Updated 170218
4.) The Primers Shell
Game –
using the right DNA and RNA to identify spirochetes to patent, but
using the wrong DNA/rDNA (the DNA known to not be
present) when assessing for spirochetes in humans.
http://www.actionlyme.org/2017_DNA_SHELL_GAME.pdf
Updates on Mechanisms of Illness, Baumgarth,
Chiu/Aucott, Duray, Rockefeller University (Lyme and LYMErix are incurable,
spirochetes target Lyme nodies, fungal antigens cause B cell
immortalizations), page 1
Background, “Clinical Violence” or “Deprivation of Rights via Color
of Law abuses”, page 14
I. Phage-vectored plasmids are variable DNA (like OspA); not to be used for
human disease, page 17
II. Borrelia Acquiring Sticky OspA, and OspA Sticking to Itself (falsified
vaccines reporting, blot smudging, Korean Chemists on OspA being sticky and
clumping) – page 19
III. Lyme spirochetes did not evolve naturally and are
closest to an African bird borreliosis, page 21
IV. Brain Permanence, Tropism and the Single Spirochete Infection
with resultant
MULTIPLE VARIANTS page 26
V. SIDESTEPPING - Alert on “Biofilms” page 32
VI. On using the correct DNA to look for spirochetes in
humans by using recombinant Borrelia-specific flagellin DNA product to
detect those specific antibodies page 33
VII. The FDA being forced to assure Lyme testing is valid according to FDA’s
own rules by the Senators (summer, 2014 1), page 33
VIII. SIDE-STEPPING - CDC’s Other Research Fraud: A) Lying about the
viability of the cyst or spheroplast form of spirochetes and B) lying about
mycoplasma not being involved in Chronic Fatigue Syndrome page 35
IX. The CDC Cabal Play the DNA and RNA Shell Game: Alan
Barbour, Durland Fish, Gary Wormser, Mark Klempner, Robert Schoen, and Allen
Steere page 36
X. The Guidelines – Who signed on to this perverted science and is
therefore responsible for endorsing this fraud? Page 57
2017 Update:
This charge sheet is a revision of the 2014 Criminal Charges Sheet called
the “DNA or Primers Shell Game.” Since that time we learned from Nicole
Baumgarth, et al, at UC Davis, and Chiu/Aucott at UCSF, that spirochetes go
right to the lymph nodes and destroy the B cell maturation or germinal
centers,… and that around half of all tick bite sepsis victims have long
term changes to their immune systems (despite claiming that it doesn’t
happen) and don’t recover:
PLoS Pathog. 2015
Jul 2;11(7):e1004976. doi: 10.1371/journal.ppat.1004976. eCollection 2015.
Suppression of
Long-Lived Humoral Immunity Following Borrelia burgdorferi
Infection.
Elsner RA1, Hastey
CJ1, Olsen
KJ2, Baumgarth N3.
“Lyme Disease caused by infection with Borrelia burgdorferi
is an emerging infectious disease and already by far the most common
vector-borne disease in the U.S. Similar to many other infections, infection
with B. burgdorferi results in strong antibody response induction, which can
be used clinically as a diagnostic measure of prior exposure. However,
clinical studies have shown a sometimes-precipitous decline of such
antibodies shortly following antibiotic treatment, revealing a potential
deficit in the host's ability to induce and/or maintain long-term protective
antibodies. This is further supported by reports of frequent repeat
infections with B. burgdorferi in endemic areas. The mechanisms underlying
such a lack of long-term humoral immunity, however, remain unknown. We show
here that B. burgdorferi infected mice show a similar rapid disappearance of Borrelia-specific
antibodies after infection and subsequent antibiotic treatment. This failure
was associated with development of only short-lived germinal centers,
micro-anatomical locations from which long-lived immunity originates. These
showed structural abnormalities and failed to induce memory B cells and
long-lived plasma cells for months after the infection, rendering the mice
susceptible to reinfection with the same strain of B. burgdorferi. The
inability to induce long-lived immune responses was not due to the
particular nature of the immunogenic antigens of B. burgdorferi, as
antibodies to both T-dependent and T-independent Borrelia antigens
lacked longevity and B cell memory induction. Furthermore, influenza
immunization administered at the time of Borrelia infection
also failed to induce robust antibody responses, dramatically reducing the
protective antiviral capacity of the humoral response. Collectively,
these studies show that B. burgdorferi-infection results in targeted and
temporary immunosuppression of the host and bring new insight into the
mechanisms underlying the failure to develop long-term immunity to this
emerging disease threat.”
https://www.ncbi.nlm.nih.gov/pubmed/26136236
And
MBio. 2016
Feb 12;7(1):e00100-16. doi: 10.1128/mBio.00100-16.
Longitudinal Transcriptome Analysis Reveals a
Sustained Differential Gene Expression Signature in Patients Treated for
Acute Lyme Disease.
Bouquet J1, Soloski
MJ2, Swei
A3, Cheadle
C2, Federman
S1, Billaud
JN4, Rebman
AW2, Kabre
B1, Halpert
R4, Boorgula
M2, Aucott
JN5, Chiu CY6.
“Lyme disease is a tick-borne illness caused by the
bacterium Borrelia burgdorferi,
and approximately 10 to 20% of patients report persistent symptoms lasting
months to years despite appropriate treatment with antibiotics. To gain
insights into the molecular basis of acute Lyme disease and the ensuing
development of post-treatment symptoms, we conducted a longitudinal
transcriptome study of 29 Lyme disease patients (and 13 matched controls)
enrolled at the time of diagnosis and followed for up to 6 months. The
differential gene expression signature of Lyme disease following the acute
phase of infection persisted for at least 3 weeks and had fewer than 44%
differentially expressed genes (DEGs) in common with other infectious or
noninfectious syndromes. Early Lyme disease prior to antibiotic therapy was
characterized by marked upregulation of Toll-like receptor signaling but
lack of activation of the inflammatory T-cell apoptotic and B-cell
developmental pathways seen in other acute infectious syndromes. Six months
after completion of therapy, Lyme disease patients were found to have 31 to
60% of their pathways in common with three different immune-mediated chronic
diseases. No differential gene expression signature was observed between
Lyme disease patients with resolved illness to those with persistent
symptoms at 6 months post-treatment. The identification of a sustained
differential gene expression signature in Lyme disease suggests that a panel
of selected human host-based biomarkers may address the need for sensitive
clinical diagnostics during the "window period" of infection prior to the
appearance of a detectable antibody response and may also inform the
development of new therapeutic targets.
https://www.ncbi.nlm.nih.gov/pubmed/26873097
The devil is in the details about this Chiu/Aucott
article:
"Importantly, Lyme disease
patients did not show any changes in the calcium-dependent T-cell apoptosis
pathway, in contrast to the marked downregulation observed in other
bacterial and viral diseases (Fig. 4B). In addition, an absence of
significant DEGs linked to B-cell development in Lyme disease relative to
other infections was observed. These findings suggest that Lyme disease may
be associated with a smaller proportion of B and T cells in peripheral blood
than other diseases. Interestingly, suppression of long-lived humoral
responses has been observed in a mouse model of Borrelia infection (31).
The absence of DEGs corresponding to B-cell maturation may also potentially
explain why prior infection with B. burgdorferi is associated with a
serological response yet does not appear to confer immunity to reinfection.
Certain alleles of HLA genes have been previously reported to be associated
with serological responses to Lyme disease infection (32). Here we found
that upregulation of certain HLA genes (HLA-DQA1, HLA-DQB1, HLA-DRB5) is
associated with seronegativity in Lyme disease and may thus constitute
potential diagnostic biomarkers for seronegative patients.
"Following the
acute phase of infection, recent treatment trials among patients with EM
have estimated that approximately 10 to 20% of patients treated for Lyme
disease experience lingering symptoms that may progress to PTLDS, although
the incidence can be as high at 50% (4). The pathogenetic mechanisms of
PTLDS remain unknown, but autoantigens and/or central nervous system
sensitization have been postulated to play a role (10, 33–35). In our study,
the relatively large proportion of posttreatment
Lyme disease patients with persistent
symptoms of fatigue, widespread musculoskeletal pain, and/or cognitive
dysfunction (13 [46.4%] of 28) can be potentially accounted for by more
stringent enrollment criteria at the time of presentation (requiring the
presence of EM and concurrent influenza-like symptoms rather than EM alone).
This may have resulted in the selection of patients with more severe disease
and thus with an increased likelihood of persistent symptoms (36). Of note,
according to the proposed formal case definition for PTLDS, which requires a
functional decline in patients in addition to lingering symptoms, only 4
(14.3%) of our 28 patients met all of the criteria, within the range of the
10 to 20% frequency reported in the literature (4).
”Notably, Lyme disease at 6 months
post-treatment (V5) had 60 and 31% of their predicted pathways
overall in common with SLE and RA, respectively. Circulating immune
complexes have been
identified as features common to all three
conditions (37, 38). Symptoms of fatigue and cognitive impairment occur in
a variety of chronic syndromes, including SLE, CFS, and PTLDS. Although
some pathways were common to Lyme disease at
V5 and CFS, melatonin signaling, prominent in CFS, was not predicted to be
involved in Lyme disease (Fig. 4D). As melatonin is a hormone that regulates
the circadian rhythms of the sleep-wake cycle and thus is strongly linked to
fatigue, the absence of increased melatonin signaling suggests that the
fatigue in Lyme disease patients with persistent symptoms is related to a
different mechanism. Overall, our results, showing only 18% of the DEGs and
34% of the pathways common to CFS and Lyme disease, are consistent with a
proteomic study of cerebrospinal fluid that clearly discriminates between
the two conditions (39).
In a news article about this report, this was said:
“Early Lyme disease
prior to antibiotic therapy was characterized by marked upregulation of
Toll-like receptor signaling but lack
of activation of the inflammatory T-cell apoptotic and B-cell developmental
pathways seen in other acute infectious syndromes,” wrote the
study’s authors. “Six months after completion of therapy, Lyme disease
patients were found to have 31 to 60% of their pathways in common with three
different immune-mediated chronic diseases. No differential gene expression
signature was observed between Lyme disease patients with resolved illness
to those with persistent symptoms at six months post-treatment.”
"Six months after
treatment, 15 of the 29 patients in the study had fully recovered, while 13
had persistent symptoms, and one had dropped out."
http://www.genengnews.com/gen-news-highlights/lyme-disease-may-be-diagnosable-via-transcriptome-signature/81252365/
The first thing Chiu, et al, do, in the actual journal report, is discount
the fairly extensive evidence that Lyme, yes is associated with B cell
changes and suppression of long lived immunity (Duray, Baumgarth, Dattwyler,
even Steere in the early days; see below). Secondly, he shows again the
association to the MS and Lupus HLAs that Klempner talked about, caught on
tape in the summer of 2001 at South County Hospital, Rhode Island, and that
means, essentially,“yes, probably EBV and/or the other herpesviruses are
reactivated.” These HLA-DQs are associated with MS and Lupus (active EBV, et
al). Thirdly, he falsely states that the sicker patients have fatigue
with EM, whereas in most cases, no one notices the EM because they are not
sick at the time it shows up.
The title of the Chiu/Aucott journal article basically
says there are changes to the “transcriptome” (which likely does not apply
to the condition we are talking about, immune blunting), and then says “not
really” in the details. In the news article they claim that half the tick
bite remain sick regardless of treatment. In the journal article they say
60% of the tick bite victims have the Lupus or reactivated EBV pathways in
common, and then they go off pooh-pah-ing Chronic Fatigue victims as having
a sleep disorder in the typically sinister way they discount people with
post tick bite sepsis.
What can everyone take away from this article? These
clowns discount what’s real and try to associate “Chronic Lyme” with the
mental disorder (“nervousness,” let’s say) of Chronic Fatigue Syndrome, when
they are both the same disease (post-sepsis) but acquired through different
immune assaults, probably. He also tries to maintain the false view that
“if you don’t have an autoimmune disease, you must have a mental illness.”
If you understand the real mechanisms of this illness,
whereby the uptake of fungal antigens (TLR2/1 agonists or triacyl
lipopeptides), causes “tolerance” or “lack of antigen processing or
inhibition of antigen processing,” and even B cell immortalization, we don’t
really think anyone should be concerned with “gene expression changes.” It
is enough to know about fungal antigen tolerance and cross tolerance or what
happens in post-septic shock from a tick bite.
OspA-ish antigens causing immune cell immortalization or inhibition of
apoptosis:
Cell Microbiol. 2007
Jan;9(1):142-53. Epub 2006 Aug 2.
“The inhibitory effect of Mycoplasma fermentans
on tumour necrosis factor (TNF)-alpha-induced apoptosis resides in the
membrane lipoproteins.”
Gerlic M1, Horowitz
J, Farkash
S, Horowitz
S.
“Mycoplasma have been shown to be involved in the
alteration of several eukaryotic cell functions, such as cytokine
production, gene expression and more. We have previously reported that
infection of human myelomonocytic U937 cell line with live Mycoplasma
fermentans (M. fermentans) inhibited tumour necrosis factor
(TNF-alpha)-induced apoptosis. Mycoplasmal membrane lipoproteins are
considered to be the most potent initiators of inflammatory reactions in
mycoplasmal infections. The aim of this study was to clarify whether the
inhibitory effect on TNFalpha-induced apoptosis is exerted by M. fermentans
lipoproteins (LPMf). A significant reduction in TNFalpha-induced apoptosis
was demonstrated by stimulation of U937 cells with M. fermentans total
proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide), but not with
M. fermentans hydrophilic protein preparation (AqMf). To investigate the
mechanism of M. fermentans antiapoptotic effect, the reduction of
mitochondrial transmembrane potential (delta psi m) was measured. M.
fermentans total proteins LPMf and MALP-2, but not AqMf, inhibited the
reduction of delta psi m. In addition, M. fermentans total proteins LPMf and
MALP-2, but not AqMf, downregulated the formation of active caspase-8.
NF-kappaB was transactivated in cells treated with M. fermentans
lipoproteins, and was essential for host cell survival, but not for the
inhibition of TNFalpha-induced apoptosis by LPMf. Our results suggest that
the inhibitory effect exerted by M. fermentans on TNFalpha-induced apoptosis
in U937 cells is due to the membrane lipoproteins of these bacteria.
https://www.ncbi.nlm.nih.gov/pubmed/16889623
OspA-ish antigens causing immune cell
immortalization or inhibition of apoptosis:
Curr Genomics. 2009
Aug;10(5):306-17. doi: 10.2174/138920209788920967.
Anti-apoptotic genes in the survival of monocytic
cells during infection.
Busca A1, Saxena
M, Kryworuchko
M, Kumar
A.
“Macrophages are cells of the immune system that protect organisms against
invading pathogens by fulfilling critical roles in innate and adaptive
immunity and inflammation. They originate from circulating monocytes and
show a high degree of heterogeneity, which reflects the specialization of
function given by different anatomical locations. Differentiation of
monocytes towards a macrophage phenotype is also accompanied by an increase
of resistance against various apoptotic stimuli, a required characteristic
that allows macrophages to accomplish their function in a stressful
environment.Apoptosis, a form of programmed cell death, is a tightly
regulated process, needed to maintain homeostasis by balancing proliferation
with cellular demise. Caspases, a family of cysteine proteases that are
highly conserved in multicellular organisms, function as central regulators
of apoptosis. FLIP (FLICE-inhibitory protein), anti-apoptotic members of the
Bcl2 family and inhibitors of apoptosis (IAP) are the main three groups of
anti-apoptotic genes that counteract caspase activation through both the
extrinsic and intrinsic apoptotic pathways. Modulation
of the apoptotic machinery during viral and bacterial infections, as well as
in various malignancies, is a well established mechanism that promotes the
survival of affected cells. The
involvement of anti-apoptotic genes in the survival of
monocytes/macrophages, either physiological or pathological, will be
described in this review. How viral and bacterial infections that target
cells of the monocytic lineage affect the expression of anti-apoptotic genes
is important in understanding the pathological mechanisms that lead to
manifested disease. The latest therapeutic approaches that target
anti-apoptotic genes will also be discussed.
M.tb also exploits TLRs to induce anti-apoptotic genes that enhance cell
survival and promote bacterial persistence [109]. Exploiting TLRs is not a
mechanism unique to M.tb. As mentioned earlier, we have shown that TLR3,
TLR4 and TLR9, when stimulated by their ligands PolyI:C, LPS and CpG DNA,
respectively, protected monocytic cells from HIV-Vpr induced apoptosis by
induction of NFκB and anti-apoptotic cIAP genes (unpublished data). Stimulation
of TLR2, found in abundance at sites of M.tb infection, by components of
M.tb cell wall, has been shown to protect human macrophages against
apoptosis. THP1-derived
macrophages when stimulated with 19kDa mycobacterial lipoprotein or
mannosylated LAM were shown to induce resistance to apoptosis via activation
of NFκB and subsequent induction of anti apoptotic cFLIP which inhibits
death receptor-mediated apoptosis [25, 109].”
http://www.ncbi.nlm.nih.gov/pubmed/20119528
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729995/?tool=pubmed
OspA-ish antigens causing immune cell immortalization or inhibition of
apoptosis:
Eur J Immunol. 1997
Sep;27(9):2450-6.
Mycobacterium bovis Bacillus Calmette Guérin
infection prevents apoptosis of resting human monocytes.
Kremer L1, Estaquier
J, Brandt
E, Ameisen
JC, Locht
C.
“Apoptosis plays an
essential role in the development and homeostasis of multicellular
organisms. Some infectious agents interfere with this programmed cell death
to their own benefit. Here, we show that infection of resting human
monocytes with Mycobacterium bovis Bacillus Calmette Guérin (BCG) increases
monocyte viability by preventing them from undergoing apoptosis. Heat-killed
BCG also prevented apoptosis, indicating that replication of BCG is not
required to prevent cell death. Analysis
of BCG-infected monocytes revealed an up-regulation of the A1 mRNA, whereas
the bcl-2 mRNA was not up-regulated. Interestingly, preinfection with BCG
renders the cells resistant to interleukin (IL)-10-induced apoptosis which
may be one of the mechanisms mycobacteria use to modulate immune responses. BCG
infection was also accompanied by an impairment of the capacity of monocytes
to secrete IL-10 and by an induction of the capacity to secrete tumor
necrosis factor-alpha, two cytokines known to induce and prevent human
monocyte apoptosis, respectively. Since
it has been reported that apoptosis is involved in killing of intracellular
mycobacteria, the prevention
of apoptosis may represent a strategy for mycobacterial survival in the
infected host.”
https://www.ncbi.nlm.nih.gov/pubmed/9341792
Gary Wormser saying – while LYMErix was still on
the market -, that how sick you become, depends on how much OspA you got
stuck with, either by ticks/spirochetes or syringe. You cant make this up:
“The
magnitude of modulation [immunosuppression – KMD] was directly dependent on
the quantity of OspA. OspA interferes with the response of lymphocytes to
proliferative stimuli including a blocking of cell cycle phase progression.”
– Gary Wormser:
FEMS Immunol Med Microbiol. 2000
Jul;28(3):193-6.
Modulation of lymphocyte proliferative responses by
a canine Lyme disease vaccine of recombinantouter surface protein A
(OspA).
Chiao JW1, Villalon
P, Schwartz
I, Wormser
GP.
