Injustice and the 2 Lone Wolves
Mort Zuckerman
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Subject: Injustice and the 2 Lone Wolves
Date: Dec 12, 2009 5:45 AM
I would like everyone to notice
that the only 2 MDs who really mattered
in Blumenthal's lawsuit were Liegner, who
performed the autopies on the dead Lyme
victims, and whose body parts tested
positive BY THE CROOKS! vua staining or
PCR for Borrelia after repeated treatments:
http://www.actionlyme.org/BRAIN_PERMANENT.htm
(#13)
http://www.actionlyme.org/CDC_Spirochetes_Brain_Liegner_Autopsy.htm
and Dr. Donta, who was basically kicked
off the 2000 IDSociety.org Lyme Guidelines
panel for insisting they include a chapter
on "Chronic Lyme" - which the Lyme crooks
have *all* written about at one time or another
in those exact terms, "Chronic Lyme":
http://www.actionlyme.org/080430_RICO_CABAL_CAVES.htm
http://www.actionlyme.org/Schoen.htm
are the two most important sci/med MDs/researchers
and who do *not* belong to ILADS.org.
That would be because they're too valuable
to belong to a retarded clique like ILADS.org
Nevertheless, we're still waiting for justice
but that won't happen because ILADS doesn't
even understand how the science is bogus-
how the *testing* is bogus.
There is only one place in the world where
you can see the FULL TEXT of what Allen
Steere did in Europe to falsify the
diagnostic standard for "Lyme Disease."
There are 2 articles:
Steere in Europe
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
and the Dressler/Steere article:
http://www.actionlyme.org/DICKSON_FDA_SUBMISSION_FULL.htm
Those two reports are bogus science.
Those two reports show Allen Steere
used recombinant OspA&B antigens in
GERMAN patients, and that his G39/40
and FRG strains were "high passage" which
was UNRECOMMENDED both by the NIH and
the CDC for use in Human Western Blotting:
http://www.actionlyme.org/Dearborn_Who_Approved.htm
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
No one in the entire US or European medical
world has reported on these FACTS: 1) that
the diagnostic standard for Lyme Disease
was falsified in Europe, and 2) that what
Allen Steere did alone in Europe with
funky illegal strains and antigens is not
something you can see in a US journal, free
full text. You have to either go to a good
medical library or order these reports and
pay for them.
No American MD has done it.
No American MD is competent to do it.
No American MD is competent to find out
what happened, such that we now have this
ridiculous test where you have to have a
20 ton paper elephant (too many antibodies
but no other illness signs), in order to be
diagnosed with a disease, but you can't be
diagnosed with the 10 ton real elephant
(Neuroborreliosis or Relapsing Fever or
"Lyme Borreliosis" or Pam3Cys Immune Dysregulation
Complex), despite a scientifically
validated test for it (US patent 5,618,533)
existing and being owned by Yale.
To me, that is amazing. There is *no*
MD in the *entire* United States who is
competent to understanding how such
testing is performed. No one at the
NIH and no one at the FDA, either, despite
these analytical validation guidelines
belonging to the FDA:
http://www.relapsingfever.org/index.htm
'And despite all the money supplied to these
crooks by the NIH and the CDC.
Nobody can say to the USDOJ, "Look, this
is not how it is done. There is no such
thing as 'Receiver Operating Characteristic'
in the real world:
http://www.relapsingfever.org/index.htm
"What does 'receiver operating characteristic'
mean?
"Does the 'receiver' even have to show that
his eyes have been calibrated?
"Allen Steere himself reported that Lyme
was a Relapsing Fever organism and that
'New IgM' meant the disease, the infection,
'the organisms were not killed by
antibiotics,' yet in the New Allen Steere
standard (CDC/Dearborn), he threw out that claim:
http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
"How in the world does one simply throw
out the means to the proof that a sick person
has an infection - the IgM antibodies?"
- - -
Nobody in the entire UDSA has the nuts
or the brains to say that to the USDOJ.
No MD in America can say to the USDOJ,
"Look, they falsified the diagnostic standard
to falsify their vaccines outcomes and to
deny the existence of a disease that needs
intravenous ceftriaxone, and this little
enterprise, the ALDF.com happened to originate
at NYMC, which is Kaiser-Permanente's new New
England Forward Base. This is a RICO. This
is an enterprise. They use coercion, false
reporting to Medical Boards,
http://www.actionlyme.org/OPMC_CORRUPTION.htm
the pinheaded pitbulls, the "Child Protective
Services"
http://www.actionlyme.org/MUNCHAUSENS.htm
http://www.actionlyme.org/HOWE_BBC_SCIENCE_EVIDENCE.htm
the *SLUTTY, DRUNKEN, DRUGGIE,* pinheaded pitbull
"CPS":
http://www.actionlyme.org/CRYME_DISEASE.htm
http://www.actionlyme.org/GAUVIN_DEATH_PENALTY.htm
(The crazy bitch Jessica Gauvin ^^ et al illegally
refused to FOI me all her emails about myself or
Donald G. Dickson because they would contain some
correspondence from some certain people we know should
not be involved in the false allegations against myself
by Nancy E. Martin and the "sociopath," Donald G. Dickson
http://www.actionlyme.org/Hilarious.htm
http://www.actionlyme.org/THE_REAL_DON_DICKSON.htm
Donald resented having to pay Child Support.
