No Conspiracy? Did someone say no conspiracy?

Hmmmm.

What did Weinstein mean when he said:

http://www.actionlyme.com/CONNOLLY_FISH_WEINSTEIN.htm

"The College has recognized that Lyme disease is a major clinical and
research interest on this campus. The main players in the development
of the program were Fish, Wormser and Connolly," Dr. Weinstein
advises. ***The entrepreneurial trio are*** Durland Fish, Ph.D.,
former director of the College's Lyme Disease Center and now a
research scientist at Yale; Gary P. Wormser, M.D., still professor of
medicine and pharmacology and chief of the Division of Infectious
Diseases at the College; and John J. Connolly, Ed.D., former College
president and current chairman of the board of the American Lyme
Disease Foundation, Inc., which had its genesis on the Valhalla campus
in 1990.

And John Connolly?

- - - - 

That was after the 1989 Infectious Disease Reviews, which said:

1: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1518-25.  

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.

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.

Publication Types:
    Review
    Review, Tutorial

PMID: 2682965 [PubMed - indexed for MEDLINE]



2: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1505-10.  

Isolation techniques for spirochetes and their sensitivity to
antibiotics in
vitro and in vivo.

Johnson RC.

Department of Microbiology, University of Minnesota Medical School,
Minneapolis.

Leptospira interrogans can be cultured from blood and cerebrospinal
fluid during
the first week of leptospirosis and from urine thereafter. Studies of
in vitro
sensitivity indicate that these organisms are sensitive to most
antibiotics.
Tetracycline and penicillin G are most often used clinically, although
laboratory studies suggest that the bactericidal activity of
penicillin G may be
inadequate. Treponema pallidum cannot be satisfactorily cultured. It
is
identified by dark-field microscopy. Studies of in vivo sensitivity
show that
penicillin G is highly active against the syphilis pathogen. Since
syphilis and
gonorrhea may occur simultaneously, ceftriaxone, which is as active as
penicillin G against T. pallidum but is also active against
penicillinase-producing gonococci, is a logical choice for therapy.
Borrelia
burgdorferi has been cultured from the blood, cerebrospinal fluid, and
skin of
patients with Lyme disease. In vitro studies have shown tetracycline
and
erythromycin to be effective against B. burgdorferi and penicillin G
to be less
so, although all are commonly used clinically. Ceftriaxone has also
proven to be
highly effective in laboratory studies and for clinical treatment.

Publication Types:
    Review
    Review, Tutorial

PMID: 2682963 [PubMed - indexed for MEDLINE]



3: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1499-504.  

Erratum in:
    Rev Infect Dis 1990 May-Jun;12(3):566.

Abnormalities of the nervous system in Lyme disease: response to
antimicrobial
therapy.

Halperin JJ.

Department of Neurology, State University of New York, School of
Medicine, Stony
Brook 11794.

Objective measures of neurologic function were used to assess response
to
treatment in patients with late Lyme borreliosis. Neurophysiologic
evidence of
peripheral neuropathy was present in 64 of 137 patients tested.
Measures of
distal axon function (sensory amplitude and conduction velocity, motor
terminal
latency) were most affected. Repeat studies following 60 patients
receiving
antimicrobial therapy demonstrated significant improvement in these
values.
Before and after therapy 17 patients with late Lyme borreliosis and
prominent
subjective cognitive dysfunction underwent neuropsychologic tests of
memory,
conceptual ability, concentration, psychomotor function, overlearned
intellectual abilities, and mood. Significant abnormalities were
evident before
treatment; all reversed with antimicrobial therapy. Many patients with
this
encephalopathy had specific abnormalities revealed by magnetic
resonance imaging
of the brain and had evidence of intrathecal synthesis of antibody to
Borrelia.
These findings indicate that late Lyme borreliosis commonly causes
nervous
system abnormalities that are reversible with appropriate antibiotic
therapy.

Publication Types:
    Review
    Review, Tutorial

PMID: 2682962 [PubMed - indexed for MEDLINE]



4: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1494-8.  