“The
modulation of human lymphocyte proliferative responses was demonstrated with
a recombinant outer surface protein A (OspA) vaccine preparation for the
prevention of Borrelia
burgdorferi infection. After
exposure to either the unaltered vaccine preparation or OspA prepared in
saline, normal lymphocyte responses to the mitogens concanavalin A,
phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were
consistently reduced. Whole cell extracts of B.
burgdorferi also modulated
immune responses but required a much greater quantity of protein than needed
for the OspA preparation. The magnitude of modulation was directly dependent
on the quantity of OspA. OspA interferes with the response of lymphocytes
to proliferative stimuli including a blocking of cell cycle phase
progression. Future studies designed to delete the particular region or
component of the OspA molecule responsible for this effect may lead to
improved vaccine preparations.
“We have previously demonstrated that proteins of B. burgdorferi are capable
of modulating human cellular immune responses [7].
Suppression of in vitro mitogen- or antigen-mediated proliferative
responses of lymphocytes and reduced production of interleukin-2 (IL-2) from
lymphocytes were demonstrated using protein extracts of B. burgdorferi.
These early studies were confirmed by a report of de Souza et al. [8],
who observed that B. burgdorferi infection in mice resulted in impaired T
and B cell proliferation to mitogens and reduced IL-2 and IL-4 production.
The nature of the B. burgdorferi proteins responsible for suppression of
cellular immunity has not been defined. In this study we examined the
modulating activity of a recombinant outer surface protein A (OspA) vaccine
preparation on cellular immune responses.”
http://femsim.oxfordjournals.org/content/28/3/193.long
Notice: “OspA blunts the immune response mechanism,” says Gary Wormser
(above), 2000, while LYMErix was still on the market. You can see that the
intention of the falsified Dearborn case definition and all the shenanigans
by this Cabal regarding what Lyme is and does, revolves around the notion
that Lyme Borrelia only cause an inflammatory disease (HLA-linked
autoimmune), and that OspA would tolerize against that, as it presumably
does in animal OspA vaccines. The reason for that baloney is because
actually OspA is a fungal toxin that causes global immunosuppression in most
humans. Ray Dattwyler said at the FDA meeting in 1998 on the Lyme vaccines
that he only sees about one such “case” a year of this arthritis-only
outcome.
1989, and 1992, Paul Duray on immortalized B cells in the spinal fluid of
Lyme victims:
“The immature B cells can also be seen in the spinal
fluid. These cells appear quite atypical – not unlike those of transformed
of neoplastic lymphocytes.”
Duray in IDSA’s journal:
Rev Infect Dis. 1989 Sep-Oct;11
Suppl 6:S1487-93.
“Clinical pathologic correlations of Lyme disease.
“The multisystem effects caused by Borrelia burgdorferi
in Lyme disease
are multiple, varied, and unpredictable. In some patients, the full extent
of the infection consists of a stage I acute systemic viral-like illness.
Stage II primarily involves the cardiovascular system (myocarditis) and/or
the central nervous system (CNS) (meningoencephalitis, polyradiculitis).
More inflammatory cells are found in the heart and nervous system structures
during this intermediate stage than are found in any tissues involved during
stage I. Stage III is characterized by peripheral neuropathy and CNS
disorders such as dementia or transverse myelitis and arthritis and
synovitis of large joints such as the knee. Chronic Lyme disease
is also associated with multiple and seemingly unrelated cutaneous
manifestations such as acrodermatitis chronica atrophicans,
sclerodermoid-like reactions, lichen sclerosus et atrophicus, subcuticular
fibrous nodules, eosinophilic fasciitis-like lesions of the extremities,
and, possibly, granuloma annulare. With care, spirochetes can be recovered
or demonstrated by silver staining in most of the above lesions. Spirochetes
have yet to be seen in the tissues of autonomic ganglia or peripheral
nerves.”
https://www.ncbi.nlm.nih.gov/pubmed/2814170
In the text of that article:
The following is from the Steven Schutzer book,
Lyme Disease, Molecular and Immunological Approaches:
https://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770
Paul Duray says in that book, “These immunoblastoid cells resemble those
found in Epstein-Barr infections. Does Bb reactivate latent viruses
infections in tissues?”
So, we know OspA inhibits apoptosis and we know
Epstein-Barr virus inhibits apoptosis and is responsible for the Great
Imitator outcomes of Lyme and Syphilis. And we know spirochetes go after
lymph nodes and cause the “B cell maturation centers” to fail. And we know
even from “Seronegative Lyme-Patients-are-the-Sickest” Dattwyler who in 1998
showed that Borrelial supernatant was responsible for the NK and other
immune cell senescence:
Ann N Y Acad Sci. 1988;539:103-11.
Modulation of
natural killer cell activity by Borrelia burgdorferi.
Golightly M1, Thomas
J, Volkman
D, Dattwyler
R.
"Effect of B burgdorferi Culture on Normal
PBL
"..when lymphocytes are cultured in
the presence of growing Bb there is a marked inhibition ( p < .0005 ) of NK
activity on days 3, 5, and 7 when compared to lymphocytes cultured in BSKII
media in the absence of spirochetes. This effect is not due to a selective
depletion or or toxicity to endogenous NK since viability studies and
monoclonal antibodies demonstrate no significant changes after culture with
the organism.
"The inhibition is directly attributable to the organism or its
supernatants (data not shown)."
https://www.ncbi.nlm.nih.gov/pubmed/3056196
AKA: “TOLERANCE” or a septic
shock-like result.
1922: Ancient history on how
spirochetes target the lymph nodes
J Exp Med. 1922
Jan 1;35(1):39-62.
A STUDY OF THE RELATION OF TREPONEMA PALLIDUM TO
LYMPHOID TISSUES IN EXPERIMENTAL SYPHILIS.
Pearce L1, Brown
WH.
A widespread dissemination of Treponema pallidum from a
local focus of inoculation in the rabbit constantly occurs by way of the
lymphatics. Spirochetes were
regularly recovered from the satellite lymph
nodes by
animal inoculation after scrotal inoculation; they were present as early as
2 days, when no specific primary reaction was detected, and at later periods
of from 5 to 61 days after inoculation. Other superficial nodes at
remote sites such as the popliteals and with no syphilitic lesions in the
drainage area have also been shown to harbor active organisms. Although spirochetes were
found in relatively few of the lymph node
emulsions, the orchitis resulting from their injection was of a rapidly
progressive type with an incubation period but slightly longer than that
produced by a testicular or skin nodule emulsion rich in spirochetes.
It has further been shown that a syphilitic infection is sufficiently
established in the rabbit body within 48 hours after scrotal inoculation so
that the primary lesion is no longer essential for its maintenance. Active
treponemata survive in the popliteal lymph
nodes for
long periods of time and have been regularly recovered from them in cases of
true latency. The lymph
nodes, therefore, function as reservoirs of the organisms. The
ability to recover the spirochetes from
lymphoid tissue through successive generations is seen in the serial passage
of lymph node
emulsion to testicle during an 18 months period. The persistence of spirochetes in
lymphoid tissue irrespective of the presence or absence of syphilitic
lesions is a characteristic and fundamental feature of syphilis of the
rabbit. The existence of infection, therefore, may be demonstrated at any
time by the recovery of spirochetes from
the popliteal lymph
nodes by
animal inoculation. This fact is of great practical importance in the
therapy of the infection and may be profitably utilized in determining the
ultimate effect of a therapeutic agent. These experiments demonstrate that
the disease is not confined to the site of local inoculation but that
lymphogenous dissemination of treponemata regularly takes place, and that
during the course of this process organisms become localized in the lymph
nodes and
exist there indefinitely irrespective of the occurrence of manifestations of
disease. The intimate relation of Treponema pallidum to lymphoid tissue is
an essential concept of syphilis of the rabbit, and from this point of view,
the infection is primarily one of lymphoid tissue.
https://www.ncbi.nlm.nih.gov/pubmed/19868586
J Exp Med. 1925
Jun 30;42(1):33-42.
STUDIES IN EXPERIMENTAL SYPHILIS : IV. THE SURVIVAL
OF TREPONEMA PALLIDUM IN THE INTERNAL ORGANS OF TREATED AND UNTREATED
RABBITS.
Chesney AM1, Kemp
JE; Assistance
of Allan K. Poole, M.D.
“Simultaneous transfers to the testes of normal rabbits
of circulating blood, heart muscle, liver, brain, spleen and bone marrow
(mixed), inoculated testicle, and popliteal lymph nodes from a series of
untreated syphilitic rabbits, demonstrated the persistence of the original
infection unifomnly in the lymph nodes and less regularly in the liver,
mixed spleen and bone marrow, and testis originally inoculated. In one
instance the circulating blood was found to be infectious. Transfer of
similar tissues from syphilitic rabbits treated with arsphenamine late in
the course of the disease failed to disclose syphilitic infection of any of
these tissues. In one animal, in which keratitis developed both before and
after treatment, the blood, internal organs, and lymph nodes were found to
be non-infectious in spite of the fact that the cornea was shown to be the
site of a syphilitic inflammation. Transfer of lymph nodes or internal
organs of treated syphilitic rabbits is probably the best method of
evaluating an antisyphilitic agent, but it must be supplemented by careful
observation of treated animals over an appreciable interval of time
following treatment. The results of this study support the idea that failure
to reinoculate a treated syphilitic animal does not necessarily mean the
existence of the first infection but might beinterpreted as indicating the
presence of an acquired resistance which persists in rabbits in which no
trace of the first infection can be demonstrated.”
https://www.ncbi.nlm.nih.gov/pubmed/19869032
Spirochetes have long been known to hang out in lymph nodes, cause
antibody-negative disease, be incurable and produce a variety show of
outcomes. It wasn’t until we found out what OspA was exactly were we able
to see that that alone, injected, could cause the same “these look like
Epstein-Barr transformed lymphocytes” and “oh, spirochetes and Epstein-Barr
both hang out in the lymph nodes” outcome, solving the 500 year old mystery
of why ancient dinosaur phyla like Spirochaeta are responsible for dementia
in white human males with “MD” after their names, where those demented “MD”
males don’t deliberately infect non-Caucasians with these organisms to find
out why spirochetal infections in African humans do not cause the dementia
they do in Caucasians (Tuskegee “Bad Blood”).
Sex Transm Dis. 2014
Jul;41(7):440-6. doi: 10.1097/OLQ.0000000000000149.
Toll-like receptor polymorphisms are associated with increased neurosyphilis risk.
Marra CM1, Sahi
SK, Tantalo
LC, Ho
EL, Dunaway
SB, Jones
T, Hawn
TR.
"Clinicians in the early 20th century
posited that race influenced susceptibility to neurosyphilis, citing a
decreased risk in African Americans compared to Caucasians (7).
Subsequent work suggested a genetic basis for such differences, with an
increased risk of syphilitic dementia, but not other forms of neurosyphilis,
in patients with certain HLA types (8)
that differed in African Americans compared to Caucasians (9).
While more recent reports suggest that there may be genetic
contributions to syphilis susceptibility (10-13),
to the best of our knowledge there have been no recent investigations of
genetic susceptibility to neurosyphilis."
https://www.ncbi.nlm.nih.gov/pubmed/24922103
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4414322/
Meanwhile, importantly, everyone will recall that the Cabal (published in
IDSA’s journal) themselves dubbed Lyme a New Great Imitator because it
causes Lupus, MS,
ALS, stroke, cancer and so forth. Yale even had a “Lyme and Lupus
Clinic,” now called “L2 (for Lyme and Lupus) Diagnostics.”
Rev Infect Dis. 1989
Sep-Oct;11 Suppl 6:S1482-6.
Neurologic manifestations of Lyme disease,
the new "great imitator".
https://www.ncbi.nlm.nih.gov/pubmed/2682960
(Note that “Reviews of Infectious Diseases” was IDSA’s own journal.)
And yet now Yale says Lupus is mostly like caused by Epstein-Barr, so what
is happening? Right, Lyme activates Epstein-Barr via immunosuppression
because not only do they both live in the lymph nodes (spirochetes and EBV),
but injecting people with OspA alone causes this same immunosuppression and
multi-system disease outcome:
This is Yale:
J Immunol. 2004
Jan 15;172(2):1287-94.
Defective control of latent Epstein-Barr virus
infection in systemic lupus erythematosus.
Kang I1, Quan
T, Nolasco
H, Park
SH, Hong
MS, Crouch
J, Pamer
EG, Howe
JG, Craft
J.
“EBV infection is more common in patients with systemic lupus erythematosus
(SLE) than in control subjects, suggesting that this virus plays an
etiologic role in disease and/or that patients with lupus have
impaired EBV-specific immune responses. In the current report we assessed
immune responsiveness to EBV in patients with SLE and healthy controls,
determining virus-specific T cell responses and EBV viral loads using whole
blood recall assays, HLA-A2 tetramers, and real-time quantitative PCR.
Patients with SLE had an approximately 40-fold increase in EBV viral loads
compared with controls, a finding not explained by disease activity or
immunosuppressive medications. The frequency of EBV-specific CD69+ CD4+ T
cells producing IFN-gamma was higher in patients with SLE than in controls.
By contrast, the frequency of EBV-specific CD69+ CD8+ T cells producing
IFN-gamma in patients with SLE appeared lower than that in healthy controls,
although this difference was not statistically significant. These findings
suggest a role for CD4+ T cells in controlling, and a possible defect in
CD8+ T cells in regulating, increased viral loads in lupus.
These ideas were supported by correlations between viral loads and
EBV-specific T cell responses in lupus patients.
EBV viral loads were inversely correlated with the frequency of EBV-specific
CD69+ CD4+ T cells producing IFN-gamma and were positively correlated with
the frequencies of CD69+ CD8+ T cells producing IFN-gamma and with
EBV-specific, HLA-A2 tetramer-positive CD8+ T cells. These results
demonstrate that patients with SLE have defective control of latent EBV
infection that probably stems from altered T cell responses against EBV.”
https://www.ncbi.nlm.nih.gov/pubmed/14707107
Amazingly stupid people injected the very thing that
causes complete ruination of the immune system, from organisms known for
almost 100 years to target and survive in lymph nodes (clue, “immune
system”), and said that thing was a “vaccine” against “a disease that does
not exist but is just hypochondria, drug-seeking, and drama queen-itis.”
You can’t make this up.
Some Normal People recently objecting to the idea that Borreliae is more
than one genus, which is what the criminal CDC cabal would like to (falsely)
claim; look how many signers!!
Int J Syst Evol Microbiol. 2016
Dec 8. doi: 10.1099/ijsem.0.001717. [Epub ahead of print]
There is inadequate evidence to support the division of
the genus
Borrelia.
Margos G1, Marosevic
D2, Cutler
S3, Derdakova
M4, Diuk-Wasser
M5, Emler
S6, Fish
D7, Gray
J8, Hunfeld
KP9, Jaulhac
B10, Kahl
O11, Kovalev
S12, Kraiczy
P13, Lane
RS14, Lienhard
R15, Lindgren
PE16, Ogden
N17, Ornstein
K18, Rupprecht
T19, Schwartz
I20, Sing
A21, Straubinger
RK22, Strle
F23, Voordouw
M24, Rizzoli
A25, Stevenson
B26, Fingerle
V27.
“As for the clinical symptoms caused by Borrelia
species, the symptomology that differentiates RF spirochaetes from the LB
group of spirochaetes has been blurred by recent case descriptions. For
example, a patient with clinical symptoms resembling those of Lyme
neuroborreliosis was diagnosed as being infected with the RF group species
B. miyamotoi (Boden et al., 2016). Interestingly, infection with the
recently described genospecies of the B. burgdorferi s.l. complex, B.
mayonii, produced high spirochaetal blood densities, akin to that seen
following infection with species of the RF group (Pritt et al., 2016).
”Thus, splitting the genus does not provide any assistance as far as
clinical evaluation is concerned. It does not help end user communities
including those in clinical medical practice, public health or those
studying the ecology of the bacteria. Collectively, in view of the
inadequate genetic evidence supporting the genus split and the biological
features shared between RF and LB group spirochaetes, at present we
strongly oppose the proposed division of the genus Borrelia. This division
complicates an already complicated situation which will serve only to lead
to further confusion among scientists, clinicians, public health authorities
and the general public. Taken together, we believe that such a change is
inadvisable based on currently available biological and clinical evidence,
and therefor respectfully request that it be repealed.”
https://www.ncbi.nlm.nih.gov/pubmed/27930271
http://ijs.microbiologyresearch.org/deliver/fulltext/ijsem/ijsem_pap.001717.zip/ijsem.0.001717.pdf?itemId=/content/journal/ijsem/10.1099/ijsem.0.001717.v1&mimeType=pdf&isFastTrackArticle=true
And here is the Cabal’s answer:
Int J Syst Evol Microbiol. 2017
Jan 27. doi: 10.1099/ijsem.0.001815. [Epub ahead of print]
Division of the genus Borrelia into
two genera (corresponding to Lyme disease and relapsing fever groups)
reflects their genetic and phenotypic distinctiveness and will lead to a
better understanding of these two groups of microbes (Margos et al. (2016)
There is inadequate evidence to support the division of the genus Borrelia.
Int. J. Syst. Evol. Microbiol. doi: 10.1099/ijsem.0.001717).
Barbour AG1, Adeolu
M2, Gupta
RS3.
“This rebuttal Letter
responds to a Letter in the IJSEM by Margos et al. challenging division of
the genus Borrelia into
two genera. We discuss here point-by-point the issues raised by Margos et
al. and show that much of their criticism is unfounded and in several cases
based on misreading of the presented results. We summarize here the
extensive evidence based on genomic, genetic and phenotypic properties
showing that the members of the family Borreliaceae (containing mainly the
genus Borrelia)
comprises two distinct and cohesive groups of microbes, differing in
diseases they cause and other phenotypes. Prior to the proposed division, Borrelia spp.
causing Lyme disease (LD) were already functionally treated as a distinct
group, referred to as "B. burgdorferi sensu lato" to distinguish them from
the other cluster of Borrelia spp.
which includes all known species causing relapsing fever (RF). With the more
explicit division of Borreliaceae species into two genus level groups, which
are distinguishable from each other based on numerous unique genetic and
molecular characteristics, the attention can now be focused on the
biological significance of different molecular characteristics
differentiating the two groups. The clear distinction of the LD and the RF
groups of microbes based on numerous highly reliable markers, which are
expected to be present even in uncharacterized members of these two groups,
should aid in the improved diagnosis as well treatment of both these
diseases, which is hindered by the conflation of a common name for agents
causing two different types of diseases.”
https://www.ncbi.nlm.nih.gov/pubmed/28141502
What would be
the advantage of claiming the Lyme Borrelia are a separate genus?
Right: ‘To maintain the lie that Dearborn was real and that “Lyme” is only
a bad knee. This response was another attempt to manufacture a Get Out of
Jail Free card. It’s all about maintaining the PRETENSE (a legal word
meaning FRAUD) that Dearborn was real, and not a crime scene.
Lyme Borrelia do not only cause “bad knees.” They’re spirochetes and do
what spirochetes do, which is shed fungal antigens and go right to the lymph
nodes where they ruin the immune system. They do not Get Out Of Jail Free
or Pass Go, Right to The Knees and Collect 200 Dollars. They do not
participate in semantics games. They are found in Alzheimer’s brains.