'A pair of jealous pinheads who did not appreciate
my growing notoreity in the sci-med world:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
)
and Color of Law tactics to blow off their
competition."
Nobody can say that to the USDOJ.
No MD in America can look at the "data"
that Steere produced, drive their little
asses to the nearest USDOJ office and say,
"This is FRAUD; this is a mass-murder crime.
This is NOT how science is done.
Allen Steere went to Europe! to falsify
this standard."
That's pretty amazing given that they're
now going to regulate nanotechnology so
that none of these little nanometer machines
gets away from them. Meanwhile, we can't
detect "Lyme Disease?" (Borreliosis)
There will be *DETECTORS*/FILTERS for these
nanobots that have to be the size of the bots
themselves or smaller, but no one in America
can figger out how to tell if antibodies
come from spirochetes?
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm
or discover a DNA method?
http://www.actionlyme.org/PRIMERSHELLGAME.htm
Or rediscover one that's been in use by
the crooks, themselves since 1992:
GARY WORMSER, 1992:
http://jcm.asm.org/cgi/reprint/30/12/3082?view=long&pmid=1452688
"Nucleotide sequence accession number. The sequences for
B. burgdorferi 16S and 23S rRNA genes have been deposited
in GenBank with accession numbers M88329 and M88330,
respectively."
1992.
???
That 16S and 23S RNA test was ever used again in
human antibiotic treatment trials of either "Lyme
Disease" *or* Lyme Borreliosis. This gang only
uses this 16S/23S RNA method when they want to
run to the US Patent Office- when they want to
patent a new organism, but NOT EVER AGAIN to
determine if people are sick from these
organisms, or if treatment failed.
This real test for the outcomes of
antibiotic treatment (outside the Mouse
Infectivity Test, which IDSA members have
referenced, meaning they read this report
http://www.actionlyme.org/IDSA_CYST_VIAHLE.htm
has never since been used to determine if
antibiotic treatment succeeded or failed,
since 1992, when Gary Wormser proved that
2/9 patients treated for tick attachment
failed the treatment (as it says in that
report).
No MD in America can wrap their brains
around it.
Amazing.
Kathleen M. Dickson
-------------------
FROM "THE LYME DISEASE DILEMMA," A
FORMER GEOCITIES WEBSITE, CREATED
in NOVEMBER 2001:
What the Authors of the Guidelines forgot about CLD and PLS
Persistent neuroborreliosis, or the Post-Lyme Syndrome (PLS) or
Chronic
Lyme Disease (CLD), as formerly reported by the authors of the IDSA
Guidelines, who now say "there is insufficient evidence to regard
'chronic Lyme disease' as a separate diagnostic entity", and PLS is a
"poorly defined" entity. Steere will be considered in chapters 5-8.
[Note: Schoen not an author of the Guidelines, but is a scientific
advisor to the ALDF.]
TITLE: Treatment of Lyme disease.
AUTHORS: Schoen RT
SOURCE: Conn Med 1989 Jun;53(6):335-7
CITATION IDS: PMID: 2667887 UI: 89337699
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.
AUTHORS: Luft BJ; Gorevic PD; Halperin JJ; Volkman DJ; Dattwyler RJ
AUTHOR AFFILIATION: Department of Medicine, University of New York,
Stony Brook 11794-8153. SOURCE: Rev Infect Dis 1989 Sep-Oct;11 Suppl
6:S1518-25
CITATION IDS: PMID: 2682965 UI: 90048527
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 standardized approach to treatment trials.
Coyle
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.
Coyle on long term effects
TITLE: Cognitive functioning in late Lyme borreliosis [see comments]
AUTHORS: Krupp LB; Masur D; Schwartz J; Coyle PK; Langenbach LJ;
Fernquist SK; Jandorf L; Halperin JJ
AUTHOR AFFILIATION: Department of Neurology, State University
of New York, Stony Brook 11794.