Immunologic aspects of Lyme borreliosis.

Dattwyler RJ, Volkman DJ, Luft BJ.

Department of Medicine, State University of New York School of
Medicine, Stony
Brook 11724-8161.

Immune responses to Borrelia burgdorferi infection are now well
characterized.
Following infection there is an early T cell response and a more
slowly evolving
B cell response. IgM antibodies appear first and are followed by IgG
and IgA.
Early antibodies are primarily against a 41-kilodalton
flagellum-associated
antigen; responses to other spirochetal antigens develop later.
Serologic assays
that use whole B. burgdorferi preparations are not always able to
detect an
early rise in antibodies above a background of crossreactive
antibodies present
in most uninfected individuals. Moreover, some individuals with
neurologic
involvement who lack diagnostic levels of serum antibody to B.
burgdorferi have
high levels of the antibody in their cerebrospinal fluid. Specific T
cell
blastogenesis to B. burgdorferi can further document infection.
Analysis of T
cell subsets in Lyme arthritis demonstrates a marked decrease in the
CD4+2H4+
subpopulation in the synovial fluid, although normal numbers of these
cells are
present in peripheral blood. Immunologic measurements are useful in
evaluating
and treating a wide array of patients who may be infected with B.
burgdorferi.

Publication Types:
    Review
    Review, Tutorial

PMID: 2682961 [PubMed - indexed for MEDLINE]



5: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1482-6.  

Neurologic manifestations of Lyme disease, the new "great imitator".

Pachner AR.

Department of Neurology, University Hospital, Georgetown University
Medical
School, Washington, D.C. 20007.

The causative agent of Lyme disease, Borrelia burgdorferi, is a highly
neurotropic organism that not only can produce symptomatic neurologic
disease
but also can exist dormant within the central nervous system (CNS) for
long
periods. Two distinct types of neuroborreliosis occur at different
stages of
Lyme disease. Second-stage Lyme meningitis resembles aseptic
meningitis and is
often associated with facial palsies, peripheral nerve involvement,
and/or
radiculopathies. Lyme meningitis may be the first evidence of Lyme
disease,
occurring without a history of erythema chronicum migrans or flu-like
illness.
Third-stage parenchymal involvement causes a multitude of nonspecific
CNS
manifestations that can be confused with conditions such as multiple
sclerosis,
brain tumor, and psychiatric derangements. Manifestations of CNS
parenchymal
involvement in Lyme disease are generally associated, however, with a
history of
erythema chronicum migrans, meningitis, or carditis. Both second- and
third-stage Lyme neuroborrelioses are commonly misdiagnosed because
they are
relatively uncommon and because they mimic many better-known
disorders.

Publication Types:
    Review
    Review, Tutorial

PMID: 2682960 [PubMed - indexed for MEDLINE]



6: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1470-4.  

The molecular biology of Borrelia.

Barbour AG.

Department of Medicine, University of Texas Health Science Center, San
Antonio,
Texas 78284.

Borrelia burgdorferi, the cause of Lyme disease, has two major
outer-membrane
proteins, OspA and OspB, which act as surface antigens. A 49-kilobase
linear
plasmid contains the genes that encode for these surface proteins.
Direct
examination of denatured plasmid molecules has revealed
single-stranded circles
with a circumference of approximately 100 kilobases (about twice the
length of
the linear duplex molecule), a finding that indicates the plasmid
strands have
covalently closed ends. This form of DNA, while present in eukaryotic
organisms
and their viruses, has not been observed in a prokaryotic organism.
Plasmid
heterogeneity has been observed in strains with surface proteins of
similar
molecular weights and similar monoclonal antibody reactivity. Thus,
plasmid
analysis may prove a sensitive tool for differentiating strains of B.
burgdorferi. Furthermore, since loss of plasmids in vitro has been
correlated
with loss of the ability of many-passaged strains to cause infection,
borrelial
plasmids may encode for virulence factors as well.

Publication Types:
    Review
    Review, Tutorial

PMID: 2682959 [PubMed - indexed for MEDLINE]



7: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1460-9.  

Epidemiology and clinical similarities of human spirochetal diseases.

Schmid GP.

Division of Sexually Transmitted Diseases, Centers for Disease
Control, Atlanta,
Georgia 30333.

Lyme disease, first identified in 1975, is the most recently
recognized of the
seven human spirochetal diseases; the evolving clinical picture of
Lyme disease
indicates it shares many features with the other diseases. These
similarities
are striking in view of the diverse epidemiology of the seven
diseases, which
are caused by Treponema species (spread by human-to-human contact) or
Leptospira
or Borrelia species (zoonoses). These similarities include the
following: (1)
skin or mucous membrane as portal of entry; (2) spirochetemia early in
the
course of disease, with wide dissemination through tissue and body
fluid; and
(3) one or more subsequent stages of disease, often with intervening
latent
periods. Lyme disease shares with many spirochetal diseases a tropism
for skin
and neurologic and cardiovascular manifestations, whereas chronic
arthritis is
unique to Lyme disease. These similarities and dissimilarities offer
opportunities to discover which properties unique to the pathogenic
spirochetes
are responsible for clinical manifestations and suggest that certain
clinical
features of patients with spirochetal diseases other than Lyme disease
may
someday be recognized in patients with Lyme disease.

Publication Types:
    Review
    Review, Academic

PMID: 2682958 [PubMed - indexed for MEDLINE]



8: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1451-9.  

Epizootiology of Borrelia in Ixodes tick vectors and reservoir hosts.

Anderson JF.

Department of Entomology, Connecticut Agricultural Experiment Station,
New Haven
06504.

Four North American and two European species of Ixodes ticks harbor
borreliae.
Three of the North American species--Ixodes dammini, Ixodes
scapularis, and
Ixodes pacificus--and two Old World species--Ixodes ricinus and Ixodes
persulcatus--feed on a wide range of hosts, including humans; the
North American
Ixodes dentatus has a predilection for cottontail rabbits and rarely
parasitizes
humans. In Lyme disease foci in North America where I. dammini is
common,
Borrelia burgdorferi or similar types of spirochetes have been
cultured from 10
species of wild or domestic mammals and from one species of songbird.
The
prevalence of infected rodents is remarkably high (greater than or
equal to 75%)
in these foci. Several different antigenic variants of B. burgdorferi
have been
cultured. Initial isolates of B. burgdorferi in North America were
remarkably
homogeneous, but documentation of different variants is increasing.
The
association of different antigenic variants with diseases in humans
and domestic
animals needs to be clarified.

Publication Types:
    Review
    Review, Academic

PMID: 2682957 [PubMed - indexed for MEDLINE]



9: Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1442-50.  

Pathophysiology of the Lyme disease spirochete, Borrelia burgdorferi,
in ixodid
ticks.

Burgdorfer W, Hayes SF, Corwin D.

Laboratory of Pathobiology, National Institute of Allergy and
Infectious
Diseases, Hamilton, Montana 59840.

The pathophysiology of Borrelia burgdorferi, the Lyme disease
spirochete, is
unique in tick/vector relationships, differing substantially from that
of other
spirochetes, e.g., Borrelia duttonii, the agent of tick-borne
relapsing fever,
and Borrelia recurrentis, the agent of louse-borne relapsing fever, in
their
respective vectors. Following ingestion by a tick, B. burgdorferi
lodges in the
midgut diverticula, in some instances penetrating the gut wall and
invading
various tissues. Certain investigators suggest that transmission of
the
spirochete occurs via infectious saliva, although, in light of the
fact that
only 5% of adult ticks are systemically infected, this mechanism is
open to
question. Alternatively, transmission may occur via periodic
regurgitation of
gut fluids during the feeding process. While ticks of the genus Ixodes
were once
thought to be the only vectors, it now appears that other genera, and
possibly
other hematophagous arthropods, may also be involved.

Publication Types:
    Review
    Review, Tutorial

PMID: 2682956 [PubMed - indexed for MEDLINE]