They’re not nanobots, and they’re not even regular bacteria, with
lipopolysaccharide as a main membrane component (LPS). When they show up in
a courtroom, such as a “Railroad
Case,” they go back to being a regular Great Imitator, instead of a bad
knee. When they show up at the FDA, Glaxo-SmithKline, themselves,
make fun of Allen Steere and say, basically, “Steere’s is a crazy idea; if
spirochetal OspA antibodies cross-attack a fragment of the HLA molecule,
they would be found everywhere in the body and not just in the knees… “
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_02_lobet.pdf
As much as delusional persons would like to will Spirochetes
into being subservient little thugs in their RICO club, well, let’s say you
really can’t train them. They don’t even live in colonies
in vivo, which is a bogus claim of another wrong-headed organization,
ILADS.org…
The following, Primer Shell Game charge sheet is
more formal training in Spirochete biology and taxonomy.
BACKGROUND: The
essence of these criminal charge sheets is that the Cabal makes false claims
based on research fraud, and our job (apparently), is to show point-
by- point, crime-by-crime, research fraud and false claims that result
in tremendous human (and even animal) harm, and billions in lost
research-dollar-lives in related diseases such as cancer, MS, RA, and Lupus,
not to mention the harm to USA’s scientific reputation. “MDs” apparently
have no responsibility to know what they’re talking about. There is no
accountability system for them in the United States. USA’s medical schools
do not require a science background.
These are the research-fraud “Guidelines,” the signers of which will be
prosecuted among others (CDC):
Clin Infect Dis. 2006
Nov 1;43(9):1089-134. Epub 2006 Oct 2.
The clinical assessment, treatment, and prevention of
lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical
practice guidelines by the Infectious Diseases Society of America.
Wormser GP1, Dattwyler
RJ, Shapiro
ED, Halperin
JJ, Steere
AC, Klempner
MS, Krause
PJ, Bakken
JS, Strle
F, Stanek
G, Bockenstedt
L, Fish
D, Dumler
JS, Nadelman
RB.
http://www.ncbi.nlm.nih.gov/pubmed/17029130
http://www.cid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=17029130
The Cabal will probably attempt to say the data we present in these criminal
charge sheets for the USDOJ is taken out of context, but you can go to all
the PubMed links in all these SASH/TruthCures criminal charge sheets and
find how many other
scientists referenced
their work when this gang was telling the truth. This CDC/ALDF organized
crime gang that hijacked IDSociety.org certainly could not have been
mistaken on EVERYTHING,
either, if that is what they will try to claim.
- - - -
START by understanding the DNA Shell Game, by finding out what DNA and RNA
primers are:
http://en.wikipedia.org/wiki/Primer_%28molecular_biology%29 and
http://en.wikipedia.org/wiki/16S_ribosomal_RNA
Primers are like a starting DNA or RNA sequence to look for a match in your
sample. If you start with the wrong primer probes, you won’t find what are
looking for. When looking for spirochetes in humans, particularly when
trying to claim “NO LYME,” either in EM rashes in Missouri, or after
“treatment,” the Cabal either uses the wrong primers (they prefer to use
OspA primers in particular, when trying to not find Lyme), or using
inadequate primers such that only one or 2 species are probed for in humans,
when there are probably a hundred formal different types of
borrelia.
It would be therefore reasonable to either sequence the DNA and not rely on
probes, or use several different probes for the commonest borrelia in the
region, be they hermsii,
and subdivisions thereof from the other relapsing fever, or several from the
new, burgdorferi clade
including some of the newer ones that have evolved from it. Recently, we
learned of a new Mass Spec--ToF-PCR method endorsed by the CDC and
Infectious Diseases Society of America to detect central nervous system
(CNS) infections:
"Unmet diagnostic
needs in infectious disease"
”…A
number of new diagnostic technologies for ID are rapidly emerging: e.g.,
broad-range PCR, next-generation sequencing, and matrix-assisted laser
desorption/ionization time of flight mass spectrometry.***
http://ein.idsociety.org/media/publications/papers/2014/Blaschke_DMID_14_Unmet_Diagnostic_Needs.pdf
And
J Clin Microbiol. 2014
Jan;52(1):212-7. doi: 10.1128/JCM.02270-13. Epub 2013 Nov 6.
Virological diagnosis of central nervous system
infections by use of PCR coupled with mass spectrometry analysis of
cerebrospinal fluid samples.
Lévêque N1, Legoff
J, Mengelle
C, Mercier-Delarue
S, N'guyen
Y, Renois
F, Tissier
F, Simon
F, Izopet
J, Andréoletti
L.
”Viruses are the leading cause of
central nervous system (CNS) infections, ahead of bacteria, parasites, and
fungal agents. A rapid and comprehensive virologic diagnostic testing method
is needed to improve the therapeutic management of hospitalized pediatric or
adult patients. In this study, we assessed the clinical performance of PCR
amplification coupled with electrospray ionization-time of flight mass
spectrometry analysis (PCR-MS) for the diagnosis of viral CNS infections.
Three hundred twenty-seven cerebrospinal fluid (CSF) samples prospectively
tested by routine PCR assays between 2004 and 2012 in two university
hospital centers (Toulouse and Reims, France) were retrospectively analyzed
by PCR-MS analysis using primers targeted to adenovirus, human herpesviruses
1 to 8 (HHV-1 to -8), polyomaviruses BK and JC, parvovirus B19, and
enteroviruses (EV). PCR-MS detected single or multiple virus infections in
190 (83%) of the 229 samples that tested positive by routine PCR analysis
and in 10 (10.2%) of the 98 samples that tested negative. The PCR-MS results
correlated well with herpes simplex virus 1 (HSV-1), varicella-zoster virus
(VZV), and EV detection by routine PCR assays (kappa values [95% confidence
intervals], 0.80 [0.69 to 0.92], 0.85 [0.71 to 0.98], and 0.84 [0.78 to
0.90], respectively), whereas a weak correlation was observed with
Epstein-Barr virus (EBV) (0.34 [0.10 to 0.58]). Twenty-six
coinfections and 16 instances of uncommon neurotropic viruses (HHV-7 [n =
13], parvovirus B19 [n = 2], and adenovirus [n = 1]) were identified by the
PCR-MS analysis, whereas only 4 coinfections had been prospectively
evidenced using routine PCR assays (P < 0.01). In
conclusion, our results demonstrated that PCR-MS analysis is a valuable tool
to identify common neurotropic viruses in CSF (with, however, limitations
that were identified regarding EBV and EV detection) and may be of major
interest in better understanding the clinical impact of multiple or
neglected viral neurological infections.”
http://www.ncbi.nlm.nih.gov/pubmed/24197874
We should be clear about this Primers
Shell Game aspect of the criminal behavior of the Cabal: The Cabal
deliberately uses the wrong DNA to assess for the presence of spirochetes
patients, yet use the correct DNA and RNA analyses when looking for
spirochetes to patent. This bait-and-switch game could be called clinical
violence or medical violence because the victims are left not only sick,
but declared mentally ill, are slandered against, or libeled against, are
denied income and disability benefits, as well as suffer social ostracism.
How different is this abuse than that suffered by the tortured African
American community all these centuries? It’s a “Deprivation of Rights
via Color of Law” criminal charge, where the Govt employees deny you
your rights. In this case, it is the CDC staff involved in these crimes who
can be charged with “Color of Law” (Alan Barbour, Barbara Johnson, etc.).
These victim-patients are deprived of their humanity, as well as
functionality. They’re tossed aside, sick, demoralized, ostracized, and
despised, yet they suffer a complex of several exhausting, neurologic
diseases at the same time. While the CDC now claims that Lyme is 10 times
underreported - meaning the new annual cases number around 300,000 rather
than 30,000 because the falsified case definition misses 85% of the cases as
shown in the other criminal charge sheets -, they of course never mention
it is only 15% reportable due to the fraud of Dearborn. That is a lot
of human cost and disability for which Uncle Sam will have to pay. Somehow
a gang of low-lives was put in charge so they could potentially capitalize
on this new vaccines and test kits racket, the emerging, global
pollution-related vector-borne-diseases. The ALDF’s was a 50 year to
roll-out plan for every new type of disease: rickettsia, babesia, borrelia,
any new viruses they find, etc. Their model was to in each instance, invent
a vaccine, and then the
falsify the serological description of the disease. Whoever did not meet
their Vaccine First disease definition was to be trashed. It’s the same
violence seen in any mob-related activity. “You do it our way or we’ll
break your legs, we’ll kill you or ruin your family, but you will be taken
out. Silenced.”
To continue your background training in the Primers Shell Game, go to the
National Library of Medicine and search for Borrelia in the Taxonomy
database. Click on the word Borrelia until you come to the genetics page
and find that flagellin – and not plasmid DNA (which is varied, added to-
and subtracted from via bacteriophages, as well as variable within each
plasmid) - is the species distinguisher.
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=138&lvl=3&lin=f&keep=1&srchmode=1&unlock
Use Google Images to discover the basic structure of a spirochete; see the
internal flagellar bundle that facilitates movement by expanding and
contracting like a muscle; the organism borrows. There may be no help from
“physicians” in this campaign, but that really doesn’t even mean anything
any more. The victims themselves have carried this campaign all these 20+
years and in the end, we’ll probably welcome robot-doctor kiosks in the
malls and at Walmart, perhaps with a nurse standing by to take blood and
write the orders for the radioimaging. ‘No need to overpay a middle-man for
their incompetence. You’ll at the end of this campaign be convinced no one
needs a man with perverted, unscientific ideas about disease and medicine
getting in the way of the machines. “Doctors” had their shot. They chose
Kool-Aid and the age-old cliquish, clannish default position of looking down
their noses and blaming their victims. “Chose,” people, and that’s a
spiritually dangerous thing from a bunch of First Do No Harm, oath-takers.
It was dangerous also, because BS is never not a boomeranger. We saw that
loud and clear with the 911 stunt and then the subsequent quintuple
financial and military superpower of Iran, Russia, Brazil, China, and South
Africa (BRICS), not to mention ISIS and losing Syria and the Middle East oil
wars.
I. Phage-vectored
plasmids are variable DNA, not to be used for probes in human disease
PHYLOGENY means how the organism evolved and how it is genetically related
to other organisms, for example, such as dogs evolving from wolves and being
related to bears. B.
burgdorferi is genetically
closest to B. anserina,
an African Bird Borreliosis. Borreliae undergo constant variation in their
plasmid DNA, and the plasmid DNA is bacteriophage-vectored and changes all
the time, also. The plasmid content is variable inside the spirochetes, and
variable phage-vectored DNA for the plasmids come from other organisms to an
important extent.
The genus, Borreliae, is the name for the relapsing fever organisms, and the
nature of the relapse is antigenic variation. Therefore
you cannot use any DNA from borrelia’s plasmids –
which is where the variable surface antigens are ordered manufactured and
remanufactured – to assess for the presence of spirochetes. No researchers
outside the United States EVER use
plasmid DNA to assess for spirochetes. They only use species-specific genes
like 5-, 16- and 23-S RNA or flagellin. When
CDC officers like Alan Barbour or Yale staff patent borrelia species, they
patent the specific flagellin that differentiates that particular bug from
the other borrelia.
Plasmid content changes all
the time within individual
spirochetes and this is known as antigenic variation. CDC officer
Alan Barbour is an expert on how this plasmid content changes and produces
the well-known antigenic variation in spirochetes. Oscar Felsenfeld once
said there was no point in differentiating Borreliae species since they were
so variable and changing to constantly due to this phage-vectored-, variable
plasmid content. Just call
them all Borreliae, the genus, is what Felsenfeld recommended. It’s
best if you see this with your own eyes:
CDC’s Barbour and NIH’s Burgdorfer on bacteriophages
transferring plasmids (the arrows point to the phages or viruses of
bacteria):
J Bacteriol. 1983 Jun;154(3):1436-9.
Bacteriophage in the Ixodes dammini spirochete, etiological agent of
Lyme disease.
Hayes SF, Burgdorfer
W, Barbour
AG.
http://www.ncbi.nlm.nih.gov/pubmed/6853449
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC217620/pdf/jbacter00247-0414.pdf
Plasmids change all the time, are
bacteriophage-vectored and responsible for intra-Kingdom gene transfer. The
antigens produced by the plasmid change all the time. So,
there is only one species-determinant, flagellin. See also Casjens on this
topic in the PubMed literature.
Spirochetes from human brains were shown
to undergo antigenic variation (Pachner, below), but we can assume they’re
all weakened over time from dropping plasmids. Spirochetes do all their
damage early in the disease by shedding these varying, fungal antigens, as
CDC officer Alan Barbour says in (the probably mis-titled) the next
article, and causing what the NIH prefers to call Post-Sepsis Syndrome:
“Researchers Finding
Rewarding Careers As Software Entrepreneurs”
"It's using some sort of
stealth-bomber-type mechanism," he says. Or, using another diversionary
tactic called blebbing, the spirochete can pinch off bits of its membrane in
order to release its surface proteins.
Explains Barbour: "It's like a bacterial Star Wars defense program," in
which released surface proteins might intercept incoming host antibodies,
keeping the spirochete safe from immunological attack.”
http://www.the-scientist.com/?articles.view/articleNo/17985/title/Researchers-Finding-Rewarding-Careers-As-Software-Entrepreneurs/
They, the shed fungal
antigens like OspA, turn off the immune response. It’s the secondary
infections, the reactivated latent infections (herpes) or the opportunistics
that mainly cause the majority of disease signs. A better and more
acceptable description of Lyme is that it is AIDS-like or Post Sepsis
Syndrome.
Says CDC officer Alan Barbour about
antigenic variation even from a single spirochete (and Section IV, below,
page 25-26):
VMP-like sequences of pathogenic Borrelia
”2.1
Methods of Treatment
”An important aspect of the invention is the
recognition that Borrelia VMP-like sequences recombine at the vls site, with
the result that antigenic variation is virtually limitless. Multiclonal
populations therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed. Thus there is
now the opportunity to develop more effective combinations of immunogens for
protection against Borrelia infections or as preventive inoculations such as
in the form of cocktails of multiple antigenic variants based on a base
series of combinatorial VMP-like antigens. “
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6,719,983.PN.&OS=PN/6,719,983&RS=PN/6,719,983
The Vmps are little different
from the Osps. They call Osps from the non-Lyme relapsing fever organisms,
VMPs or variable major proteins. There is no data on whether or not the
VMPs are triacyl lipopeptides; we just know spirochetes and
Mycoplasma/Mycobacteria (and Brucella) are lumped together as producers of
these TLR2/1-agonists. The take home point is that Osps/Vmps undergo
constant variation such as to adapt to new hosts and tissues, within
themselves and among the genus, Borrelia. They can’t be used to assess
human cases of Lyme. Non-variable DNA/RNA should be used. See more at:
J Bacteriol. 2006 Jun; 188(12):
4522–4530.
Crystal Structure of Neurotropism-Associated
Variable Surface Protein 1 (Vsp1) of Borrelia
turicatae†
Catherine L. Lawson,1,* Brian
H. Yung,1 Alan
G. Barbour,2 and Wolfram
R. Zückert2,3,*
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1482977/
II. Borrelia Acquiring Sticky
OspA, and OspA Sticking to Itself (falsified vaccines reporting, blot
smudging, Korean Chemists on OspA being sticky and clumping)
We’ve wondered how Lyme spirochetes “took” to hard-bodied, Ixodes ticks,
as they were originally found in the guts of soft-bodied Ornithodoros ticks.
OspA or Pam3ys is a ligand for chitinous or collagenous tissue.
OspA/Pam3Cys also binds plasminogen and maintains the plasminogen as
biologically active even when OspA is as a free molecule (Philipp, Tulane). Mycoplasma, Brucella and
Lyme spirochetes all cause arthritis, so one may wonder if these molecules
just stick to joint tissue? And do they, as bearers of biologically active
plasminogen, aid the spirochetes in penetrating the hard bodies of hard
bodied ticks?
We know these Pam3Cys molecules tick to each other and to intracellular
components, gumming up the immunity works as seen in other charge sheets for
the U. S. Justice Department. We also suspect that the fact that OspA
sticks to itself is a probable reason the LYMErix vaccines had unreadable
Western Blots as well as is the reason for the large number of strokes,
cancer, and other “vascular events” resulting from LYMErix or OspA
vaccination. Next, Yale’s Robert T. Schoen on LYMErix damage, the Phase IV
data (strokes, cancer, “vascular events”):
Clin Ther. 2003
Jan;25(1):210-24.
An open-label, nonrandomized, single-center,
prospective extension, clinical trial of booster dose schedules to assess
the safety profile and immunogenicity of recombinant outer-surface protein A
(OspA) Lyme disease vaccine.
Schoen RT1, Deshefy-Longhi
T, Van-Hoecke
C, Buscarino
C, Fikrig
E. or (OspA_4.htm)
https://www.ncbi.nlm.nih.gov/pubmed/12637121
Korean Chemistry Journal on
the Structure of OspA/Pam3Cys
Bull.
Korean Chem. Soc. 1996, Vol. 17 Number 11
Characterization of Extremely Hydrophobic Immunostimulatory Lipoidal
Peptides by Matrix-Assisted Laser Desorption ionization Mass Spectrometry
Jung-Suk Jang,
Sung-Taek Lee, et al, Korea
”We are currently using mass spectral
techniques to characterize the amino acid sequence of the Pam3Cys peptides
found in the envelope glycoproteins of HIV-1 and the Simian Immunodeficiency
Virus (SIV) (17). Conventional FAB-MS analysis using standard matrices such
as glycerol and nitrobenzyl alcohol is not particularly effective for these
molecules, largely due to their tendency to aggregate.”
http://newjournal.kcsnet.or.kr/main/j_search/j_download.htm?code=B961118
As shown by the Korean chemists, OspA sticks to
itself. We suspect that while OspA molecules are in vaccine vial they are
not completely micellized. It would seem this could be responsible for the
strokes, cancer, and other vascular events described by Schoen and Steere in
their Phase IV trial results and also the totally unreadable Western Blots
in both OspA vaccine trials, ImuLyme and LYMErix as shown in this next
report by Persing (Mayo and Corixa), Molloy (Imugen), and Sigal:
Clin Infect Dis. 2000
Jul;31(1):42-7. Epub 2000 Jul 17.
Detection of multiple reactive protein species by
immunoblotting after recombinant outer surface protein A lyme disease
vaccination.
Molloy PJ1, Berardi
VP, Persing
DH, Sigal
LH.
”… 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.”
http://www.ncbi.nlm.nih.gov/pubmed/10913394
Let’s hypothesize that OspA molecules in a vaccine vial was probably
never 100% micellized and was probably injected into people in clumps. The
unreadable, smudged Western Blots of the LYMErix and ImuLyme victims make
this appear to be the case. The Cabal did not report to the FDA that they
could not read their Western Blots. Instead they falsely claimed they had
76% and 92% safe and effective OspA vaccines based on the falsified Dearborn
Western Blot criteria without mentioning to the FDA and the public that the
blots in the trials were unreadable. This is clearly in itself a FRAUD
AGAINST THE GOVERNMENT charge.
https://www.law.cornell.edu/uscode/text/18/1031
We don’t know for sure if this particular ligand for plasminogen and
chitinous tissue, OspA, was, say added or spliced in or “evolved” such that
Lyme spirochetes were allegedly, suddenly found in New England ticks, Ixodes. But
we can look at the other circumstantial evidence.
III. Lyme
spirochetes are closest to an African bird borreliosis and evolutionarily
“contrary to its arthropod vector,” Plum Island
You can believe the CDC’s theory that Lyme spirochetes/West Nile blew/flew
from Africa to the northeastern United States on seabirds during hurricanes,
or, you can consider the circumstantial scientific evidence against the
backdrop of CDC’s other lies. For the sake of believing this hurricane BS
from your own eyes, see the following report:
Emerg Infect Dis. 2000 Jul-Aug;6(4):319-28.
Migratory birds and
spread of West Nile virus
in the Western Hemisphere.
Rappole JH1, Derrickson
SR, Hubálek
Z.
“Displacement of West African Birds to the New World by Tropical Storms
”A very few birds, particularly seabirds, are carried by tropical storms
across the Atlantic each summer from their normal environs on or near the
coast of West Africa (39). A number of such storms form each summer and fall
near the Cape Verde Islands off the western coast of Africa, travel across
the Atlantic, and occasionally reach land along the East Coast of North
America, depositing birds that were carried thousands of kilometers from
their homes. Species known to have been infected by West Nile virus and
whose habitat and distribution indicate
that they might be
affected by such displacement include the Gray Heron (Ardea cinerea), the
Little Egret (Egretta garzetta), the Cattle Egret (Bubulcus ibis), the
Black-headed Gull (Larus ridibundus), and the Yellow-legged Gull (Larus
cachinnans) (Table 1). The same objections apply to this scenario for the
introduction of the virus to the New World as for normal migration, i.e.,
low numbers and the likelihood that a storm transported bird would be
infected with the West African rather than the Middle Eastern form of the
virus.”
http://wwwnc.cdc.gov/eid/pdfs/vol6no4_pdf-version.pdf
The following is a key report from the
NIH's NLM's Taxonomy (Fukunaga, et al) database showing burgdorferi
is closest to anserina, an
African bird borreliosis. They just happen to do this kind of
African-Diseases-With-North-American-Vectors-kind of "Research" on
Plum Island, as you will see.
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 M1, Okada
K, Nakao
M, Konishi
T, Sato
Y.
http://ijs.sgmjournals.org/content/46/4/898.long
1995 -- Next, New York
Medical College (NYMC) and Marconi at Medical
College of Virginia at Virginia Commonwealth University, Richmond, VA, say anserina is
an “out-group” when comparing burgdorferi or
the Lyme group from other borrelia. It is not some random out-group. It is
the origin of burgdorferi as
you will see when we talk more about 1) Plum Island as the original outbreak
area, where 2) UPenn says this vector-pathogen match-up was evolutionarily
unlikely, and 3) where they just happen to do that kind of
African-diseases-with-North-American Vectors kind of research on Plum, not
to mention, 4) all the CDC’s lies and attempts to have us believe “Lyme
disease” is not even a spirochetal disease, but autoimmune arthritis
(Dearborn).
J
Clin Microbiol. 1995
Sep;33(9):2427-34.
Identification of novel insertion elements, restriction fragment length polymorphism patterns,
and discontinuous 23S rRNA in Lyme disease spirochetes: phylogenetic analyses of rRNA genes and
their intergenic spacers in Borrelia japonica sp. nov.
and genomic group 21038 (Borrelia andersonii sp. nov.) isolates.
Marconi RT1, Liveris
D, Schwartz
I.
https://www.ncbi.nlm.nih.gov/pubmed/7494041
UPenn on Lyme spirochetes being evolutionarily unlikely:
Evolution. 2010
Sep;64(9):2653-63. doi: 10.1111/j.1558-5646.2010.01001.x.
Uncoordinated phylogeography of Borrelia burgdorferi
and its tick vector, Ixodes scapularis.
Humphrey PT1, Caporale
DA, Brisson
D.
”Despite the
intimate association of B. burgdorferi and I. scapularis, the population
structure, evolutionary history, and historical biogeography of the pathogen are all
contrary to its arthropod vector.”
http://www.ncbi.nlm.nih.gov/pubmed/20394659
More on evolution and expansion north and west from eastern Long Island of
the anserina-come-burgdorferi-Plum-Island phenomenon; SUNY-SB on Lyme/Plum
Island as the original outbreak area (Ed Bosler):
Zentralbl Bakteriol Mikrobiol Hyg A. 1986
Dec;263(1-2):65-71.
Evolution of a focus of Lyme disease.
Schulze TL, Shisler
JK, Bosler
EM, Lakat
MF, Parkin
WE.
http://www.ncbi.nlm.nih.gov/pubmed/3577493
1998-- Yale’s Durland Fish performing vector-pathogen studies on Plum Island
(Borrelia are also found in these pig ticks in Africa):
African swine fever
virus infection in the argasid host, Ornithodoros porcinus porcinus.
J Virol. 1998
Mar;72(3):1711-24.
Kleiboeker SB1, Burrage
TG, Scoles
GA, Fish
D, Rock
DL.
1Plum Island Animal Disease Center, Agricultural Research Service, U.S.
Department of Agriculture, Greenport, New York 11944, USA.
“The pathogenesis of African swine fever virus (ASFV) infection in
Ornithodoros porcinus porcinus was examined in nymphal ticks infected with
the ASFV isolate Chiredzi/83/1. At times postinfection (p.i.) ranging from 6
h to 290 days, ticks or dissected tick tissues were titrated for virus and
examined ultrastructurally for evidence of virus replication. The ASFV
infection rate in ticks was 100% in these experiments, and virus infection
was not associated with a significant increase in tick mortality. Initial
ASFV replication occurred in phagocytic digestive cells of the midgut
epithelium. Subsequent infection and replication of ASFV in undifferentiated
midgut cells was observed at 15 days p.i. Generalization of virus infection
from midgut to other tick tissues required 2 to 3 weeks and most likely
involved virus movement across the basal lamina of the midgut into the
hemocoel. Secondary sites of virus replication included hemocytes (type I
and II), connective tissue, coxal gland, salivary gland, and reproductive
tissue. Virus replication was not observed in the nervous tissue of the
synganglion, Malpighian tubules, and muscle. Persistent infection,
characterized by active virus replication, was observed for all involved
tick tissues. After 91 days p.i., viral titers in salivary gland and
reproductive tissue were consistently the highest detected. Successful
tick-to-pig transmission of ASFV at 48 days p.i. correlated with high viral
titers in salivary and coxal gland tissue and their secretions. A similar
pattern of virus infection and persistence in O. porcinus porcinus was
observed for three additional ASFV tick isolates in their associated
ticks...
“African swine fever (ASF) is a highly
lethal disease of domestic pigs for which animal slaughter and area
quarantine are the only methods of disease control. …
http://www.ncbi.nlm.nih.gov/pubmed/9499019
Note that the end-point, here, slaughtering your
infected livestock, is a Plum Island-, or as we call it, Von Traub Island-,
goal. We should mention there is at least one “Plum Island” strain of
Mycoplasma:
J Hyg (Lond). 1983
Jun;90(3):441-9.
Immunogenic variation among the so-called LC strains
of Mycoplasma mycoides subspecies mycoides.
Smith GR, Oliphant
JC.
“Much
evidence of immunogenic heterogeneity among the LC strains of Mycoplasma mycoides
ssp. mycoides emerged from cross-immunization and -hyper-immunization
experiments in mice in which three LC strains (Vom/Plum Island,
74/2488, and Mankefår 2833) were
used for challenge purposes. All heterologous LC-strain vaccines
cross-immunized against the three challenge strains, but protection was
usually only 'partial', i.e. significantly less than that given by
homologous vaccine. Cross-hyperimmunization with all heterologous LC but not
SC strains produced protection against challenge with
Vom/Plum Island that
was virtually 'complete', i.e. similar to that produced by homologous
vaccine. Challenge with 74/2488 gave generally similar results; but against
Mankefår 2833 six heterologous LC vaccines gave complete protection and six
did not. Vaccines prepared from the Smith (1423) strain of M. mycoides ssp.
capri gave some protection against Vom/Plum Island
but none against 74/2488 or Mankefår 2833. The cross-immunizing ability of
three further M. mycoides ssp. capri strains appeared to resemble that of
Smith (1423). In a cross-hyperimmunization experiment, vaccines prepared
from SC strains of M. mycoides ssp. mycoides varied greatly in their ability
to protect against challenge with strains 74/2488 and Mankefår 2833”
http://www.ncbi.nlm.nih.gov/pubmed/6190898
"Mycoplasma mycoides
mycoides” = “Fungal-plasma fungal,
fungal,” nice. Triple fungal mycoplasma on Plum Island. That’s adorable.
J
So, challenging various vectors (bugs) with diseases from Africa is what
Plum Island does. Naturally, an odd one could have escaped, one way or
another – an African bird borreliosis -, genetically unlikely, and Plum
Island was the original outbreak area. That’s all the real data we’ll ever
have because we’ll never have the lab notebooks from Plum Island.
If we were prosecuting a murder trial, this all would probably fly
circumstantial evidence case as “beyond a reasonable doubt,” especially
considering all the other lies about Lyme disease, like the hurricane fairy
tale, IDSA’s “Guidelines on the Diagnosis and Treatment of Lyme disease,”
the Dearborn “case definition,” and most of all the very idea that everyone
should get a vaccine against an imaginary disease. No one has ever met or
heard from a person who can come up with a sound reason there would be a
vaccine against a disease that does not exist and needs no treatment.
IV. Brain
Permanence, Tropism and the Single Spirochete Infection
with resultant MULTIPLE
VARIANTS
J Bacteriol. 1951
Aug;62(2):215-9.
Relapse phenomena in rats infected
with single spirochetes
(Borrelia recurrentis var. turicatae).
SCHUHARDT VT, WILKERSON
M.
“Antigenic variation by the
spirochete is generally believed to be responsible for the relapse phenomena
in spirochetal relapsing fever. Schuhardt (1942) has reviewed the literature
prior to 1942 on this subject, and little if any evidence has been presented
subsequently to alter or extend this concept. Among the unanswered questions
in spirochetal relapse phenomena are: (a) the antigenic variation capacity
of a single spirochete, and (b) the capacity of an antigenic variety to
recur in a series of relapses in a given animal. Although Cunningham,
Theodore, and Fraser (1934) believe that antigenic varieties do not recur,
other workers are not convinced that this possibility has been ruled out.
Consequently we undertook a study of single spirochete infections in white
rats in an effort to answer these two and possibly other questions related
to the relapse phenomenon in spirochetal relapsing fever.”
https://www.ncbi.nlm.nih.gov/pubmed/14861181
http://jb.asm.org/cgi/reprint/62/2/215?view=long&pmid=14861181
Oscar Felsenfeld, CDC officer Alan
Barbour, Russell Johnson (ALDF member), and Diego Cadavid talking
about/referencing this Single Spirochete Phenomena:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed_citedin&uid=14861181
Oral spirochetes infecting Alzheimer’s
brains and traveling along inside nerves (this is not the only report that
says this, you’ll find it in syphilis reports too; from the older published
data and from the Cabal on the
incurability of relapsing fever; an independent study on spirochetes in the
brain from dentists and they say:
Oral Microbiol Immunol. 2002
Apr;17(2):113-8.
Molecular and immunological evidence of oral
Treponema in the human brain and their association with Alzheimer's disease.
Riviere GR1, Riviere
KH, Smith
KS.
“The purpose of this
investigation was to use molecular and immunological techniques to determine
whether oral Treponema infected the human brain. Pieces of frontal lobe
cortex from 34 subjects were analyzed with species-specific PCR and
monoclonal antibodies. PCR
detected Treponema in 14/16 Alzheimer's disease (AD) and 4/18 non-AD donors
(P < 0.001), and AD specimens had more Treponema species than controls (P <
0.001). PCR also detected Treponema in trigeminal ganglia from three AD and
two control donors. Cortex from 15/16 AD subjects and 6/18 controls
contained Treponema pectinovorum and/or Treponema socranskii
species-specific antigens (P < 0.01). T.
pectinovorum and/or T. socranskii antigens were also found in
trigeminal ganglia and pons from
four embalmed cadavers, and 2/4 cadavers also had Treponema in the
hippocampus. These findings suggest that oral Treponema may infect the
brain via branches of the trigeminal nerve.”
http://www.ncbi.nlm.nih.gov/pubmed/11929559
1975 -- Jay Sanford, Uniformed Services University School of Medicine,
Bethesda, Maryland, page 391, in the
book, The Biology of Parasitic Spirochetes, 1976
edited by ALDF.com’s Russell C. Johnson
”The Biology of parasitic
spirochetes” / edited by Russell C. Johnson
Bib ID 2160125, New York ; Academic Press, 1976, ISBN 012387050X
"The ability of the borrelia, especially tick-borne strains to persist in
the brain and in the eye
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).”
http://www.actionlyme.org/Biology_of_Parasitic_Spirochetes1976.htm
See more at: The History of Relapsing
Fever: http://www.actionlyme.org/RICOCHRON.htm
There was never any issue with persistence or
neurotropism or even lymph node tropism of Borreliae despite the CDC’s
attempts to defraud and have everyone believe Lyme is not a spirochetal
disease. They do play a shell game, though, so as not to find borrelia in
humans – and especially, eaning ALL Borreliae (see the
Taxonomy database), not just burgdorferi.
Says CDC officer Alan Barbour in 1986:
Microbiol Rev. 1986
Dec;50(4):381-400.
Biology of Borrelia
species.
Barbour AG, Hayes
SF.
”When
relapsing fever borreliae are no longer detectable in the blood, they may
still be found in organs (120). Although borreliae can usually be recovered
from such organs as the spleen, liver, kidneys, and eyes of infected animals
(37, 120), the organ usually with the most persistent infections is the
brain. Humans with relapsing fever have had borreliae recovered from the
cerebrospinal fluid (72). Borreliae can be recovered from the brains of
animals that are immune to challenge with that strain (119, 127, 148, 178).
Detection or isolation of borreliae from brains of animals that had been
infected several months and up to 3 years previously has been reported (12,
181, 197, 223). Before the advent of modem ultracold freezers, strains were
kept in the brains of rodents and passed once or twice a year (92).”
https://www.ncbi.nlm.nih.gov/pubmed/3540570
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC373079/pdf/microrev00055-0033.pdf
Rodent brains use to be the storage media says
Barbour, above. And borrelia are often absent from blood even with valid DNA
methods like flagellin DNA or species specific 16S genes, because, as Alan
Barbour says, they are in the organs, especially the brain and lymph nodes.
Obviously a culture method from blood can’t be used for the same reason –
they’re not always in the blood.
CDC officer Alan Barbour also says in
the same report:
”A
strain of B. duttonii that had been passed many times in mice was found to
have lost virulence for humans (212). When using borreliae for pyrotherapy
of neurosyphilis, the authors of this report recommended that no more than
30 to 40 passages in mice be made before inoculation of the strain back into
humans (212).”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC373079/pdf/microrev00055-0033.pdf
It is fair to say this CDC
officer, Alan Barbour, was not too confident in antibiotics if he suggested
giving people a fever from a weakened (high passage) relapsing fever
organism as a way to cure syphilis. Barbour shows
us above that he is aware that one should not use high-passage strains –
which Steere did to develop the Dearborn method -, since the point of high
passages is to weaken the strain and have the organisms drop plasmids. We
assume the reason Steere falsified the testing for the CDC’s Dearborn case
definition panel (leaving OspA and B out; OspA and B are encoded on the same
plasmid, so you can’t drop one without dropping the other), using
high-passage strains, was that he and his co-conspirators intended to develop
a test for Lyme that would be okay to use in a population “where the
vaccination status was unknown.” The Schoen-Persing-Steere RICO method
patent, US 6,045,804, uses a strain of Borrelia that had dropped the OspA-B
plasmid. It’s possible to do that with repeat passages; you can get the
bugs to drop plasmids and “virulence determinants” in this way.
We will see from this report CDC officer
Allen Steere played the shell game while he falsified the case definition
strains, identifying borrelia using the correct primers when he developed
that bogus Dearborn method in 1992. Later Steere used mainly the wrong DNA
(OspA and in one instance 1 primer probe of 16S RNA) to assess human
treatment results. Despite using the wrong primers, Steere found DNA
persisted in a third of his spinal-fluid, and synovial-fluid patients to the
tune of at least a third of the patients.
1990 – Pachner, on human brain strains changing plasmid DNA code in mice:
Neurology. 1990
Oct;40(10):1535-40.
Borrelia burgdorferi
infection of the brain: characterization of the organism and response to
antibiotics and immune sera in the mouse model.
Pachner AR1, Itano
A.
“To learn more about the
neurologic involvement in Lyme disease, we inoculated inbred mice with the
causative agent of Lyme disease, Borrelia burgdorferi.
We cultured brains and other organs, and measured anti-B burgdorferi
antibody titers. We further studied a brain isolate
for its plasmid DNA content and its response in vitro to immune sera and
antibiotics. One strain of B burgdorferi, N40, was consistently infective
for mice, and resulted in chronic infection of the bladder and spleen. SJL
mice developed fewer culture-positive organs and had lower antibody titers
than Balb/c and C57Bl/6 mice. Organism was cultured from the brain early
in the course of infection, and this isolate, named N40Br, was further
studied in vitro. The plasmid content of N40Br was different from that of
the infecting strain, implying either a highly selective process during
infection or DNA rearrangement in the organism in vivo. N40Br was very
sensitive to antibiotics, but only after prolonged incubation. Immune sera
from both mice and humans infected with B burgdorferi were unable to
completely kill the organism by complement-mediated cytotoxicity. These data
demonstrate that B burgdorferi infects the brain of
experimental animals, and is resistant to immune sera in vitro but sensitive
to prolonged treatment with antibiotics.”
http://www.ncbi.nlm.nih.gov/pubmed/2215944
After a time the plasmid content was different from the original strain,
says Pachner. That would be because Lyme is just another relapsing fever
borreliosis. Antibiotics merely cause the organisms to convert into a
spheroplast form, but that is a topic for another DOJ criminal charge
sheet. The cyst or spheroplast form is not an “end-stage,” as some claim.
It is a replication form. Previously we said, “The thing to do about Lyme
is to catch it early before the shed Osp or fungal antigen-related
immunosuppression invites (cross-tolerance) other pathogens or reactivates
old, dormant ones like the herpes viruses, do most of the damage.” But
apparently this damage is done right away, according to Baumgarth and Chiu.
Where else to we find these fungal, OspA-like antigens?
J Biol Chem. 1999
Nov 19;274(47):33419-25.
Toll-like receptor 2 functions as a pattern
recognition receptor for diverse bacterial products.
Lien E1, Sellati
TJ, Yoshimura
A, Flo
TH, Rawadi
G, Finberg
RW, Carroll
JD, Espevik
T, Ingalls
RR, Radolf
JD, Golenbock
DT.