SOURCE: Arch Neurol 1991 Nov;48(11):1125-9
CITATION IDS: PMID: 1953395 UI: 92061616
COMMENT: Comment in: Arch Neurol 1992 Oct;49(10):1011
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 systemic infection or other toxic-
metabolic
factors may be partly responsible.
more here:
http://www.lymenet.de/literatur/niches.htm
Wormser and Nadelman
TITLE: Isolation of Borrelia burgdorferi from the blood of seven
patients with Lyme disease.
AUTHORS: Nadelman RB; Pavia CS; Magnarelli LA; Wormser GP AUTHOR
AFFILIATION:
Department of Medicine, New York Medical College, Valhalia.
SOURCE: Am J Med 1990 Jan;88(1):21-6
CITATION IDS: PMID: 2294761 UI: 90102528
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.
AUTHORS: Nadelman RB; Wormser GP
AUTHOR AFFILIATION: Department of Medicine, New York Medical
College,
Valhalla.
SOURCE: Mt Sinai J Med 1990 May;57(3):144-56 CITATION IDS: PMID:
2196462 UI: 90318435
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 migrans. 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. 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.
AUTHORS: Dattwyler RJ; Luft BJ; Kunkel MJ; Finkel MF; Wormser GP;
Rush
TJ; Grunwaldt E;
Agger WA; Franklin M; Oswald D; Cockey L; Maladorno D
AUTHOR AFFILIATION: Department of Medicine, State University of New
York, Stony Brook, 11794-8161, USA.
SOURCE: N Engl J Med 1997 Jul 31;337(5):289-94, CITATION IDS: MID:
9233865 UI: 97365037
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 in 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.
AUTHORS: Steere AC; Green J; Hutchinson GJ; Rahn DW; Pachner AR;
Schoen RT; Sigal LH;
aylor E; Malawista SE
SOURCE: Zentralbl Bakteriol Mikrobiol Hyg [A] 1987 Feb;263(3):352-6
CITATION IDS: PMID: 3109144 UI: 87237041
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 continued 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.
AUTHORS: Schoen RT; Aversa JM; Rahn DW; Steere AC
AUTHOR AFFILIATION:
Department of Medicine, Yale University School of Medicine, New
Haven,Connecticut 06510.
SOURCE: Arthritis Rheum 1991 Aug;34(8):1056-60,CITATION IDS: PMID:
1859481 UI: 91315620
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.
So, 20 patients 7 still not recoveed.
I guess it depends on which side of 65 % you are on, as regards
efficacy
of this treatment.
-------------------------------------
TITLE: Fate of Borrelia burgdorferi DNA in tissues of infected mice
after antibiotic treatment [see comments]
AUTHORS: Malawista SE; Barthold SW; Persing DH
AUTHOR AFFILIATION: Department of Internal Medicine, Yale University
School of Medicine, New Haven, Connecticut.
SOURCE: J Infect Dis 1994 Nov;170(5):1312-6
CITATION IDS: PMID: 7963735 UI: 95052860
COMMENT: Comment in: J Infect Dis 1995 May;171(5):1379-80
ABSTRACT: Persistence of Borrelia burgdorferi DNA in tissues
following
antibiotic treatment
was evaluated in C3H mice inoculated intradermally with 10(3) B.
burgdorferi N40
or sterile medium. Half of the infected mice and all of the uninfected
mice were treated with ceftriaxone 15 days after inoculation for 5
days.
Ear and urinary bladder samples were collected on days 20, 30, and 60
after inoculation for culture and for
extraction of DNA and amplification of specific spirochetal DNA by
polymerase chain reaction (PCR). PCR primers were specific for a 280-
bp
portion of a highly conserved region of the gene encoding outer
surface
protein (Osp) A of B.
burgdorferi and for a 328-bp part of the OspB gene. There was
excellent
concordance
between culture and PCR for ears (35/36 mice) and bladders (33/36).
Both
tissues became uniformly negative at the earliest interval tested
after
antibiotic treatment. Thus, the ability to amplify B. burgdorferi DNA
quickly disappeared from tissues
that had become culture-negative after antibiotic treatment,
suggesting
that serial study of PCR-positive tissues and fluids may be useful for
evaluating the efficacy of antibiotic therapy in human Lyme disease.
We patients know peripheral spirochetes can be cleared, but as shown
by
Alan Barbour, it is the spirochetes in the brain and CNS that are
giving
us the most trouble:
TITLE: Localization of Borrelia burgdorferi in the nervous system and
other organs in a nonhuman primate model of lyme disease.
AUTHORS: Cadavid D; O'Neill T; Schaefer H; Pachner AR AUTHOR
AFFILIATION:
Department of Neuroscience, University of Medicine and Dentistry of
New
Jersey-New Jersey Medical School, Newark 07103, USA.
SOURCE: Lab Invest 2000 Jul;80(7):1043-54
CITATION IDS: PMID: 10908149 UI: 20363441
ABSTRACT: Lyme borreliosis is caused by infection with the spirochete
Borrelia burgdorferi.
