Valhalla., Mt Sinai J Med 1990
May;57(3):144-56
ABSTRACT: Lyme disease (also known as Lyme borreliosis) is an
emerging, newly
described infectious disease with diverse clinical manifestations. The
disease is
caused by the spirochetal agent Borrelia burgdorferi,
which is transmitted to humans by the bite of certain species of Ixodes
ticks
harboring the organism. The most readily identifiable clinical feature
is the
distinctive skin lesion, erythema migrans. If recently infected
patients go
untreated, approximately 15% will develop neurologic conditions (most
commonly
facial nerve palsy), 8% will develop myocarditis (typically with heart
block),
and 60% will develop migratory mono- or pauci-articular arthritis.
Diagnosis
depends on clinical suspicion, recognition of the characteristic signs
and
symptoms, and appropriate testing for antibody to B. burgdorferi.
Serology for
Lyme disease, although in need of better standardization, is most
useful in
diagnosing patients with manifestations of Lyme disease other than
erythema
migran
s. All manifestations of Lyme disease are potentially treatable with
either a
beta-lactam antibiotic (for instance penicillin, amoxicillin, or
ceftriaxone) or
a tetracycline preparation. However, the optimal antimicrobial regimen,
including
choice of drug, drug dose, route of administration, and length of
therapy, is
unknown. Other important areas for future research include Ixodes
biology and
control, improved laboratory tests for diagnosis and for assessing
response to
therapy, and vaccine development.

Rush

This study was about the treatment results of acute disseminated Lyme
disease,
which is within the first month of infection AND NOT DISSEMINATED INTO
THE CNS.
This is not a treatment study about Chronic Lyme disease. There are no
other
publications by this scientist other than the Guidelines and possibly
one on
AIDS.

TITLE: Ceftriaxone compared with doxycycline for the treatment of
acute
disseminated Lyme disease., Dattwyler RJ; Luft BJ; Kunkel MJ; Finkel
MF; Wormser
GP; Rush TJ; Grunwaldt E; Agger WA; Franklin M; Oswald D; Cockey L;
Maladorno D,
Department of Medicine, State University of New York, Stony Brook,
11794-8161,
USA., N Engl J Med 1997 Jul 31;337(5):289-94
ABSTRACT:
BACKGROUND: Localized Lyme disease, manifested by erythema migrans, is
Usually treated with oral doxycycline or amoxicillin. Whether acute
disseminated
Borrelia burgdorferi infection should be treated differently from
localized
infection is unknown. METHODS: We conducted a prospective, open-label,
randomized, multicenter study comparing parenteral ceftriaxone (2 g
once daily
for 14 days) with oral doxycycline (100 mg twice daily for 21 days) in
patients
with acute disseminated B. burgdorferi infection but without
meningitis. The
erythema migrans skin lesion was required for study entry, and
disseminated
disease had to be indicated by either multiple erythema migrans lesions
or
objective evidence of organ involvement. RESULTS: Of 140 patients
enrolled, 133
had multiple erythema migrans lesions. Both treatments were highly
effective.
Rates of clinical cure at the last evaluation were similar among the
patients
treated with ceftriaxone (85 percent) and those treated with
doxycycline (88 percent);
treatment was considered to have failed in only one patient in
each group. Among patients whose infections were cured, 18 of 67
patients i
n the ceftriaxone group (27 percent) reported one or more residual
symptoms at
the last follow-up visit, as did 10 of 71 patients in the doxycycline
group (14
percent, P > or = 0.05). Mild arthralgia was the most common persistent
symptom.
Both regimens were well tolerated; only four patients (6 percent) in
each group
withdrew because of adverse events. CONCLUSIONS: In patients with acute

disseminated Lyme disease but without meningitis, oral doxycycline and
parenterally administered ceftriaxone were equally effective in
preventing the
late manifestations of disease.


Rahn

TITLE: Treatment of Lyme disease., Steere AC; Green J; Hutchinson GJ;
Rahn DW;
Pachner AR; Schoen RT; Sigal LH; Taylor E; Malawista SE, Zentralbl
Bakteriol
Mikrobiol Hyg [A] 1987 Feb;263(3):352-6
ABSTRACT: We compared phenoxymethyl penicillin, erythromycin, and
tetracycline,
in each instance 250 mg four times a day for 10 days, for the treatment
of
early Lyme disease (stage 1). None of 39 patients given tetracycline
developed
major late complications compared with 3 of 40 penicillin-treated
patients and 4
of 29 given erythromycin (p = 0.07). However, with all three
antibiotic
agents, nearly half of patients had minor late symptoms. For neurologic

abnormalities (stage 2), 12 patients were treated with high-dose
intravenous
penicillin, 20 million U a day for 10 days. Pain usually subsided
during
therapy, but a mean of 7 to 8 weeks was required for complete recovery
of motor
deficits. For the treatment of established arthritis (stage 3), 20
patients were
assigned treatment with intramuscular benzathine penicillin (7.2
million U) and
20 patients received saline. Seven of the 20 penicillin-treated
patients (35%)
were apparently cured, but all 20 patients given placebo contin
ued to have attacks of arthritis (P less than 0.02). Of 20 arthritis
patients
treated with intravenous penicillin G, 20 million U a day for 10 days,
11 (55%)
were apparently cured.
Thus, all 3 stages of Lyme disease can be treated with antibiotic
therapy, but
some patients with late disease may not respond.

Rahn, Steere, Schoen

TITLE: Treatment of refractory chronic Lyme arthritis with
arthroscopic
synovectomy. Schoen RT; Aversa JM; Rahn DW; Steere AC, Department of
Medicine,
Yale University School of Medicine, NewHaven,Connecticut 06510.,
Arthritis Rheum
1991 Aug;34(8):1056-60
ABSTRACT: Of 20 patients who underwent arthroscopic synovectomy for
refractory
chronic Lyme arthritis of the knee, 16 (80%) had resolution of joint
inflammation during the first month after surgery or soon thereafter,
and they
have remained well during the 3-8-year followup period. Three of these
16
patients who were more disabled preoperatively, still had mild
functional
limitation at long-term followup. The remaining 4 patients (20%) had
persistent
or recurrent synovitis. We conclude that arthroscopic synovectomy is
effective in
treating chronic Lyme arthritis in patients in whom the disease does
not respond to antibiotic therapy.

----Kathleen M. Dickson

--
http://www.actionlyme.org

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