”Toll-like
receptors (TLRs) 2 and 4 are signal transducers for lipopolysaccharide, the
major proinflammatory constituent in the outer membrane of Gram-negative
bacteria. We observed that membrane lipoproteins/lipopeptides from Borrelia
burgdorferi, Treponema pallidum,
and Mycoplasma fermentans activated
cells heterologously expressing TLR2 but
not those expressing TLR1 or TLR4. These TLR2-expressing
cells were also stimulated by living motile B. burgdorferi, suggesting that TLR2 recognition
of lipoproteins is relevant to natural Borrelia infection. Importantly, a TLR2 antibody
inhibited bacterial lipoprotein/lipopeptide-induced tumor necrosis factor
release from human peripheral blood mononuclear cells, and TLR2-null
Chinese hamster macrophages were insensitive to lipoprotein/lipopeptide
challenge. The data suggest a role for the native protein in cellular
activation by these ligands. In addition, TLR2-dependent
responses were seen using whole Mycobacterium
avium and Staphylococcus
aureus, demonstrating that
this receptor can function as a signal transducer for a wide spectrum of
bacterial products. We conclude that diverse pathogens activate cells
through TLR2 and
propose that this molecule is a central pattern recognition receptor in host
immune responses to microbial invasion.”
http://www.ncbi.nlm.nih.gov/pubmed/10559223
http://www.jbc.org/content/274/47/33419.long
What you should do when
reading this general science material, particularly like the 1999 one above
and see related and see cited by on PubMed.
These triacyl-lipopeptides are only initially inflammatory.
After a time, this same researcher, Radolf, wrote that these fungal
lipoproteins cause immunosuppression and a lack of antibody production:
J Immunol. 2001
Jul 15;167(2):910-8.
Toll-like receptor 2-dependent inhibition of
macrophage class II MHC expression and antigen processing by 19-kDa
lipoprotein of Mycobacterium tuberculosis.
Noss EH1, Pai
RK, Sellati
TJ, Radolf
JD, Belisle
J, Golenbock
DT, Boom
WH, Harding
CV.
”Mycobacterium
tuberculosis (MTB)
induces vigorous immune responses, yet persists inside macrophages, evading
host immunity. MTB bacilli or lysate was found to inhibit macrophage
expression of class II MHC (MHC-II) molecules and MHC-II Ag processing. This
report characterizes and identifies a specific component of MTB that
mediates these inhibitory effects. The inhibitor was extracted from MTB
lysate with Triton X-114, isolated by gel electroelution, and identified
with Abs to be MTB 19-kDa lipoprotein. Electroelution- or
immunoaffinity-purified MTB 19-kDa lipoprotein inhibited MHC-II expression
and processing of both soluble Ags and Ag 85B from intact MTB bacilli.
Inhibition of MHC-II Ag processing by either MTB bacilli or purified MTB
19-kDa lipoprotein was dependent on Toll-like receptor (TLR) 2 and
independent of TLR 4. Synthetic analogs of lipopeptides from Treponema
pallidum also inhibited Ag processing. Despite the ability of MTB 19-kDa
lipoprotein to activate microbicidal and innate immune functions early in
infection, TLR 2-dependent inhibition of MHC-II expression and Ag processing
by MTB 19-kDa lipoprotein during later phases of macrophage infection may
prevent presentation of MTB Ags and decrease recognition by T cells. This
mechanism may allow intracellular MTB to evade immune surveillance and
maintain chronic infection.”
http://www.ncbi.nlm.nih.gov/pubmed/11441098
Spirochetes create multiple variants and all the individual spirochetes
do their own thing, varying their surface antigens on their own, shedding
these fungal antigens in a process called blebbing, ruining a person's
immune system. And a ruined immune system is
the DAMAGE and is
the ILLNESS and is
the specific goal of a bioweapon:
AND
"Methods of using antipersonnel agents undoubtedly
wary so that no uniform pattern of employment or operation is evident [make
sure it does not produce antibodies, so
assess the HLAs in the population you intend to abuse like the defecting
Russian scientists at NYMC have been doing, is the short version-
KMD]. It
is likely that agents will be used in combinations so that disease symptoms
will confuse diagnosis and interfere with proper treatment. It is also
probable that biological agents would be used in heavy concentrations to
insure a high percentage of infection [or
just use the OspA vaccine- KMD] in
the target area. The use of such concentrations [or
the multiple infections it causes, due to the immunosuppression like HIV,
Lyme, or LYMErix as acquired
immune deficiencies -
KMD] could
result in the breakdown
of individual immunity because
the large number of micro-organisms entering the body could overwhelm the
natural body defenses [or
just infect or inject people with an immune suppressor like OspA from a tick
or a syringe, and the reverse will happen: people will acquire multiple
infections because their immunity is trashed by fungal OspA- KMD].
Do you see the disease now? It's
fungal (shed borrelial antigens are TLR2/1-agonists or fungal); it is about
“overwhelming the immune system” (which is another way to way, “post-sepsis
syndrome”); it is about not producing identifiable antibodies; your
bioweapon should be like a Trojan Horse, setting off other latent
infections; your immune system is now turned off (“overwhelmed”
means “turned off”); you don't have "biofilms" at least of borrelia; Lyme
was the "perfect
stealth disabler." See more in the Occam’s Razor chapter.
V. SIDESTEPPING
- Alert on “Biofilms”
Use “Borrelia Staining” or “Borrelia Silver Staining”
as search
terms in PubMed to
discover that Borrelia in
vivo do
not cluster at all, much less under a “biofilm.” Here is one. Look closely
for the “clustered spirochetes hiding under a biofilm” (there is no such
thing):
J Med Microbiol. 1987
May;23(3):261-7.
Demonstration of spirochaetes in patients with Lyme disease with
a modified silver stain.
De Koning J, Bosma
RB, Hoogkamp-Korstanje
JA.
https://www.ncbi.nlm.nih.gov/pubmed/2438410
http://jmm.sgmjournals.org/content/23/3/261.long
Here is another one by Paul Duray [same guy who revealed that congenital
Lyme brain damage kills babies and
who revealed that Lyme- and LYMErix- diseases cause a leukemia-like illness
and that the cells in the CSF of Lyme patients "look like Epstein-Barr
transformed (mutated, pre-cancerous) cells]:
J Clin Microbiol. 1991
Apr;29(4):764-72.
Morphology of Borrelia burgdorferi: structural
patterns of cultured borreliae in relation to staining methods.
Aberer E1, Duray
PH.
"The microscopic recognition of Borrelia burgdorferi
in biologic fluids and tissues is difficult and challenging because of low
numbers of organisms occurring as single isolated spirochetes, the
apparent lack of colony formation in tissues, and differing lengths and
structural morphologies."
http://www.ncbi.nlm.nih.gov/pubmed/1716264
Additionally, some biofilms are covered in TLR2/1
agonists so
the body does not even see them at all any more, if they are there in this
post-sepsis disease called Chronic Lyme, with the multiple reactivated
herpes viruses, etc., and the expansion of tolerance to other
toll-like-receptor-managed antigen types. The biofilms could be covering
other organisms, but spirochetes are all independent operators and the
illness and the damage is mainly from the secondary, “Post Sepsis Syndrome,”
infections.
REVIEW: Biofilms
covering spirochetes are NOT responsible for the persistent symptoms in
Chronic Lyme Disease. Spirochetes, while permanent, and while they have
been shown to be draped in lymphocyte membrane, or have a “mucopeptide
layer” (or while were always known to be covered in a slime layer), are not the
main cause of the disease or the reason antibiotics fail.
Yes, spirochetal diseases are incurable. No, the disease is not about
spirochetes, since they shed fungal antigens and ruin the immune system,
inviting in other opportunistics or reactivating old ones. We learned this
from LYMErix disease where the vaccine gave people the same systemic disease
we know of as Chronic Lyme or Chronic Fatigue Syndrome. It is a NO-IMMUNE
disease, post-sepsis.
VI. On using the
correct DNA to look for spirochetes in humans by using recombinant
Borrelia-specific flagellin DNA product to detect those specific antibodies
Says Yale:
Infect Immun. 1991
Oct;59(10):3531-5.
Molecular characterization of the humoral
response to the 41-kilodalton flagellar antigen of Borrelia burgdorferi, the Lyme disease agent.
Berland R1, Fikrig
E, Rahn
D, Hardin
J, Flavell
RA.
"The earliest humoral response in patients infected
with Borrelia burgdorferi, the agent of Lyme disease, is directed against
the spirochete's 41-kDa flagellar antigen. In order to map the epitopes
recognized on this antigen, 11 overlapping fragments spanning the flagellin gene
were cloned by polymerase chain reaction and inserted into an Escherichia
coli expression vector which directed their expression as fusion proteins
containing glutathione S-transferase at the N terminus and a flagellin fragment
at the C terminus. Affinity-purified fusion proteins were assayed for
reactivity on Western blots (immunoblots) with sera from patients with
late-stage Lyme disease. The same immunodominant domain was bound by sera
from 17 of 18 patients. This domain (comprising amino acids 197 to 241) does
not share significant homology with other bacterial flagellins and therefore
may be useful in serological testing for Lyme disease."
http://www.ncbi.nlm.nih.gov/pubmed/1894359
Yale says that their method (same method patented as US
patent 5, 618, 533) detects, early, late, neurological, and every
other possible kind of Lyme outcome and
that it detects 94.4% of the cases, which means it is the closest
possible method we could possibly have to detect Lyme ("should be 100% of
the cases," says the FDA, verbatim), and
this method was made SPECIFIC, which means it does not detect any other
flagellins from non-Borreliae organisms.
When the FDA says "sensitivity," they really mean
"LIMIT OF DETECTION" and refer to the METHOD and not the "CASES."
“Accuracy” addresses cases. Yale, as you can see, took care of all that in
1991 and went ahead and patented it. They did not, however, use this method
to qualify LYMErix, their other patent, which is the essence of this False
Claims Act case.
The only way to detect a spirochetal disease is to use recombinant specific
flagellins antibody test from most of the Borreliae species that we know to
be at least in the United States. THAT is what is "VALID," and the FDA and
NIH agree.
VII. The FDA being forced to
assure Lyme testing is valid according to their own rules by the Senators
(summer, 2014):
Here we have to talk about the FDA and what their rules are for the
"Validation of an Analytical Method." As you can see there is Accuracy (should
detect 100% of the instances when the analyte in question is present), Specificity (only
detects one thing), Linearity,
Ruggedness, Precision (refers
to instrumentation), Limit of Detection (this
would be something like, "How low in concentration of the analyte in
question can your method detect?").
This is from the new announcement July 31, 2014 regarding the FDA now about
to ENFORCE their validation rules:
http://www.fda.gov/downloads/MedicalDevices/ProductsandMedicalProcedures/InVitroDiagnostics/ucm407409.pdf
The FDA says: “Under
the FD&C Act, the FDA assures both the analytical validity (e.g., analytical
specificity and sensitivity, accuracy, and precision) and clinical validity
of diagnostic tests through its premarket clearance or approval process.”
"Sensitivity" MEANS "Limit of Detection." The closest
thing to Sensitivity in the FDA (real) requirements is “Limit of
Detection.” Keep that in mind because the Cabal misuses that word all the
time.
FDA Rules on the Validation of an Analytical Method:
http://www.fda.gov/downloads/drugs/guidancecomplianceregulatoryinformation/guidances/ucm368107.pdf
Specificity (only
detects one thing)
Accuracy (Should
detect 100% of the instances where the analyte is present, and the
concentration should be close to 100% of that known to be spiked in, and
never should detect "none" as is the case with Lyme Western Blotting and the
Lyme ELISA, especially)
Limit of Detection (means
"What is the lowest concentration of the analyte in question does your
method detect?")
Precision (system
has integrity in performance)
Ruggedness (anyone
can run the test with their own equipment and get the same results)
Linearity (concentration
range of analyte for which the test is valid in and out of matrix or "inert
ingredients")
Your test should primarily detect all the
cases in question, - or be 100% ACCURATE - and that means, in the case of
Lyme, the only analyte for which we can test is flagellin or anti-flagellar
antibodies. Anti-flagellar antibodies can be found in probably 95% of Lyme
cases. So, Yale went ahead and made that Specific (also
described in US patent 5,618,533) in 1991, as shown previously, above.
Infect Immun. 1991
Oct;59(10):3531-5.
Molecular characterization of the humoral
response to the 41-kilodalton flagellar antigen of Borrelia burgdorferi, the Lyme disease agent.
Berland R1, Fikrig
E, Rahn
D, Hardin
J, Flavell
RA.
http://www.ncbi.nlm.nih.gov/pubmed/1894359
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC258917/pdf/iai00046-0199.pdf
For the other Borrelia in North America and Europe, at
least, such a recombinant-specific-multiple-flagellins method should be
developed and the NIH agrees with this (May, 2012, phone conversation).
There is no other way to detect most cases of Borreliosis. All the other
antigens are plasmid-encoded and variable. Borrelia spirochetes are not
always in the blood, so there is point to using a blood DNA method.
Flagellin is the only reliable antibody and it can be made specific. There
is no “end point” to treatment, since late Lyme is more about the other
opportunistics. But early Lyme, all agree that the flagellar antibody test
is the only test that captures the majority of cases and meets the FDA
criteria for “ACCURACY.”
Lyme and LYMErix cause immunosuppression and an
AIDS-like disease or an acquired immune deficiency, or as the NIH describes
it, post-sepsis with the all kinds of still-active herpes and other
infections. It should be said that Lyme and LYMErix diseases are far worse
than just spirochetes. Apparently that has always been the case. The
Great Imitator, Syphilis was probably really the Great Detonator of the
latent herpes and other infections. Syphilis was probably the original
AIDS, via OspA-like or fungal-antigen-like immunosuppression and the
reactivation of mostly Epstein-Barr.
VIII. SIDE-STEPPING - CDC’s Other Research Fraud: A) Lying about the
viability of the cyst or spheroplast form of spirochetes and B) lying about
mycoplasma not being involved in Chronic Fatigue Syndrome
CDC and IDSA claimed the cyst form was not viable, and
that Borrelia DNA-positive human samples were “just dead DNA” (never
happens, the body cleans up such debris). Yet here is the CDC in 1964
explaining how to dessicate and weaponize your Borrelia (freeze-drying – and
good for at least a year, they say):
J Bacteriol. 1964
Sep;88:811.
RECOVERY OF TREPONEMA AND BORRELIA AFTER LYOPHILIZATION.
HANSON AW, CANNEFAX
GR.
https://www.ncbi.nlm.nih.gov/pubmed/14208528
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC277387/pdf/jbacter00438-0287.pdf
Next we see the CDC is
throwing out the blood cells (throwing out whole cells of any
kind), including red blood cells and immune cells or white cells to which
mycoplasma adhere, while alleging to look for mycoplasma in Chronic Fatigue
Syndrome. Mycoplasma or epERTHROzoa are called epERYTHROzoa because they
attach to red blood cells. Such epERYTHROzoa are famous for changing the
erythrocyte membrane potential and the ability of oxygen to cross the red
blood cell membrane, causing tremendous fatigue even in animals.
CDC did this to allegedly show Mycoplasma were not
involved in Chronic Fatigue Syndrome:
J Med Microbiol. 2003
Nov;52(Pt 11):1027-8.
Absence of Mycoplasma species DNA in chronic fatigue syndrome.
Vernon SD, Shukla
SK, Reeves
WC.
"Plasma, the liquid portion of peripheral blood that is devoid of cells,
is known to contain remnants of numerous physiological and disease
processes. We used plasma DNA to detect and characterize bacterial 16S rDNA
sequences in a group of individuals with CFS and a group of non-fatigued
controls (Vernon et al., 2002). Whilst a variety of bacterial sequences were
detected in both fatigued and non-fatigued groups, no Mycoplasma sp. 16S
rDNA sequences were found."
https://www.ncbi.nlm.nih.gov/pubmed/14532349
http://jmm.sgmjournals.org/cgi/pmidlookup?view=long&pmid=14532349
That is important. The CDC does not want anyone to
know fungal antigens and/or fungal antigen tolerance cause(s) extreme
fatigue. They must be important bioweapons, a problem with the pediatric
vaccines causing Autism, or both.
Next up the specific DNA Shell
Game played by members of the Cabal. You will see it is almost entirely CDC
officers committing this fraud. The data you have seen so far reveals 1)
how to test for all Borrelioses, 2) how we got this particularly
evolutionarily unlikely bird borreliosis in New England “on hurricanes?” and
3) catching the CDC staff committing research fraud in other arenas.
IX. The
CDC Cabal Play the DNA and RNA Shell Game (we learned what is
proper detection DNA: flagellin, and other non-variable specific RNA)
Alan Barbour playing the DNA/RNA shell game.
You will want to look at The Patents Criminal Charge sheet for this
multi-Crymes Disease to
see that CDC
officer and former head of the NIH’s Rocky Mountain Bioweapons Montana Lab
(you’re familiar with Montana, the place where there are tons of relapsing
fever borrelia but no “Lyme?”), Alan Barbour, reported
that, basically, “antigenic variation in one spirochete, times all the
spirochetes you have, leaves the immune system ‘overwhelmed’ with ‘an
infinite number of new antigens.’” This is a characteristic or attribute
of bioweapons, well described by the US Army when speaking to Congress as
shown previously in this document.
With all this malarkey about “Lyme disease” as opposed to relapsing fever,
and how the pediatric Autism vaccines fail and give children the very brain
infections they’re meant to prevent (same mechanisms; immunosuppression
either via fungal exposure or some other exposure, or genetic immune
insufficiency, plus live, attenuated viruses that become un-attenuated), you
get the impression that the CDC was never mentally or morally competent to
maintaining theirs and the USDA’s fallacies. We’ve longed called the CDC
the Centers for Disease Confabulation.
Alan Barbour states below that OspA undergoes true antigenic variation
and basically that, therefore you cannot use this as a vaccine (while he
owns the patent for the ImmuLyme OspA non-vaccine). If it undergoes “true
antigenic variation,” it certainly cannot be used for DNA diagnostics as Klempner
allegedly did in his “BREAKING NEWS!!!” bogus
“re-treatment” "study" that is now the data used by IDSA for their
"Guidelines on Lyme” from 2001 and 2006. Klempner said he looked for DNA of
Borrelia in the spinal fluid of his victims – and used OspA primers (ones
that will CHANGE and therefore not be there).
J Exp Med. 1992
Sep 1;176(3):799-809.
Antibody-resistant mutants of Borrelia burgdorferi:
in vitro selection and characterization.
Sădziene A1, Rosa
PA, Thompson
PA, Hogan
DM, Barbour
AG.
Says Barbour above: “Second,
previous studies had shown antigenic differences in outer membrane proteins,
OspA and OspB, between strains (21-26) and also true antigenic variation of
these proteins within a strain (25, 27-30).”
http://www.ncbi.nlm.nih.gov/pubmed/1339462
,
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119346/
None of the
OspA vaccines ever prevented Lyme or spirochetes in any animal. OspA
vaccination may have prevented arthritis by tolerance, but no animal study
showed prevention of spirochetes.
Remember, “mutants” is code language. They’re
all mutants. Antigenic variation or “selection pressure” is the nature of
the relapse in relapsing fever. To call them mutants is silly and redundant,
and not the least bit correct as you’ve seen in Barbour’s patents and in the
older data such as the Single Spirochete outcome.
Here are Fikrig and
Flavell, Yale employees and inventors
of the LYMErix patent saying the same thing: Due to antigenic variations
and antibodies forcing the bugs to change surface antigens, OspA or variable
DNA can never be a vaccine against Lyme or Relapsing Fever:
Infect Immun. 1995
May;63(5):1658-62.
Selection of variant Borrelia burgdorferi isolates
from mice immunized with outer surface protein A or B.
Fikrig E1, Tao
H, Barthold
SW, Flavell
RA.
“…B. burgdorferi organisms expressing wild-type OspA
(data not shown), showing that immunization against a clonal population of
spirochetes is also dependent upon the challenge dose. Therefore, we
postulate that during tick-borne infection, a population of antigenically
heterogeneous spirochetes may be transmitted to the host (27) and that the
spirochetes that persist in the immune host during the evolution of
infection and the development of chronic disease are more likely to be
partially resistant to borreliacidal immune responses.
”This report describes the ability of OspA and OspB antibodies to cause
the in vivo selection of B. burgdorferi organisms with subtle genetic
alterations that result in the expression of OspA or OspB which do not bind
to, or weakly bind with, antibodies that are protective in nature. These
data suggest a potential reason for the lack of complete efficacy of an
Osp-based Lyme disease vaccine. Over extended periods of time, the
administration of an OspA- or OspB-based vaccine to hosts that are involved
in the natural life cycle of the spirochete may result in the expansion of
variant B. burgdorferi isolates within ticks at a higher frequency than
would normally be found in the general population. If this selection
pressure was to be maintained, the number of variant spirochetes could rise
to a significant level, such that the efficacy of a monovalent OspA- or
OspB-based vaccine could be impaired in the future.”
http://www.ncbi.nlm.nih.gov/pubmed/7729870
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC173206/
Alan Carbour’s patent saying antigenic variation
and "overwhelms the immune system":
Patent filed in 2002 -
VMP-like sequences of pathogenic Borrelia
"2.1 Methods of Treatment
"… An important aspect of the invention is the recognition that Borrelia
VMP-like sequences recombine at the vls site, with the result that
antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological defenses
are severely
tested if not totally overwhelmed."
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6,719,983.PN.&OS=PN/6,719,983&RS=PN/6,719,983
So, you can’t use the OspA gene for a vaccine, for post-treatment or late
Lyme DNA diagnostics, or for “Lyme case” detection in antibodies. The only
thing you can do or say about OspA is that it apparently helped the
normally, formerly non-borreliae-bearing Ixodes (hard
bodied) ticks acquire a ligand (OspA-B plasmid) with which to attach to and
invade the hard bodies of hard bodied (Ixodes) ticks. Lyme
spirochetes were probably adapted on Plum Island to local vectors.
Genetically, the Lyme spirochete is closest to anserina, an
African bird borreliosis, likely making potentially likely to spread around
fast.
1995 – Barbour’s patent for Lyme in Missouri, using 16S
RNA sequencing and flagellin primer
probes that many of the Lyme Cabal members did not use when assessing human
treatment outcomes.
Barbour says this is in Lone Star ticks in Missouri:
Diagnostic tests for a new spirochete, Borrelia lonestari sp. nov.
“Bites from Amblyomma americanum,
a hard tick, have been associated with a Lyme disease-like illness in the
southeastern and south-central United States. Present in 2% of ticks
collected in four states were uncultivable spirochetes. Through use of the
polymerase chain reaction, partial sequences of the flagellin and 16s rRNA
genes of microorganisms from Texas and New Jersey were obtained. The
sequences showed that the spirochete was a Borrelia sp. but distinct from
other known members of this genus, including B. burgdorferi, the agent of
Lyme disease. Species-specific differences in the sequences of the flagellin
protein, the flagellin gene and the 16s rRNA gene between the new Borrelia
species and previously known species provide compositions and methods for
assay for determining the presence of this new spirochete, or for providing
evidence of past or present infection by this spirochete in animal
reservoirs and humans...
”…SUMMARY OF THE INVENTION
”The present invention provides
compositions, methods, and kits for the detection of a new spirochete that
is associated with a Lyme disease-like illness. The compositions are
based on a Borrelia lonestari sp. nov.-specific allotype or combination of
allotypes of the flagellin protein, or a Borrelia lonestari sp.
nov.-specific allele or combination of alleles of the flagellin or 16s rRNA
genes of the new spirochete. The allotypes and alleles provided by the
present invention have been determined by nucleic acid sequencing of
portions of the flagellin and rRNA genes from this new spirochete. Detection
of a species-specific amino acid or nucleotide as defined herein, or a
species-specific combination of amino acids or nucleotides as defined
herein, in a subject sample is indicative of infection with Borrelia
lonestari sp.
nov.”
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=5%2C932%2C220.PN.&OS=PN%2F5%2C932%2C220&RS=PN%2F5%2C932%2C220
Barbour sequenced the RNA and DNA, obviously and did not use someone else’s
primers. Using primer probes from Borreliae not expected to be there
(burgdorferi flagellin and another specific lonestari gene) rather than
sequencing. Therefore, Borreliae cannot be ruled out as Wormser did when
assaying EM rashes in Missouri. This patent of Barbour’s also shows Barbour
knows what are the species-distinguishers: NOT THE OSPS, VMPS or the PLASMID
DNA. He then can’t sign on to any claims about Lyme that mimic the CDC’s
and IDSA’s current fraudulent positions without expecting to be indicted.
Barbour does claim however, that the species identifier is… FLAGELLIN.
Gary Wormser playing the DNA/RNA shell game.
Next we are going to look at Gary Wormser who is in 1992 using the
correct primers; this proves he knows exactly how to identify Borrelia
species. Later, in order to “prove” there is no Lyme in Missouri, he does
not apply this same technique.
J Clin Microbiol. 1992
Dec;30(12):3082-8.
Diagnosis of early Lyme disease by polymerase chain
reaction amplification and culture of skin biopsies from erythema migrans
lesions.
Schwartz I1, Wormser
GP, Schwartz
JJ, Cooper
D, Weissensee
P, Gazumyan
A, Zimmermann
E, Goldberg
NS, Bittker
S, Campbell
GL, Pavia
CS.
”rRNA-based PCR detection assay for B.
burgdorferi.
”The organization of the rRNA genes of B. burgdorferi and the sequences of
the corresponding rRNAs have been determined (32). Figure 1 presents a
schematic diagram of the rRNA operon and the positions of the primers and
probes employed for PCR amplification and detection. The 23S rRNA sequence
was compared for homology to other rRNA sequences in the GenBank data base.
On the basis of these comparisons, a region near the 5' end of the 23S RNA
sequence (nucleotides 689 through 948) was chosen as a likely target for
amplification. The equivalent regions of the 23S rRNA genes in the related
species Borrelia hermsii and B. anserina and several isolates of B.
burgdorferi were also sequenced (Fig. 2). PCR primers (designated JS1 and
JS2) were designed to contain perfect homology to the B.
burgdorferi sequence
but maximum mismatch at their 3' ends with the related Borrelia species
(Fig. 2). The sensitivity of the PCR assay was determined with serially
diluted, titered B. burgdorferi samples. Fewer than 10 spirochetes in a
total sample could be detected efficiently (Fig. 3). The sensitivity and
specificity of the assay were also investigated by performing PCR
amplification with 10 different isolates of B.
burgdorferi, B. hermsii, B. anserina, and Borrelia
turicatae. Samples
containing 50 spirochetes were subjected to PCR amplification, and one-fifth
of the amplified product (equal to 10 spirochetes) was detected by
hybridization with a radiolabeled probe (FS1) corresponding to a portion of
the amplified sequence. All isolates of B. burgdorferi were detected by the
procedure with essentially equal efficiency (Fig. 4). These included
isolates from North America (isolates 24430, 24352, HK, B31, 297), Europe
(20004, Gl, 20047), and Russia (IP90, IP3). Furthermore, only B. burgdorferi
was detected by this method; samples containing the other closely related
Borrelia species produced no amplified product.
”To provide a second primer pair that could be employed for specific
detection of B. burgdorferi, we took advantage of the unusual and unique
tandem duplication of the 23S rRNA gene (Fig. 1). This feature was observed
in all B. burgdorferi isolates tested and, furthermore, was not found in
other Borrelia species (32). Thus, a PCR amplimer pair with the forward
primer targeted to a sequence at the 3' end of the first copy of 23S RNA
gene and a reverse primer complementary to a sequence near the 5' end of the
second 23S RNA gene copy should have absolute specificity for B.
burgdorferi. The locations of this primer pair (designated IS1 and IS2,
respectively) relative to the rRNA operon are presented in Fig. 1. The
sensitivity and specificity of this primer pair were tested in a manner
similar to that described above for the JS1-JS2 primer pair. The IS1-IS2
amplimer set displayed a degree of specificity and sensitivity similar to
that of JS1-JS2 (Fig. 5).
http://www.ncbi.nlm.nih.gov/pubmed/1452688
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC270592/pdf/jcm00036-0064.pdf
In 2005, in Missouri, Wormser did not use these same methods.
We’ll see that report shortly.
In this next report, Gary Wormser in 1999, when using the correct
primers (16S) finds some people
are infected with more than one species of Borrelia burgdorferi (yet,
ignoring the other Borrelia) and that you can't really use
Barbour-Kelly-Stoener culture media, the only one anyone sells in the USA.
It shows Wormser knows what DNA to use when looking for spirochetes, yet he
is a signer of the IDSA “Guidelines” which are based on Klempner’s bogus
“re-treatment” “study,” which is based on the falsified Dearborn case
definition, and
which is based on the bogus OspA gene to determine “no Lyme” after
“treatment.”
J Clin Microbiol. 1999
Mar;37(3):565-9.
1999 - Genetic diversity of Borrelia burgdorferi in lyme disease patients
as determined by culture versus direct PCR with clinical specimens.
Liveris D1, Varde
S, Iyer
R, Koenig
S, Bittker
S, Cooper
D, McKenna
D, Nowakowski
J, Nadelman
RB, Wormser
GP, Schwartz
I.
”… The
data confirmed the presence of the three major RFLP types previously
described (17).
Of 183 skin isolates, 46 (25.1%) were type 1, 70 (38.3%) were type 2, and 55
(30.1%) were type 3; the
remaining 6.6% (12 of 183) were mixed cultures composed of at least two
genotypically distinct isolates.”
http://www.ncbi.nlm.nih.gov/pubmed/9986813
1995-6—Alan Barbour does proper sequencing for the analysis of the
spirochetes in the Lone Star tick (compare to what Wormser does, following
this report):
J Infect Dis. 1996
Feb;173(2):403-9.
Identification of an uncultivable Borrelia species in
the hard tick Amblyomma americanum: possible agent of a Lyme disease-like
illness.
Barbour AG1, Maupin
GO, Teltow
GJ, Carter
CJ, Piesman
J.
“…The deduced amino acid sequences for flagellin proteins of the 2
microorganisms found in A. americanum were identical over 213 residues; the
nucleotide differences between strains were synonymous. Figure 3 shows the
alignment of part of the deduced flagellin sequences of the spirochetes
found in A. americanum in Texas and New Jersey with the comparable variable
regions of the flagellin proteins of 8 Borrelia species and Treponema
pallidum, the spirochete that causes syphilis. The amino acid positions are
numbered according to the full length B. burgdorferi flagellin protein. The
flagellin proteins of microorganisms found in A. americanum differed from
other borrelial flagellins at several positions and, uniquely among the
Borrelia species, lacked most of a proline-alanine-rich region beginning
around residue 220. The spirochetes found in A. americanum resembled B.
turicatae, B. hermsii, B. parkeri, B. crocidurae, and B. anserina in being
without the QAA at residues 204-206 of the Lyme disease agents B.
burgdorferi, B. garinii, and B. afzelii...
“Analysis of 16S rRNA genes. Further phylogenetic classification was
provided by comparison of 16S rRNA gene sequences (figures 4 and 5). The
sequence of the spirochete found in A. americanum from Texas had the
following identities with selected other spirochete 16S rRNA genes:
T.pallidum, 79.6%; B. burgdorferi, 96.0%; B. anserina, 97.5%; B. hermsii,
97.8%; B. miyamotae sp. nov., 98.3%; and the "Florida canine borrelia,"
98.4%. By distance matrix and parsimony analyses of the aligned sequences
(figure 4), the spirochete found in A. americanum clustered with a group
containing the relapsing fever species B. hermsii, B. anserina, the unnamed
organism recovered from the blood of 2 dogs in Florida [25], and B.
miyamotae sp. nov. (accession no. 045192).”
”Figure 4. Unrooted distance matrix phylogenetic tree of Borrelia species
with Treponema pallidum as out group. 16S rRNA sequences corresponding to
base positions 36- 1371 of Borrelia burgdorferi 16S rRNA gene were aligned
and analyzed with PHYLIP program package. Exhibited tree in New Hampshire
standard format is: «(Florida canine borrelia: 100, (Borrelia anserina: 100,
Borrelia hermsii, 100): 52): 42, (borrelia from A. americanum: 100, Borrelia
miyamotae sp. nov.: 100): 96): 88, T. pallidum: 100, B. burgdorferi: 100).
Circled numbers indicate number of times (in 100) that particular node was
supported by bootstrap analysis. Approximate evolutionary distances are
measured along line segments; bar represents distance by Jukes-Cantor
criteria of 0.005. Similar tree (not shown) was obtained by parsimony
analysis of 100 bootstrapped datum sets: «««borrelia from A. americanum:
100, B. miyamotae: 1(0): 94, B. hermsii: 1(0): 34, Florida canine borrelia:
100): 25, B. anserina 100): 81, B. burgdorferi: 100): 100, T. pallidum:
100).”
http://www.ncbi.nlm.nih.gov/pubmed/8568302
jid.oxfordjournals.org/content/173/2/403.full.pdf
Barbour actually sequenced for flagellin and 16S RNA
and found all kinds of spirochete in this way.
For the Missouri Lyme Masters’ Disease spirochete, Barbour said…
… while Wormser tried to say “No Lyme In Missouri.” (By the way, no one
cares if they have burgdorferi or antarcticii or siberii
or freakin jupiterii. They just want to know if the science shows
they’re sick.)
Here is Wormser trying to fool Edwin Masters, using the wrong DNA and RNA so
he can say,” There is no Lyme in Missouri”
Clin Infect Dis. 2005
Feb 1;40(3):423-8. Epub 2005 Jan 10.
Microbiologic evaluation of patients from Missouri
with erythema migrans.
Wormser GP1, Masters
E, Liveris
D, Nowakowski
J, Nadelman
RB, Holmgren
D, Bittker
S, Cooper
D, Wang
G, Schwartz
I.
“PCR amplifications were performed in a 50-μL reaction
mixture containing 10 mmol/L Tris-HCl (pH 8.3); 1.5 mmol/L MgCl2; 50 mmol/L
KCl, 0.1% (w/v) gelatin; 100 μmol/L each of dATP, dGTP, dCTP, and TTP; 1.25
units Taq polymerase; and 20 pmol of each primer. Detection of borrelial
DNA in patient specimens and ticks was accomplished by the nested PCR
amplification of flaB using
primers FlaLL, FlaLS, FlaRL, and FlaRS as described by Barbour et al [11]. PCR
of 16S rDNA was performed with broad-range eubacterial primers 8FPL and
1492RPL [26], which yields a product of ∼1.5 kbp. In cases in which no
detectable product was obtained, second-round heminested PCR was performed
with 8FPL and a reverse primer (519R: 5′-TTACCGCGGCTGCTGGC-3′) targeted at
residues 535–518 (numbering corresponds to residues in the 16S RNA sequence
of Escherichia coli) in 16S rDNA; this resulted in a fragment of 500 bp.
Some specimens were also tested by PCR targeted at ospA (forward primer,
5′-CTGCAGCTTGGAATTCAGGCACTTC-3′; reverse primer,
5′-GTTTTGTAATTTCAACTGCTGACCCCTC-3′) and/or recA [27].”
http://www.ncbi.nlm.nih.gov/pubmed/15668867
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773674/
Wormser did not use the correct Borreliae-specific (for
non-burgdorferi or from any other relapsing fever groups) flagellin
genes, or 16S rDNA specific to Borreliae species, nor did he actually try to
sequence any of these Borreliae as Barbour did (and Telford, below).
Wormser would have known to use the correct method to detect spirochetes in
Lone Star ticks, since he referenced Barbour’s work (ref 11 was: Identification
of an uncultivable Borrelia species
in the hard tick Amblyomma
americanum:
possible agent of a Lyme disease–like illness. (shown
above). Wormser
knows how to do this kind of DNA analysis and that there are all sorts of
Borrelia in Lone Star ticks – and ones that cause human disease.
The enzyme Wormser talks
about, GlpQ (next reference here, by the NIH) is specific to B.
lonestari, but that
does not mean there are no disease-causing Borreliae in Lone Star ticks or
Missouri.
J Bacteriol. 2003
Feb;185(4):1346-56.
Glycerol-3-phosphate acquisition in spirochetes:
distribution and biological activity of glycerophosphodiester
phosphodiesterase (GlpQ) among Borrelia species.
Schwan TG1, Battisti
JM, Porcella
SF, Raffel
SJ, Schrumpf
ME, Fischer
ER, Carroll
JA, Stewart
PE, Rosa
P, Somerville
GA.
http://www.ncbi.nlm.nih.gov/pubmed/12562805 ,
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC142843/
Wormser’s whole
point was to say there are no Borrelia causing disease or “Lyme” in
Missouri. The very last statement he makes in that report is: “Although
it is unknown whether this rash illness has an infectious etiology, it is
important to emphasize that this study does not indicate the absence of a
therapeutic role for antibiotic treatment.” (AKA, CYA, in the common
vernacular.) It could have been some other Borrelia, just not
burgdorferi or lonestari. Check the Taxonomy database for all
the Borrelia in the USA alone.
Additionally, these were Wormser’s actual results:
Here is Wormser’s abstract:
Clin
Infect Dis. 2005
Feb 1;40(3):423-8. Epub 2005 Jan 10.
Microbiologic evaluation of patients from Missouri
with erythema migrans.
Wormser GP1, Masters
E, Liveris
D, Nowakowski
J, Nadelman
RB, Holmgren
D, Bittker
S, Cooper
D, Wang
G, Schwartz
I.
“Borrelia lonestari infects Amblyomma
americanum, the tick species that is the most common cause of tick
bites in southeast and south-central United States, and this spirochete has
been detected in an erythema migrans (EM)–like skin rash in 1 patient.
Therefore, B. lonestari is
considered to be a leading candidate for the etiologic agent of EM in this
region.
“Skin biopsy specimens
obtained from patients from the Cape Girardeau area of Missouri who had
EM-like lesions were cultured in Barbour-Stoenner-Kelly medium and evaluated
by polymerase chain reaction (PCR) targeting multiple genes. Serum specimens
were tested by enzyme-linked immunosorbent assay for antibodies against
sonicated whole-cell Borrelia
burgdorferi. Results were compared with those obtained over the same
period for patients from New York State who had EM.
“B. lonestari was
not detected by PCR in any of 31 skin biopsy specimens collected from 30
Missouri patients. None of 19 cultures of Missouri skin samples that were
suitable for evaluation were positive for B.
burgdorferi, compared with 89 (63%) of 142 cultures of samples
collected from New York State patients (P <
.001). None of the 25 evaluable Missouri patients were seropositive for
antibodies against B.
burgdorferi, compared with 107 (75%) of 143 New York State patients (P <
.001).
“Neither B.
lonestari nor B.
burgdorferi is likely to be
the cause of EM-like skin lesions in patients from the Cape Girardeau area
of Missouri. The etiology of this condition remains unknown.
https://www.ncbi.nlm.nih.gov/pubmed/15668867
So, just to reiterate Wormser’s Take-Home Message here: ”There is no Lyme
in Missouri except for those 5 out of ~30, and we were playing around with
the DNA primers. (Shhh: It’s closer to B. miyamotae and
Florida Canine Lyme disease Borrelia. Also, Shhhh, the Barbour culture
medium is specific to burgdorferi spirochetes and does not grow all
spirochetes.) The EM-Lyme illness in Missouri could have been from some
other Relapsing Fever or Ehrlichial pathogen but we are pretending there is
no such thing as an illness from a tick bite. Lyme is imaginary so get the
placebo vaccine. We used no hermsii or other common spirochetes
known to be in the west and south of the United States. The end game is to
not find illness and to say that there is no illness from a tick bite,
while Barbour patented the lonestari bug right under Masters’ nose for later
use as a vaccine against this disease that does not exist and no one has so
get the vaccine….especially in Missouri.”
It is, yes. This is a dizzying kaleidoscope of lies, is what you’re
thinking now. The whole point of it all, and the reason this scam
continues, is because the Cabal does not want anyone to know they falsified
the case definition at Dearborn. They LIED to everyone and said, “No, ‘Lyme
Disease’ is a self-limiting autoimmune monoarticular joint disease. It does
not cause any illness.” (It’s “pretense.”)
Well, why do modern
spirochetes not cause any illness? Because OspA injections had the same
outcome. These criminal dummy wannabee scientists are mortified, really,
over being discovered to be not only that stupid, but crooked. Think about
it. They never were “the smartest guys in the room,” but they
wanted to be seen as an authority on something, didn’t they? It’s obvious.
Why else would they e-stalk us and e-trash us for going on 3 decades now, as
way to allegedly be “scientific?”
Mark Klempner, playing the DNA/RNA shell game.
You have previously seen that the OspA gene undergoes antigenic variation
and is not found in all Borreliae. You can't use this DNA for anything,
especially not vaccines or detection. We move on to the Klempner “study”
which unfortunately resulted in the 2001 and 2006 IDSA “Guidelines” and
where he references which DNA he used to assess "NO LYME IN LYME VICTIMS."
Klempner doesn’t actually say what DNA he uses (only by reference) to
determine “No Lyme” in Lyme victims, and the peer reviewers at the New
England Journal of Medicine (NEJM) never noticed he did not list his
primers:
N Engl J Med. 2001
Jul 12;345(2):85-92.
Two controlled trials of antibiotic treatment in patients with persistent symptoms and
a history of Lymedisease.
Klempner MS1, Hu
LT, Evans
J, Schmid
CH, Johnson
GM, Trevino
RP, Norton
D, Levy
L, Wall
D, McCall
J, Kosinski
M, Weinstein
A.
https://www.ncbi.nlm.nih.gov/pubmed/11450676
http://www.nejm.org/doi/full/10.1056/NEJM200107123450202#t=articleMethods
“Laboratory Studies
“Western blotting for IgG antibodies against B. burgdorferi antigens
was performed with the IgG MarBlot (MarDx Diagnostics, Carlsbad, Calif.)
according to the manufacturer's instructions.6 The
intrathecal production of antibodies against B. burgdorferi was
measured as previously described.20 Base-line specimens of cerebrospinal fluid and
plasma specimens obtained at base line and on days 3, 5, 21, and 45 were
tested by PCR for the presence of B. burgdorferi DNA, as
previously described.21 All
samples of cerebrospinal fluid were cultured in Barbour–Stoenner–Kelly II
medium to detect B.
burgdorferi and
were monitored by dark-field microscopy for six weeks.22 Some
blood samples were cultured for B. burgdorferi in
hypertonic medium.23”
So, what was that mysterious REFERENCE 21 above ^^ DNA that
Klempner failed
to report and
the so-called peer-reviewers did not notice?
Steere’s
J Infect Dis. 1996
Sep;174(3):623-7.
Detection of Borrelia
burgdorferi DNA by polymerase
chain reaction in
cerebrospinal fluid in Lyme
neuroborreliosis.
Nocton JJ1, Bloom
BJ, Rutledge
BJ, Persing
DH, Logigian
EL, Schmid
CH, Steere
AC.
https://www.ncbi.nlm.nih.gov/pubmed/8769624
http://jid.oxfordjournals.org/content/174/3/623.full.pdf
WHICH SAYS:
ONLY an OspA gene and later added an OspB gene (read the whole report). And
where Steere found many positive patients, Klempner says he found none (2001
RI “Diseases of Summer” conference at South County Hospital, audiotaped).
The Cabal – including Klempner in his 2001 bogus non-retreatment report that
is now the basis of the IDSA “Guidelines” - say if the OspA gene is not
there, there is no Lyme, right? This, despite the fact that 1) Lyme is a
relapsing fever borrelia and OspA is a variable plasmid gene and therefore
not likely to be in the same form or produced by the exact same genetic code
as one produced inside a tick, late in the disease in humans; 2) they’ve
used and sequenced for16S or flagellin DNA (non-variable, although
species-specific and for which there are more copies) in the past,
particularly to patent and therefore own species; 3) and referenced the NIH
recommendation for using these 16 and 23S probes.
Durland Fish, using the
correct primers to
look for new species of Borreliae to patent in 2001, yet is a signer of the
IDSA “Guidelines” once again, based only on an OspA gene and Dearborn as
“Lyme” or the chronic illness caused by a tick bite.
Vector Borne Zoonotic Dis. 2001
Spring;1(1):21-34.
A relapsing fever group spirochete transmitted by
Ixodes scapularis ticks.
Scoles GA1, Papero
M, Beati
L, Fish
D.
"A 1,347-bp portion of 16S rDNA was amplified from a
pool of infected nymphs, sequenced, and compared with the homologous
fragment from 26 other species of Borrelia. The analysis showed 4.6%
pairwise difference from B.
burgdorferi, with the closest relative being Borrelia miyamotoi (99.3%
similarity) reported from Ixodes
persulcatus in
Japan. Phylogenetic analysis showed the unknown Borrelia to cluster with
relapsing fever group spirochetes rather than with Lyme disease spirochetes.
A 764-bp fragment of the
flagellin gene was also compared with the homologous fragment from 24 other
Borrelia species. The flagellin sequence of B. burgdorferi was 19.5%
different from the unknown Borrelia and showed 98.6% similarity with B.
miyamotoi."
http://www.ncbi.nlm.nih.gov/pubmed/12653133
What that means is the probably-Plum-Island-and-unlikely-hurricane-borrelia, B.
burgdorferi, migrated to Japan and back to the United States again,
“mutating” to adapt to a Japanese Ixodes tick. Yet,
a year later, we
see Durland Fish using the WRONG DNA (OspA gene again), to
assess treated mice, to determine if there is any Borrelia, coming to the
conclusion that there is pretty much no Borrelia:
Detection of Attenuated, Noninfectious
Spirochetes in Borreliaburgdorferi–Infected
Mice after Antibiotic Treatment
"PCR of DNA.DNA was isolated from individual ethanol-fixed nymphs or pooled
larvae by means of the Isoquick DNA isolation kit (ORCA Research) and was
resuspended in 20 μL of double-distilled H2O. Primers used for amplification
were as follows: *** ospA *** (GenBank accession no. M57248, product
amplicon coordinates 80–781): forward, 5′-AAAACAGCGTTTCAGTAGATTTGCCTGGTG-3′,
and reverse, 5′-CAACTGCTGACCCCTCTAATTTGGTGCC-3′; BBE21.1 (GenBank accession
no. AE000785, product amplicon coordinates 14663–14921): forward,
5′-AGAATTATGTCGGTGGCGTTGT-3′, and reverse, 5′-ATTAAAGCCGCCTTTTCCTTGGT-3′;
and p37-47 (GenBank
accession no. AE000794, product amplicon coordinates 1309–1457): forward,
5′-TTCTGATGGCACTGAGCAAACCA-3′, and reverse,
5′-AACCCTTTACACTTTCTTCGATTGCGCT-3′. The primer set for p37–47 has 100%
homology to sequences in both B. burgdorferi strains B31 and N40, and the
gene has been localized to lp28-1 in both strains [26, 27]. The primer set
for BBE21.1 amplifies a unique region in lp25 of
B. burgdorferi strain B31 downstream of BBE21 (amplicon coordinates
13403–14530) [28]. BBE21 is located on a similar-size plasmid
within B. burgdorferi strain N40 [29]. We have been able to amplify by PCR
the region corresponding to GenBank accession number AE000785, product
amplicon coordinates 14195–14921, indicating that BBE21 and BBE21.1 reside
on the same plasmid in
N40 (authors' unpublished data)"
http://jid.oxfordjournals.org/content/186/10/1430.long
Those are plasmids ,
those "lp” things. Plasmids are from where the variable surface protein
antigens vary themselves. So, that is a classical Durland Fish type “bogus
article.” See:
http://www.actionlyme.org/TICK_BITE_CONSPIRACY.htm where
Durland admits that he writes “bogus articles,” not that you’re not already
convinced. Anyway, previously he used the correct DNA, 16rDNA and
flagellin, but then in a post-treated case or cases, he used a gene not
likely to be there, OspA.
It probably is true that the spirochetes become
attenuated as we have seen with Jay Sanford stating that spirochetes
“persist in the brain and eye even after apparent cure” (or they do all
their damage early), and Alan Barbour recommending infecting syphilis
patients with old, wimpy, high-passage borrelia spirochetes to raise a
fever. Spirochetal diseases are all un-eradicable, as shown above. And
surely it is true that older spirochete populations in the same host lose
plasmids [NEVER use plasmid DNA to assess Lyme in humans], but the end game,
and the point of all this crime, is that the Cabal is trying to say that
their chronically ill victims are not sick, just crazy. In the end it was
OspA itself, a fungal antigen causing the reactivation of the herpesviruses,
Post-Sepsis Syndrome, and humoral immunosuppression with chronic
inflammation in the brain due to all the neurotropic herpes viruses and
Mycoplasma, etc., that blew up their intended RICO “enterprise” scam
(ALDF.com). It was a very dumb choice for a vaccine.
All of what you see in these SASH criminal charge sheets is evolving
criminal fraud in an attempt to hide all their previous lies. The most
serious offense, falsifying the case definition and rendering the 85%
without the arthritis HLAs - the million or so per year - permanently
disabled, is the one offense the Cabal so vigorously tries to mask by
issuing “Guidelines.” The “Guidelines,” based on Klempner, which is based
on Dearborn, is a way of Offense being the Best Defense. It’s Pretense, or
FRAUD. The Cabal would have the world believe that they all
believe the case definition was real and valid. We know for sure they know
it was not valid acceptable based on the non-consensus at Dearborn alone.
To put such debased individuals in charge of humans and vector-borne
diseases? That’s the United States; everything happens exclusively for
profit. Greed is our nature. It is synonymous with Exceptional! It’s ALL
ABOUT ME!! And it’s ALL ABOUT MONEY!! Hence, the new and totally novel in
human history, the BS de-scrambler Society for the Advancement of Scientific
Hermeneutics. Now we have Scientific Hermeneutics because this BS has
become like a religion or belief system, a DOCTRINE, if you will, that to
date, no “doctor” ever unscrambled on behalf of humanity.
Sam Telford's
2001 report saying “Southern Lyme” is closest to theileri or
bovine relapsing fever (the former “Tick Fever” that the cowboy/farmer wars
were all about):
J Clin Microbiol. 2001
Feb;39(2):494-7.
Lone star tick-infecting borreliae are most closely
related to the agent of bovine borreliosis.
Rich SM1, Armstrong
PM, Smith
RD, Telford
SR 3rd.
“Although Borrelia
theileri, the agent of bovine borreliosis, was described at the turn of
the century (in 1903), its relationship with borreliae causing Lyme disease
or relapsing fever remains undescribed. We tested the previously published
hypothesis that spirochetes infecting Lone Star ticks (Amblyomma americanum)
may comprise B.
theileri by
analyzing the 16S ribosomal DNAs (rDNAs) and flagellin genes of these
spirochetes. 9,
the Amblyomma agent, and B.
miyamotoiformed a natural group or clade distinct from but most closely
related to that of the relapsing fever spirochetes. B. theileri and
the Amblyomma agent were 97 and 98% similar at the nucleotide level within
the analyzed portions of the 16S rDNA and the flagellin gene respectively,
suggesting a recent divergence. The agent of bovine borreliosis might be
explored as a surrogate antigen for the as-yet-uncultivatable Amblyomma
agent in studies designed to explore the etiology of a Lyme disease-like
infection associated with Lone Star ticks.”
http://www.ncbi.nlm.nih.gov/pubmed/11158095
You can see that the Cabal had already sequenced the 3
similar strains of flagellar and genus specific 16S RNA spacer genes that
are derived from a cow or bovine relapsing fever (theileri, barbouri,
and lonestari).
But there is no “Lyme” in Missouri. You can see it is a shell game.
TO THIS DATE – from 1995 to 2015 - still, no one is
using any other of this proper DNA or RNA or SEQUENCING rather than using
bogus primer probes they know will not be found in humans to detect human
illness. They
all know the
only way to detect Lyme/Relapsing Fever is with specific recombinant
flagellins from all the Borreliae, similar to Yale’s Lyme specific flagellin
patented method, US 5,618,533.
1995- Yale’s Robert Schoen and Erol Fikrig say, essentially, “OspA is
bogus due to antigenic variation”
J Immunol. 1995
Dec 15;155(12):5700-4.
An ospA frame shift, identified from DNA in Lyme arthritis
synovial fluid,
results in an outer surface protein A that does not bind protective
antibodies.
Fikrig E1, Liu
B, Fu
LL, Das
S, Smallwood
JI, Flavell
RA, Persing
DH, Schoen
RT, Barthold
SW, Malawista
SE.
“Passive immunization
with murine or human Abs to outer surface protein A (OspA) can protect mice
against Borrelia burgdorferi, but OspA Abs elicited during natural infection
in mice or humans are unable to clear the spirochete from the infected host.
To examine Ab binding by OspA during the course of human infection, we
amplified the operon encoding full-length ospA and ospB from synovial fluids
of a patient with chronic Lyme arthritis, the first such recoveries from
human material, at four separate time points over 4.5 mo, and expressed OspA
in Escherichia coli. OspA mAbs that passively protected mice from infection
did not bind one of the expressed OspAs, because of a deletion in ospA that
resulted in a frame shift and premature stop codon near the carboxyl
terminus. However, expressed OspA from a later synovial fluid sample did not
contain this deletion. Thus, although altered forms of OspA, which
potentially can influence host immune effectiveness, do occur in the human
host, they cannot be the only factors responsible for microbial persistence.”
http://www.ncbi.nlm.nih.gov/pubmed/7499856
Oh, you mean Lyme is a Relapsing Fever organism, so you can’t use the OspA
gene for human treatment outcomes assessment or vaccines, huh Mr. Schoen, or
to detect “Lyme” in EM rashes in Missouri?
Telford, Fish, Schoen, Steere, Persing, Barbour, etc., were able to find any
kind of Borrelia anywhere America – and they are everywhere, North, South,
Central, West -, sequencing for species-specific non-variable, non-plasmid
DNA.
Yale's Robert Schoen (who says Lyme is not a real disease,
says, “I call it Lyme paranoia,” and needs no treatment) using 23S RNA
primers to assure his RICO
monopoly strain (and
later patent with Dave Persing, US Patent 6,045,804) is burgdorferi.
On page 235 of the .pdf, Schoen says:
J Clin Microbiol. 1997
Jan;35(1):233-8.
Borrelia burgdorferi enzyme-linked
immunosorbent assay for discrimination of OspA vaccination from spirochete
infection.
Zhang YQ1, Mathiesen
D, Kolbert
CP, Anderson
J, Schoen
RT, Fikrig
E, Persing
DH.
“…Subsequent evaluation of this isolate in our laboratory showed that this
strain was nonreactive with an OspA-based PCR assay designed to detect all
North American and European isolates of B. burgdorferi but that it contained
23S ribosomal DNA sequences indistinguishable from those of most
North American strains of B. burgdorferi sensu stricto such as strains B31
and N40 (22). Genomic macrorestriction analysis of this isolate by PFGE is
shown in Fig. 1. By PFGE, the isolate is related to B. burgdorferi N40,
relatives of which are widely distributed in the northeastern United States,
the Upper Midwest, and California (22). These isolates are also closely
related to type strain B31, in contrast to isolates from moderate-climate
regions of the southeastern and southwestern United States, which are often
related to strain 25015 (19, 22). However, in contrast to strain N40, strain
49736 apparently lacked the ca. 53-kb linear plasmid species presumed to
encode OspA and B. To verify this observation, we hybridized Southern blots
of the MluI digest with a probe specific for the OspA gene. In contrast to
strains N40 and B31, which were strongly OspA probe positive, no detectable
signal was observed in the digest derived from strain 49736 (not shown).
This observation was consistent with the absence of the 53-kb plasmid
species. Similar results were obtained from N40-like isolates 46047, 48510,
and B31-like isolates 46794 and 50772 (1).”
http://www.ncbi.nlm.nih.gov/pubmed/8968914
http://jcm.asm.org/content/35/1/233.full.pdf
and also reveals there is "Lyme" in the Southern and Western states in 1996:
Says Schoen, “These
isolates are closely related to type strain B31, in contrast to isolates
from moderate-climate regions of the southeastern and southwestern United
States which are often related to strain 25015 (19,22).”
And what are those references, 19 and 22?
REF 19 -
Res Microbiol. 1995
Jun;146(5):415-24.
Two geographically distinct isolates of Borrelia
burgdorferi from
the United States share a common unique ancestor.
Kolbert CP1, Podzorski
DS, Mathiesen
DA, Wortman
AT, Gazumyan
A, Schwartz
I, Persing
DH.
“The genetic diversity of Borrelia burgdorferi isolates from several
geographic regions was evaluated by nucleotide sequence analysis of the
genes encoding 23S ribosomal RNA and outer surface protein A.
Comparison of nucleotide sequences spanning 738 bp of the 23S ribosomal DNA
from two unusual isolates, DN127 (Del Norte County, California) and 25015
(Millbrook, New York), to homologous sequences from other
B. burgdorferi isolates from the United States and Russia identified several
nucleotide sequence polymorphisms that are unique to these two isolates.
Sequence analysis of a 615 nucleotide segment of the gene encoding outer
surface protein A also revealed greater similarity of strains DN127 and
25015 (94.1%) compared to other US and Eurasian isolates. These data were
further corroborated by genomic macrorestriction analysis, in which DN127
and 25015 demonstrated unique restriction digestion patterns. Our findings
suggest that substantial genetic diversity of B. burgdorferi, rivaling that
of European strains, exists among isolates from the United States. Strains
DN127 and 25015 are unique among all B. burgdorferi isolates tested to date,
and though isolated from opposite longitudinal extremes of the North
American continent, are closely related.”
http://www.ncbi.nlm.nih.gov/pubmed/8525058
In other words, this funny-, like, accidental- Ixodes-come-Plum Island
borrelia had already reached the American West, not to mention Europe, by
1995. Are we to believe Missouri has an invisible anti-bird and anti-rodent
barrier?
REF 22- 1997 – Persing and Telford, again (and you’ll just have to
look at the full text pdf of this article because you’re not going to
believe how many different kinds of Borrelia are found in just about every
state):
J Infect Dis. 1997 Jan;175(1):98-107.
Genetic
heterogeneity of Borrelia
burgdorferi in
the United
States.
Mathiesen DA1, Oliver
JH Jr, Kolbert
CP, Tullson
ED, Johnson
BJ, Campbell
GL, Mitchell
PD, Reed
KD, Telford
SR 3rd, Anderson
JF, Lane
RS, Persing
DH.
"To examine in detail Borrelia
burgdorferi strain
diversity in the United
States, 186 isolates from human, tick, and rodent sources were
analyzed from multiple distinct geographic regions of the United
States and
abroad. Strains were characterized by genomic macrorestriction analysis and
ospA and 23S rDNA gene sequencing followed by phylogenetic analysis.
Results indicate that spirochetal isolates from the United
States fall
into two major divisions and nine or more subdivisions; human isolates fell
into five of these subdivisions. Greater genetic diversity
was observed among B. burgdorferi isolates
from moderate climatic regions, consistent with increased tick vector and
reservoir diversity. All of the Borrelia isolates
were reactive by ospA polymerase chain reaction except for Borrelia hermsii
controls and several tick isolates from the Northeast, which were shown to
lack the 49-kb plasmid encoding outer surface protein A (OspA). The data
suggest that US B. burgdorferi isolates
demonstrate substantial genetic
heterogeneity, with regional differences in spirochete
populations.
http://www.ncbi.nlm.nih.gov/pubmed/8985202
http://jid.oxfordjournals.org/content/175/1/98.long
Citing Authors:
http://jid.oxfordjournals.org/cgi/crossref-forward-links/175/1/98
This is all in comparison to what IDSA says about Lyme and particularly what
Klempner did with his research-fraud re-treatment study published in 2001,
which is now the basis of the IDSA “Guidelines.” Klempner allegedly looked
for the OspA gene in people, so he could declare that no one had Lyme after
“re-treatment”: http://www.ohioactionlyme.org/wp-content/uploads/2015/02/Biomarkers1.pdf
Allen Steere playing the DNA-RNA Shell Game;
from 1992 when he falsified the Dearborn case definition (ref Marconi and
the NIH re 16S probes), his 2 DNA analyses of post-treatment of humans
where he found treatment failed in at least a third of the cases, and in the
spinal fluid analysis where he used only an OspA probe, dropping the 16S
probe he used in bad knees. Steere signs the “Guidelines” anyway and denies
that treatment fails.
Allen Steere in 1992 when he falsified the Dearborn case definition,
see his reference to Marconi and assessments of strains with 16S RNA;
notice references 11, 24...
1992-1994 -- J
Infect Dis. 1994
Feb;169(2):313-8.
Antibody responses to the three genomic groups of
Borrelia burgdorferi in European Lyme borreliosis.
Dressler F1, Ackermann
R, Steere
AC.
“The group 1 strain of B. burgdorferi, G39/40, used in this study and in
the previous study of US patients was isolated from an Ixodes damini tick in
Guilford, Connecticut [21]. The group 2 strain, FRG [Federal Republic of
Germany], was isolated from Ixodes ricinus near Cologne [22]. The
group 3 strain, IP3, was isolated from Ixodes persulcatus near Leningrad
[23]. All three strains used in this study were high passage isolates,
which were classified by Richard Marconi (Rocky Mountain Laboratory,
Hamilton, MT) using
16S ribosomal RNA sequence determination as described [11,
24]. The recombinant preparations of OspA and OspB used in this study were
purified maltose- binding protein-Osp fusion proteins derived from group 1
strain B31 [25]. The fusion proteins contained the full-length OspA or OspB
sequence without the lipid moiety or the signal sequence -"
http://www.ncbi.nlm.nih.gov/pubmed/8106763
And what are those references, 11 and 24? See the full
text at:
http://www.actionlyme.org/dressler1994.pdf
Steere’s Dearborn Reference 11: 1992, Marconi and Garon, NIH Bioweapons Lab,
Montana--
J Clin Microbiol. 1992
Mar;30(3):628-32.
Species-specific identification of and distinction
between Borrelia burgdorferi genomic groups by using 16S rRNA-directed
oligonucleotide probes.
Marconi RT1, Lubke
L, Hauglum
W, Garon
CF.
“Examination of a
number of previously published aligned Borrelia 16S rRNA
sequences revealed the presence of regions which could serve as
oligonucleotide probe targets for both species-specific identification
of Borrelia burgdorferi
and distinction between genomic groups. Total cellular RNA isolated from Borrelia cultures
was used in slot blot analysis. Radiolabeled oligonucleotides designed to
hybridize to specific 16S rRNA
targets were used as probes. These probes allowed for both species-specific identification
and genomic group typing of B. burgdorferi...
“… Using
Borrelia 16S rRNA sequences, we constructed probes that serve to distinguish
B. burgdorferi from other Borrelia species and to distinguish between the
genomic groups of B. burgdorferi. Other
groups have developed B. burgdorferi species-specific probes by using
polymerase chain reaction amplification (13, 15, 19, 22). We chose rRNA as
the target molecule since it is present in large quantities within a cell,
so rRNA targets can be considered to be naturally highly amplified. In
addition, rRNA molecules are highly conserved and presumably are subject to
a very low mutation frequency. The specificity of the probes was
demonstrated through the use of slot blots with total cellular RNA as the
target. This approach allows the reliable identification and genomic typing
of B. burgdorferi from cultures, typically within 36 h.
http://www.ncbi.nlm.nih.gov/pubmed/1372620
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC265123/pdf/jcm00027-0106.pdf
Steere’s Dearborn Reference 24: 1992, Marconi and Garon, NIH:
J Clin Microbiol. 1992
Nov;30(11):2830-4.
Development of polymerase chain reaction primer sets
for diagnosis of Lyme disease and for species-specific identification of
Lyme disease isolates by 16S rRNA signature nucleotide analysis.
Marconi RT1, Garon
CF.
“We have determined and compared partial 16S rRNA
sequences from 23 Lyme disease spirochete isolates and aligned these with 8
sequences previously presented. The 16S rRNA
signature nucleotide compositions were defined for each isolate and compared
with the genomic species signature
nucleotide sets previously established. To
identify positions truly indicative of species classification
which could serve as targets for polymerase chain reaction species-specific identification
primers, 16S rRNA-based
phylogenetic analyses were conducted. On the basis of the identified
signature nucleotides, we designed polymerase chain reaction primer sets
which (i) amplify all spirochete species associated
with Lyme disease and (ii) differentiate between these species. The
primer sets were tested on 38 Borrelia isolates
associated with Lyme disease and were found to be sensitive and specific.
All Lyme disease isolates tested were amplification positive. These primers
allow for the rapid species identification
of Lyme disease isolates.”
http://www.ncbi.nlm.nih.gov/pubmed/1280643
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC270537/
Steere’s Treatment DNA/RNA Shell Game, synovial (knees) and spinal fluid.
In the first report, knees, Steere finds treatment fails. He is using 3
OspA probes and one 16S rDNA probe. He finds about 1/3 of the
patients were positive with these probes after treatment and concludes
longer than 30 days is necessary, as the longer the treatment, the lower the
frequency of DNA-positive cases. After he makes these claims, he never
again says treatment fails, only that everyone is cured and there are no
positive cases after treatment by signing the “Guidelines”:
N Engl J Med. 1994
Jan 27;330(4):229-34.
Detection of Borrelia burgdorferi DNA by polymerase
chain reaction in synovial fluid from patients with Lyme arthritis.
Nocton JJ1, Dressler
F, Rutledge
BJ, Rys
PN, Persing
DH, Steere
AC.
”BACKGROUND:
”Borrelia burgdorferi is difficult to detect in synovial
fluid, which limits our understanding of the pathogenesis of
Lyme arthritis, particularly when arthritis persists despite antibiotic
therapy.
”METHODS:
”Using the polymerase chain reaction (PCR), we attempted to detect B.
burgdorferi DNA in
joint-fluid samples
obtained over a 17-year period. The samples were tested in two separate
laboratories with four sets of primers and probes, three of which target
plasmid DNA that
encodes outer-surface protein A (OspA).
”RESULTS:
”B. burgdorferi DNA was
detected in 75 of 88 patients with Lyme arthritis (85 percent) and in none
of 64 control patients. Each of the three OspA primer-probe sets was
sensitive, and the results were moderately concordant in the two
laboratories (kappa = 0.54 to 0.73). Of 73 patients with Lyme arthritis that
was untreated or treated with only short courses of oral antibiotics, 70 (96
percent) had positive PCR results. In contrast, of 19 patients who received
either parenteral antibiotics or long courses of oral antibiotics (> or = 1
month), only 7 (37 percent) had positive tests (P < 0.001). None of these
seven patients had received more than two months of oral antibiotic
treatment or more than three weeks of intravenous antibiotic treatment. Of
10 patients with chronic arthritis (continuous joint inflammation for one
year or more) despite multiple courses of antibiotics, 7 had consistently
negative tests in samples obtained three months to two years after
treatment.
”CONCLUSIONS:
”PCR testing can detect B. burgdorferi DNA in synovial
fluid. This test may be able to show whether Lyme arthritis
that persists after antibiotic treatment is due to persistence of the
spirochete.
“…In 7 of the 19 patients, B. burgdorferi DNA was
detected in samples obtained 1 day to 17 months after the completion of
antibiotic therapy. Three of these patients were treated with both oral and
intravenous antibiotics, two received three weekly doses of intramuscular
penicillin G benzathine, and two were given only oral antibiotics. The
median duration of their oral treatment was 37 days (range, 20 to 58), and
the median duration of intravenous therapy was 14 days (range, 14 to 20). In
the remaining 12 patients, samples obtained one day to four years after
antibiotic treatment were all negative. Seven of these patients were treated
with intravenous antibiotics, two received intramuscular penicillin, and
three were given only oral antibiotics. Their median duration of oral
treatment was 48 days (range, 21 to 120), and the median duration of
intravenous therapy was 30 days (range, 7 to 44). Although the patients with
negative PCR results tended to have been treated longer than those with
positive PCR results, the differences were not statistically significant. Of
10 patients who had chronic Lyme arthritis despite multiple courses of
antibiotic therapy, 7 had negative test results in all post-treatment
samples.
“Altogether, of 73 patients with Lyme arthritis who
were untreated or treated with short courses of oral antibiotics before
testing, 70 (96 percent) had positive PCR results. In contrast, of 19
patients who received either parenteral antibiotics or long courses of oral
antibiotics, only 7 (37 percent) had positive test results after
treatment (P<0.001). In the 29 patients for whom serial samples were
available, all pretreatment samples were positive. Once post-treatment
samples became negative, all subsequent samples remained negative.”
http://www.ncbi.nlm.nih.gov/pubmed/8272083
http://www.nejm.org/doi/full/10.1056/NEJM199401273300401
And
J Infect Dis. 1996
Sep;174(3):623-7.
Detection of Borrelia
burgdorferi DNA by polymerase
chain reaction in
cerebrospinal fluid in Lyme
neuroborreliosis.
Nocton JJ1, Bloom
BJ, Rutledge
BJ, Persing
DH, Logigian
EL, Schmid
CH, Steere
AC.
“A polymerase chain reaction (PCR) assay that detects Borrelia burgdorferi DNA in cerebrospinal
fluid (CSF)
was evaluated as a diagnostic test for acute or chronic Lyme
neuroborreliosis. In one laboratory, 102 samples were tested blindly, and 40
samples were retested in a second laboratory. In the first laboratory, B.
burgdorferi DNA was
detected in CSF samples in 6 (38%) of 16 patients with acute
neuroborreliosis, 11 (25%) of 44 with chronic neuroborreliosis, and none of
42 samples from patients with other illnesses. There was a significant
correlation between PCR results and the duration of previous intravenous
antibiotic therapy. The overall frequency of positive results was similar in
the second laboratory, but concordance between the laboratories and among
primer-probe sets was limited because many samples were positive with only
one primer-probe set. Thus, PCR testing can sometimes detect B. burgdorferi DNA in
CSF in patients with acute or chronic neuroborreliosis, but with current
methods, the sensitivity of the test is limited.
“…Previous studies using PCR to detect B. burgdorferi
DNA in cerebrospinal fluid (CSF) have been done primarily in small numbers
of patients with early, acute neuroborreliosis [5-10]. In these studies,
which have used several different probes and techniques, the PCR test had
sensitivities of 24%-100%. We previously reported that a PCR assay targeting
outer surface protein A (OspA) DNA is highly sensitive and specific for the
detection of B. burgdorferi DNA in joint fluid of patients with Lyme
arthritis [11]. We report here on the evaluation of this assay as a
diagnostic test for the detection of spirochetal DNA in CSF in a large
number of patients with acute or chronic Lyme neuroborreliosis..”
http://www.ncbi.nlm.nih.gov/pubmed/8769624
http://jid.oxfordjournals.org/content/174/3/623.long
From this report:
You can see that Steere does not use the 16S RNA probe in this
Neuroborreliosis assessment, whereas he had before in knees and found more
than a third of the patients were positive after treatment. The OspA gene
was seen more frequently in those arthritis knees patients probably due to
the exosomes or blebs, which contain DNA (Dorward, 1990, PMID:
16348232
). And as shown by Pachner, above, using a human neuroinvasive strain
(N40 was taken from the spinal fluid of a human patient), the plasmids
change. It is quite evident that Steere does not want to find
Neuroborreliosis. He referenced Garon and Marconi’s work and
recommendations for using the 16S probe to assure the Dearborn strains were burgdorferi.
Steere used DNA he knew would not likely be found in human brains to falsely
show that people are not infected with spirochetes, the CDC’s goal from the
beginning. Not every strain of Borrelia has OspA, and one should use DNA
that detects the GENUS, or at least more of the common species, flagellin or
the spacer DNAs.
The CDC deployed Allen Steere in the first place – a rheumatogist -- to
manage a vector-borne, neurologic disease? This never made any sense unless
the CDC wanted to spin it from the beginning, once they found out, “Oops
(Plum Island).” Nevertheless, here in these two reports, despite the shell
game, Steere found treatment fails at least a third of the time in both
knees and spinal fluid. Yet, he never mentioned this again and signed the
“IDSA Guidelines” that state that spirochetes do not persist after 2 weeks
to 30 days.
Surely by the late 1980s, this Cabal knew antibiotic treatment failed
because spirochetes cause damage via activating Epstein-Barr and the like,
and that no spirochetal infection has ever been “curable,” or eradicable.
All of their nonsense is about the OspA vaccines causing the same
immunosuppression-and-not-arthritis disease and that they performed the
Dearborn stunt to hide this fact.
X. The Guidelines – Who signed on to
this perverted science and are therefore
responsible for
endorsing this fraud?
The IDSA “Guidelines” are based on the Dearborn-Falsified case definition,
Klempner’s 2001, bogus “re-treatment” “study” where Klempner neglected to
mention to the NEJM – who did not catch this flaw – that he used OspA
primers to detect “No Lyme” (yet found some and rejected them from the
study, but did not report this), knowing OspA changes, knowing not all
borrelia are bearers of OspA, and knowing that Lyme was incurable since he
had published that it was in the past?
Clin Infect Dis. 2006
Nov 1;43(9):1089-134. Epub 2006 Oct 2.
The clinical assessment, treatment, and prevention of lyme disease,
human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by
the Infectious Diseases Society of America.
Wormser GP1, Dattwyler
RJ, Shapiro
ED, Halperin
JJ, Steere
AC, Klempner MS, Krause
PJ, Bakken
JS, Strle
F, Stanek
G, Bockenstedt
L, Fish
D, Dumler
JS ,Nadelman
RB.
http://www.ncbi.nlm.nih.gov/pubmed/17029130
Search the references for “Klempner” in the above
report. You will see the basis of the “Guidelines” is Klempner’s
research-fraud article on the non-retreatment of 2/3rds of his victims,
using the falsified case definition and a bogus psychiatric check-list
instead of the Cabal’s own valid biomarkers.
Notice that the authors say:
”Another study similarly was unsuccessful in recovering B.
burgdorferi from
the blood of 12 patients with chronic post–Lyme disease symptoms, using both
conventional and hypertonic media (M.S.K., unpublished data) [288].
The latter study also cultured 128 CSF specimens for B.
burgdorferi and
evaluated blood specimens and CSF specimens by PCR. None of the 843
specimens tested in total was either culture or PCR positive [288, 289].
Therefore, the most plausible explanation for the positive results using the
novel blood culture method reported by a single group of investigators [303]
is that the microscopic findings were not, in fact, due to B.
burgdorferi.
“In another study, B.
burgdorferi DNA
was detected by PCR in urine samples of 74.2% of 97 United States patients
who were diagnosed as having “chronic Lyme disease” and who were previously
treated with antibiotics for extended periods of time [306].
Few additional details were provided by the authors as to the
characteristics of the patient population.***Because the authors did not
sequence the amplicons to confirm their identity, the results should be
regarded as questionable in the absence of confirmation by other
investigators.”***
Klempner in his bogus non-retreatment article (Ref 288)
used bogus OspA (which were not listed, one had to dig and find he used
OspA) primers, and
this entire criminal gang is guilty of the same thing – not sequencing for
Borrelia DNA or
using proper primers
(Wormser in Missouri, for instance). Wormser just used bogus probes of DNA
not necessarily expected to be there (burgdorferi Fla and a specific
lonestari enzyme, knowing there were plenty of other borrelia in
ticks in Missouri, as shown above by Telford, Schoen, and Barbour).
This proves Wormser, et al, know they should have done
the same thing. All their own bogus articles have to be retracted in
addition to the Cabal’s prosecution.
------
And the 2001 “Guidelines” signers:
http://www.guideline.gov/content.aspx?id=9537
Guideline Title
Infectious Diseases Society of America practice guidelines for clinical
assessment, treatment and prevention of Lyme disease, human granulocytic
anaplasmosis, and babesiosis.
Bibliographic Source(s)
Wormser GP,
Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC, Klempner MS,
Krause PJ, Bakken JS, Strle F, Stanek G, Bockenstedt L, Fish D,
Dumler JS, Nadelman RB. The clinical assessment, treatment, and
prevention of lyme disease, human granulocytic anaplasmosis, and
babesiosis: clinical practice guidelines by the Infectious Diseases
Society of America. Clin Infect Dis. 2006 Nov 1;43(9):1089-134. PubMed |
Guideline Status
This is the current
release of the guideline.
This guideline updates a
previous version: Wormser GP, Nadelman RB, Dattwyler RJ, Dennis DT, Shapiro
ED, Steere AC, Rush TJ, Rahn DW, Coyle PK, Persing DH, Fish D, Luft BJ. Practice
guidelines for the treatment of Lyme disease. Clin Infect Dis 2000
Jul;31(Suppl 1):1-14.
The guideline was
reaffirmed for currency by the developer in 2010.
What else can you say? The Cabal and the CDC do not
want anyone to discover a Borreliosis infection much less treat it. If you
understand that the disease is far more devastating than a common infection
with a common bacteria – it’s functionally and physiologically like Post
Sepsis Syndrome -, there really is no treatment for it at this time. But
there is the threat that these walking cesspools of disease called humans
with Lyme or Chronic Fatigue Syndrome might just be the cauldron from which
emerges the next pandemic. There are a million such new cases of Tick Bite
Sepsis (Disability) per year in the USA alone.
It’s going to be pretty bad Karma to abuse and neglect
(Deprivation of Rights Under Color of Law) the very sick, one way or
another. Either by natural disaster or the other nations will decide to
boycott American businesses and especially ban the CDC staff from traveling
to their countries. Are they not criminal terrorists? Who else but the
NAZIs and the Japanese during World War II repeatedly and blatantly
experimented on races and or with bioweapons?
Right. The CDC.
Tuskegee.
Guatemala.