Nonhuman primates inoculated with the N40 strain of B. burgdorferi
develop infection of multiple tissues, including the central (CNS) and
peripheral nervous system. In immunocompetent nonhuman primates,
spirochetes are present in low numbers in tissues. For this reason, it
has been difficult to study their localization and changes in
expression
of surface proteins. To further investigate this, we
inoculated four immunosuppressed adult Macaca mulatta with 1 million
spirochetes of the N40 strain of B. burgdorferi, and compared them
with
three infected immunocompetent animals and two uninfected controls.
The
brain, spinal cord,
peripheral nerves, skeletal muscle, heart, and bladder were obtained
at
necropsy 4 months later. The spirochetal tissue load was first studied
by polymerase chain reaction (PCR)-ELISA of the outer surface protein
A
(ospA) gene.
Immunohistochemistry was used to study the localization and numbers of
spirochetes in tissues and the expression of spirochetal proteins and
to
characterize the inflammatory response. Hematoxylin and eosin and
trichrome stains were used to study inflammation and tissue injury.
The
results showed that the number of spirochetes was significantly higher
in immunosuppressed animals. B. burgdorferi in the CNS localized to
the
leptomeninges, nerve roots, and dorsal root ganglia, but not to the
parenchyma. Outside of the CNS, B. burgdorferi localized to
endoneurium
and to connective tissues of peripheral nerves, skeletal muscle,
heart,
aorta, and bladder. Although ospA, ospB, ospC, and flagellin were
present at the
time of inoculation, only flagellin was expressed by spirochetes in
tissues 4 months later. Significant inflammation occurred only in the
heart, and only immunosuppressed animals had cardiac fiber
degeneration
and necrosis. Plasma cells were abundant in inflammatory foci of
steroid-treated animals. We concluded that B. burgdorferi has a
tropism
for the meninges in the CNS and for connective tissues elsewhere in
the
body.
Barbour
TITLE: In vivo activities of ceftriaxone and vancomycin against
Borrelia spp. in the mouse
brain and other sites.
AUTHORS: Kazragis RJ; Dever LL; Jorgensen JH; Barbour AG
AUTHOR AFFILIATION:
Department of Medicine (Infectious Diseases), University of Texas
Health
Science
Center at San Antonio 78284, USA.
SOURCE: Antimicrob Agents Chemother 1996 Nov;40(11):2632-6
CITATION IDS: PMID: 8913478 UI: 97070552
ABSTRACT: Borrelia burgdorferi, the agent of Lyme disease, and B.
turicatae, a neurotropic
agent of relapsing fever, are susceptible to vancomycin in vitro, with
an MIC of 0.5
microgram/ml. To determine the activity of vancomycin in vivo,
particularly in the
brain, we infected adult immunocompetent BALB/c and immunodeficient
CB-17 scid mice with B. burgdorferi or B. turicatae. The mice were
then
treated with vancomycin, ceftriaxone as a positive control, or normal
saline as a negative control.
The effectiveness of treatment was assessed by cultures of blood and
brain and other tissues. Ceftriaxone at a dose of 25 mg/kg of body
weight administered every 12 h for 7 to 10 days eliminated cultivable
B.
burgdorferi or B. turicatae from all BALB/c or scid mice in the study.
Vancomycin at 30 mg/kg administered every 12 h was effective in
eliminating infection from immunodeficient mice if treatment was
started
within 3 days of the onset of infection. ***If treatment with
vancomycin
was
delayed for 7 days or more, vancomycin failed to eradicate infection
with B. burgdorferi or B. turicatae from immunodeficient mice. The
failure of vancomycin in eradicating established infections in
immunodeficient mice was associated with
the persistence of viable spirochetes in the brain during antibiotic
treatment.***
The experiment regarding efficacy of antibiotics in the the non-human
primate model including non-immunocompromized animals infected with Bb
and left untreated for one month or more has not been
performed. Therefore, there is no non-human primate experimental
model
of the post-Lyme Syndrome.
Right now there are two NIH studies underway which address treatment
of
"Chronic Lyme".
We patients hope the NIH and CDC know that Chronic Lyme is not a
separate diagnostic entity. They might be mad about all the nearly 10
million dollars they are spending on these two studies.
They might also be mad about all the grant money they've handed out so
far to study the Post-Lyme Syndrome. We wonder how one asks for a
grant for an entity that does not exist.
Many of Steere's Chronic Lyme NIH grant study patients are the chronic
Lyme arthritis kind of Lyme disease patient, and not the late
relapsing/persisting neuroborreliosis patients.
These studies are not complete and Steere's will not be about
neuroborreliosis, specifically.
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"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci