Re: Fallon responds to WP article
- From: Snappy <freyfaxi@xxxxxxxxxxxxx>
- Date: 23 May 2007 19:02:40 -0700
On May 23, 8:32 pm, Tempo <nob...@xxxxxxxxxxxxxxxxx> wrote:
Legitimate debate exists as to whether persistent symptoms are due to
persistent infection, a post-infectious process, or both.
In 2001, the New England Journal of Medicine published an article
documenting persistent "severe impairment" after treatment among
patients with well-documented Lyme disease. In 2003, Neurology
published an article documenting that repeated antibiotic treatment
results in clinically meaningful improvement three times more often
than placebo. Acknowledgment of this uncertainty would diminish
polarization and advance the interests of both scientists and patients.
Brian A. Fallon, MD
Director, Lyme and Tick-Borne Diseases Research Center
Columbia University
New York
I was touched by Dr. Fallon's attempt to try to mediate and bring
reconciliation into this polarized situation. Sadly, however peace is
dependent on justice and truth. Most of us in the Lyme community know
the truth about antibiotics-- that they clear up many of our symptoms,
but do not eradicate the infection, which relapses when we go off
antibiotics. Most of us choose to endure antibiotics because it gives
us some relief and hope. We are adults, and we should be able to make
the choice about our treatment along with our doctors.
Scientists in the EIS and IDSA who are paid by the insurance and
bioweapons industry, and who hold crucial patents on the organisms--
have suppressed information about persistence of spirochete infection
in a large percentage of those infected with Lyme. This is a pattern
very similar to that seen in Gulf War Illness, which is probably also
caused by an intracellular stealth organism. This suppression of the
truth is not in the best interest of patients, nor is it in the best
interest of science, and it is damaging to the reputation of the
medical profession in the long run. It is, however in the best
interest of the insurance industry and of the bioweapons industry.
Chronic Lyme patients will prevail when the truth about persistent,
intracellular infection, and the truth about the cover-up in
diagnostic testing is finally vetted. We will all be able to move on
and get to the work of finding treatments. The low levels of funding
available for research on new treatments for chronic spirochete
infections has hurt patients and has made American Lyme research a
laughing stock in Europe. The high levels of funding of prominent
Lyme reserachers for biowarfare research is a national disgrace and
should be examined with a fine microscope. Why is a hypothetical
Tularemia outbreak in America more important that the current
suffering of thousands infected with the relapsing, intracellular
spirochete known as Lyme?
There is a very large body of evidence on persistent infection:
Mechanisms of persistence
While B. burgdorferi is susceptible to a number of antibiotics in
vitro, there are contradictory reports as to the efficacy of
antibiotics in vivo. B. burgdorferi may persist in humans and animals
for months or years despite a robust immune response and standard
antibiotic treatment, particularly when treatment is delayed and
dissemination widespread. Numerous studies have demonstrated
persistence of infection despite antibiotic therapy.[46][47][48][49]
[50][51][52][53][54]
Various survival strategies of B. burgdorferi have been posited to
explain this phenomenon,[55] including the following:
Physical sequestration of B. burgdorferi in sites that are
inaccessible to the immune system and antibiotics, such as the
brain[56] and central nervous system. New evidence suggests that B.
burgdorferi may use the host's fibrinolytic system to penetrate the
blood-brain barrier.[57]
Intracellular invasion.
B. burgdorferi has been shown to invade a variety of cells, including
endothelium,[58] fibroblasts,[59] lymphocytes,[60] macrophages,[61]
keratinocytes,[62] synovium,[63][64] and most recently neuronal and
glial cells. [65] By 'hiding' inside these cells, B. burgdorferi is
able to evade the immune system and is protected to varying degrees
against antibiotics,[66][67] allowing the infection to persist in a
chronic state.
Altered morphological forms, i.e. spheroplasts (cysts, granules).
The existence of B. burgdorferi spheroplasts, which lack a cell wall,
has been documented in vitro,[68][69][70][71][72][73][74] in vivo,
[64]
[70][75][76] and in an ex vivo model.[77]The fact that energy is
required for the spiral bacterium to convert to the cystic form[68]
suggests that these altered forms have a survival function, and are
not merely end stage degeneration products. The spheroplasts are
indeed virulent and infectious, able to survive under adverse
environmental conditions, and have been shown to revert back to the
spiral form in vitro, once conditions are more favorable.[70][78][79]
[80][81]
A number of other factors make B. burgdorferi spheroplasts a key
factor in the relapsing, chronic nature of Lyme disease. Compared to
the spiral form, spheroplasts have dramatically reduced surface area
for immune surveillance. They also express different surface proteins
- another reason for seronegative disease (i.e. false-negative
antibody tests), as current tests only look for antibodies to surface
proteins of the spiral form. In addition, B. burgdorferi spheroplasts
are generally not susceptible to the antibiotics traditionally used
for Lyme disease. They have instead shown sensitivity in vitro to
antiparasitic drugs such as metronidazole,[82] tinidazole,[83] and
hydroxychloroquine,[84] to which the spiral form of B. burgdorferi is
not sensitive.
.
- References:
- Combat Zone (WP)
- From: Tempo
- Fallon responds to WP article
- From: Tempo
- Combat Zone (WP)
- Prev by Date: Re: Fallon responds to WP article
- Next by Date: Re: Anti-inflammatory properties of antibiotics...right for the wrong reasons?
- Previous by thread: Re: Fallon responds to WP article
- Next by thread: How Borrelia Persists in the Body During Antibiotic Treatment
- Index(es):
Relevant Pages
|
