Re: Cod et al: I MIGHT Have been Wrong about NIH/FOIA of Raw Data


eugeneshapiroisapig wrote:
> they've got to do tissue studies including and especially brain
tissue.


Editorial by Tom Grier:

Chronic Lyme Post-Mortem Study Needed

KEY WORDS:

Antibody -------- A protein produced by a white-blood-cell to attack
bacteria and viruses

Titer ------------- Another word for level, as in level or amount of
antibody measured in the blood

Seronegative --- Despite an infection there is an absence of antibodies
in the blood or serum of the patient.

Spirochete ------ A spiral bacteria in the same family of bacteria as
Syphilis.

Borrelia burgdorferi --- The spirochete bacteria that causes Lyme
disease
Erythema Migrans ---- A red expanding rash on the skin caused by an
infected tick bite. An EM rash is diagnostic for Lyme disease even in
absence of a positive test.

Antigen --------------refers to a foreign substance in our blood that
is
capable of causing an immune response

There isn't a disease in the past 100 years that has polarized the
medical community more than Lyme disease.

>>From the very beginning Lyme disease was misunderstood. In the early
1970s two concerned mothers Polly Murray and Judith Mensch were
convinced that the epidemic of Juvenile Rheumatoid Arthritis (JRA)
cases that they were seeing in their neighborhoods, were being
contracted as a result of some kind of environmental exposure rather
than a genetic disorder.

After the State Health Department admitted that the JRA incidence rate
in
Old Lyme CT was at least eight times the national average, they
somewhat
reluctantly decided to investigate the observations of these two woman.

(Murray and Mensch had to present actual patient case histories that
they
collected before an investigation was started.)

In 1975 a rheumatologist named Dr. Alan Steere first described these
abnormal cases of "JRA" in the medical literature as a new type of
arthritic disorder. He coined the term "Lyme Arthritis". This led to an

immediate misunderstanding of the disease, and Lyme disease was
incorrectly thought of for many years as strictly an arthritic disease.


Six years later in 1981 the actual cause of Lyme disease was discovered
to be a new species of spirochetal bacteria that was transmitted to
humans from the bite of infected "deer" ticks.

Almost ten years after Steere's description of Lyme disease as an
arthritic disorder, it was now becoming recognized that Lyme Disease
was in fact much more than just a new type of arthritis. Lyme disease
was now being recognized as being equally capable of causing severe and
devastating neurological disorders!

Pachner AR, Steere AC. The triad of neurologic manifestations of Lyme
Disease: Meningitis, cranial neuritis, and radiculoneuritis. Neurology
1985;35:47-53

The cause of Lyme disease was discovered in 1981 to be caused by a
bacteria transmitted by the bite of infected ticks. Dr. Willy
Burgdorfer was the first to isolate the spirochetal bacteria from the
midgut of Ixodes "Deer" Ticks from ticks from the Shelter Island Area.
(Shelter Island is near the coast of New York and New Jersey)

Shortly after 1981 when the cause of "Lyme Arthritis" was known to be
a bacteria, Lyme articles that appeared in the medical literature
quickly
assumed that the Lyme spirochete was similar to other bacterial
infections.

Many treatment studies based there protocols of antibiotic treatment on

other bacterial infections such as strep throat.

The conclusions of most early studies that had short patient follow-ups

concluded that you could expect Lyme disease to respond to 10-14 days
of
antibiotics. The antibiotics that were tested in the test tube and
deemed to be effective at that time included: erythromycin,
tetracycline, and
penicillin.

>>From the very beginning treatment failures were seen in virtually every

antibiotic study done. The longer the patient follow up the higher the
incidence of treatment failure.

The medical community blamed early treatment failures on the older
antibiotics, erythromycin, tetracycline, and penicillin and has long
since accepted that these antibiotics are mostly ineffective at curing
Lyme disease. What was being ignored was that the newer antibiotics
were also consistently failing at preventing relapses of active
infection.

Ever since these early treatment studies the concept that two weeks of
antibiotic therapy is adequate treatment for Lyme disease has remained
ingrained into the medical communities collective consciousness. This
is
despite the fact that in the first fifteen years since the discovery of
the disease in 1975, virtually every antibiotic treatment study
consistently recognized treatment failures?

Further the longer patients were followed up after they received
antibiotic treatment, the higher the relapse rates would climb. (See
Nantucket Island Study Dr. Nancy Sha*** et al.)

The Long-Term Follow-up of Lyme Disease: A Population-Based
Retrospective
Cohort Study Authors: Sha*** NA; Phillips CB; Sangha O et al. Ann
Intern Med 1999 Dec 21;131(12):919-26

* Data from the Nantucket Island study was presented By Dr. Nancy
Sha*** at an International Lyme Symposia. Those patients in the study
that were followed for up to 5.2 years after initial antibiotic
treatment had ever climbing relapse rates. Relapse rates in patients
that received two weeks of IV Rocephin (ceftriaxone) could expect a
relapse rate to exceed 50 % after 5 years.

Other factors that contribute to relapse post treatment seem to include

length of infection before diagnosis, choice of antibiotic used, and
the
severity of symptoms at time of evaluation.

While from the very beginning there have been thousands of patients
that
have complained of still being sick and symptomatic despite supposed
adequate antibiotic treatments, most of the medical community has
ignored
the patient's observations, and labeled them as being cured. This is
despite the fact that they still have most of the same symptoms that
brought them to their doctors in the first place?

So what determines a cure if the patient still has the symptoms of the
disease?

In many cases it is not the patient's disability that determines the
disease state but rather the presence or absence of natural immune
factors or antibodies. The problem is antibodies are not a direct
measurement of active infection either.

How could this have happened?

Part of the problem was the newly emerging science and technology of
antibody serology testing known as ELISA tests. (Enzyme Linked Immuno
Sera Assays)

[ ELISA tests, look for an enzymatic color change that indicates the
presence or absence of Lyme antibodies in a patient's serum. If you
still
see a color change when a patient's serum is diluted with 512 parts
water
then it is said a patient has a dilution titer of 1:512 note - higher
titer numbers do not have any correlation to how sick a patient is
feeling! In fact a high number indicates the presence of lots of
immunity. A that patient with a high titer is better able to fight the
infection than someone who is producing low numbers of antibody or has
a borderline or even negative titer. ]

Not only was it clear that ELISA tests were quick and easy to develop,
but they were cheap and easy to administer. The convenience of ELISA
tests was a powerful enticement to both doctors and patients. Let's
face it 10 CCs of blood is more convenient than having several brain,
skin, bladder or heart, biopsies that would cost thousands of dollars!

The problem was that from the very beginning it was assumed and
generally
accepted that these tests were a better diagnostic tool than patient
evaluations based on symptoms and a response to treatment.

It was erroneously accepted that the absence of antibodies in the blood

meant no infection was present anywhere in the patient's body. Even
more
disturbing was the incorrect assumption that the drop in antibody
levels
during treatment indicated a microbiological cure. Thus, many studies
concluded that patients were cured if they eventually tested negative
for
Lyme antibodies.

Both assumptions were and continue to be incorrect!

It certainly looks good on paper for a doctor if he can tell a patient
that based on the test that they are negative for Lyme disease, but in
reality the more accurate statement is that the patient is simply
negative for the presence of those antibodies for which that particular
test is sensitive for! But absence of antibodies does not mean the
patient cannot have active infection.

ELISA tests can vary greatly from lab to lab. Since each lab holds
there own patent on their own test, they are all competing to say they
have the best test. It is a competitive business, and certain buzz
words like specificity, sensitivity, efficacy, and accuracy are used to
try and out sell one competitor's lab test over another.

This gives rise to many methods of testing efficacy, which are
implemented by competing labs to be able to say that their test is
better than the competition's tests. This is usually based on
predetermined laboratory standards. Unfortunately, laboratory methods
of determining an ELISA test's efficacy and accuracy does not directly
correlate to accuracy of determining infection in a human being.

If a laboratory tests its ELISA test on 100 test tubes of an identical
known sample, and simultaneously on 100 test tubes of distilled water
(the control group), and it picks up 99 of the 100 samples and only one
of the control samples the lab can claim their test is 99 % accurate.
It had a 1% rate of false negatives and a 1 % rate of false positives.
(The lab chooses what dilution titer it accepts as positive. For one
lab it maybe 1:256 for others it is as high as 1:1024)

A 99% sensitivity sounds great and most doctors and lay people would
say if they heard this data that this ELISA test is 99 % effective, and
accurate.

But these tests cannot tell you if a patient who is infected but makes
no
antibodies (seronegative patients) has active Lyme disease. Also there
is
eveidance that in humans with high titers the tests can still be as
high as 55 % inaccurate!

What if I told you that some manufacturer's tests are only sensitive to
only one of the antibodies we produce to the Lyme bacteria, and it is
an antibody that is rarely elevated in late Lyme? What if I told you
this test only had moderate sensitivity and requires highly positive
serum to have a reagent color change? Now what if I told you that out
of over 100 different Lyme ELISA tests by different labs that they were
all slightly different? And now what would you think if I told you
each lab that holds a patent on its ELISA test want to make a profit on
the test so they present their data in a way to make their test to
appear to look better than the competition.

Now what would you say if I told you that many medical institutions are

actually corporations that own patents on these Lyme tests, and that
the
reputations of those institutions, and the researchers that developed
them are all on the line if their test is found to be fallible.

What are the consequences to the reputations of these institutions if
patient who say they are still sick after treatment are denied
treatment
because of these fallible tests? What if a patient becomes disabled or
dies?

The admission that the Lyme bacteria is alive and sequestered in some
seronegative patients is not welcome news to the developers of these
tests.

But rather than do the type of autopsy and tissue studies to truly
compare their tests, the manufacturers have chosen to manufacture
patient studies that don't compare their tests to tissue studies but
instead to other equally bad serum tests.

If a carpenter only has a yard stick 29 inches long, and he only tests
its precision with another yardstick 29 inches long it will always
appear that his yardstick is accurate!

So how do the lab's claims to the efficacy of these tests actually
stand up in the real world for the diagnosis of Lyme disease?

Hundreds of labs and ELISA tests were evaluated by an independent
sources, and were found several times to be less that 65 % accurate.
(This was based on triple-paired identical positive serum samples that
were sent to 516 labs across the US) In some cases some labs were far
below this average.

So without even arguing that some Lyme patient's blood can be antibody
negative despite an active infection, even in the patient whose blood
is
highly positive, that patient still runs as much as a 45 % chance or
higher of still testing negative with an ELISA test. So a patient can
be antibody negative and still have infection, but they can also have
loads of antibody and still test negative simply by virtue of the lab's
inability to deliver consistently accurate results.

Now consider this. By today's diagnostic criteria if you test negative
by
ELISA you don't have Lyme disease. But if you test positive you still
do not have Lyme disease until you test positive by Western Blot. I
will site a recent study that shows that the Western Blot can be less
than 50 % accurate too. So statistically if the ELISA test is 65 %
accurate and a Western Blot is 50% accurate if you multiply these
probabilities there is now less than a 33% chance of testing positive
using the two tiered testing approach!

The biggest problem for Lyme patients today is that the medical
community
still by and large makes the same two incorrect assumptions about blood

based testing. (This includes the more recent PCR DNA blood tests,
which
still have the same pitfalls as antibody serologies in that the absence
of infection of the bloodstream does not mean absence of infection in
the
body.)

Two important points to remember about Antibody and PCR testing:

1) The absence of antibody (or bacterial DNA) does not prove absence of

infection.

2) The drop in antibodies (or the absence of Bb DNA) does not guarantee
that a patient is cured, and that the patient won't relapse from
active infection.

Illustrated example: Let's consider that antibodies or bacterial DNA in
the patient's serum are like hailstones you see during a hail storm. If
you go out in your front yard during a hailstorm with a 5-gallon pail.
You stand there for several seconds but you don't collect a single
hailstone. What can you conclude about whether it is hailing out? The
absence of a hail stone in a small bucket doesn't exclude that it could
have been hailing in your backyard. We can use a larger bucket and
increase our odds, but what if the hailstorm is just on one corner of
your yard? Likewise a small 10 cc vial of blood may be inadequate to
find an infection that isn't even in the blood!

A very important observation: There is a history in medical literature
of symptomatic seronegative Lyme patients that have received aggressive

long-term antibiotic therapy that have been culture positive for active

infection post therapy! So tests can be and are fallible, and the
infection can persist despite lengthy and aggressive antibiotic
therapy.

Other persistent infection studies have shown the presence of Borrelia
burgdorferi antigens, bacterial particles, bacterial DNA/RNA, and found
the presence of the bacteria in tissue biopsies in patients despite
antibiotic therapy.

Using staining techniques that are sensitive for spirochetes,
researchers
have found the bacteria in the tissue biopsies from both in living
patients, and sequestered in patient's tissues at autopsy. All of
these methods are a much more direct measurement of the presence of the
Lyme bacteria than antibody blood tests. But they are impractical tests
for the average doctor to perform on a daily basis.

Why can an infection be present in the body without the immune system
making measurable antibodies?

Once an infection has left the bloodstream, a patient may not make
enough
antibodies to test positive. Once the infection has found a safer place
in the body to hide, it can avoid the immune system, and also avoid any

antibiotics that are circulating mainly in the blood.

Mechanisms of Immune escape: Bb can be coated by human blocking
antibody and become invisible to killer immune cells. Bb can coat it
self with B-cell membrane and cloak itself in human proteins. Bb can
find places like inside joints and tendons where it is sequestered from
the immune system and even antibiotics. It can go metabolically
inactive.

It can hide in the brain, heart, bladder, and possibly skin cells. It
is motile so it seeks out survivable places.

Bb may have another form that lacks cell wall, and there fore lacks
many
of the antigens the human immune system would use to attack. It may
hide
inside some human cells?

(Diagram of Antibody production against Lyme Disease)

B-cell

(plasma cell)

Anti-Lyme Antibody (Bacteria attacked an dies)

B-Cell - When stimulated by the Lyme bacteria will produce anti-Lyme
antibodies

Without the infection being in constant contact with the (blood-borne)
immune system, the body shuts off antibody production. Antibody levels
will fall even despite the fact that the infection is still sequestered
deep in the body such as the brain, tendons, heart, nerves, bladder,
eyes, and joints.

How do we know this?

Patients who have been repeatedly seronegative for antibodies, have
been
culture positive for the Lyme bacteria. Patients who have been
aggressively treated with antibiotics have been culture positive for
the Lyme bacteria.

Despite repeated negative Lyme antibody tests these patients still had
symptoms and still had active infection. Symptoms that in most cases
responded to extended antibiotic therapies. (See attached references)

Because the medical community has by and large refused to accept a
patient's symptoms as proof of infection, and have continually based
their diagnosis of Lyme disease on Lyme serologies, there has been an
ever growing schism between so called "Chronic Lyme Patients", and a
medical community that refuses to accept their claims as still having
active infection post treatment.

In many cases not only are serologies used to determine the diagnosis
but
the drop in antibodies is often used to indicate a biological cure.

It has been the variable nature of the disease and its wide range of
symptoms, and the reliance on unreliable tests that has given rise to
two
different camps concerning the diagnosis and treatment of Lyme disease.
The evolution of these two opposed paradigms of diagnosis and treatment
will be discussed in the next section.

(Break point if it is printed in two parts)

Part Two "The Need For A Post-Mortem Lyme Disease Syudy" by Tom Grier

"The Need For A Post-Mortem Lyme Study"

The medical community is unevenly divided into two opposing camps on
three major issues concerning Lyme Disease:

1) What constitutes a proper diagnosis of Lyme disease?

2) What Constitutes proper treatment for patients with Lyme disease who
have symptoms that persist beyond four weeks of antibiotic therapy?

3) What role should Lyme tests play in both diagnosis and treatment?

The first camp on the diagnosis and treatment of Lyme disease:
The first camp, which I will call Camp A, represents the majority of
the
medical community and is spearheaded by researchers from Yale Medical,
the American College of Physicians (ACP), and several other major
medical
institutions. In general terms, this camp believes that Lyme disease is
best diagnosed through the use of two consecutive serology tests; the
ELISA test followed by a confirming Western Blot. This is known as
two-tiered testing.


(With very little opposition by the medical community, two-tiered
testing
has now become the diagnostic standard of most major medical centers.)

Camp A also maintains that Lyme disease, despite the stage or severity,
is usually cured with just a few weeks of oral antibiotics. (This is
the by far the most popular position within the medical community and
the health insurance industry at this time.)

How does Camp A make a diagnosis of Lyme Disease? In the past a
history of a tick bite followed by a bull's-eye skin rash or erythema
migrans rash was diagnostic of the disease, but a diagnosis based on
the rash and symptoms alone has come under increasing attack by several
advocates of two tiered testing including Yale Medical (see Yale
Medical Report) and the ACP.

A video training tape by the ACP is quite explicit in its portrayal of
Lyme patients that in the absence of an erythema migrans (EM) rash, the
diagnosis must be made by dual serologies and more than two weeks of
antibiotics is almost always unnecessary.

In one of the video scenarios, the tape suggests to treating physicians
that patients who insist that they have persistent symptoms
post-treatment should be referred to psychiatrists. The logic of this
psychiatric referral stems from the premise that since antibiotics are
accepted as curative, any persistence of symptoms has to be purely
psychological. So if a patient doesn't feel better post treatment; send
them to a shrink!

The second camp on the diagnosis and treatment of Lyme disease:

The second camp, often referred to as "Lyme advocates," and which I
will
call Camp B, believes that most of the persistent symptoms
post-antibiotic treatment are caused by persistent infection. This camp
maintains that antibody serologies are poor at detecting a spirochetal
bacterial infection that has sequestered in deep tissues and no longer
found within the bloodstream. They believe spirochetes that have found
sequestered, or privileged, sites tend to hide in the body and are
poorly detected by any means. As proof of their position, this camp
offers numerous studies which have shown persistence of Borrelia
infection post-antibiotic treatment.

Listed below are several of these published cases of persistent
infection in humans and animals post-treatment as confirmed by either
culture or tissue biopsy and stain:

(For further information, please refer to the compendium of references
to
the persistence or relapse of Lyme disease at
http://www.geocities.com/HotSp­rings/Oasis/6455/lyme-links.ht­ml )

· Schmidli J, Hunzicker T, Moesli P, et al, Cultivation of Bb from
joint
fluid three months after treatment of facial palsy due to Lyme
Borreliosis. J Infect Dis 1988;158:905-906

· Liegner KB, Shapiro JR, Ramsey D, Halperin AJ, Hogrefe W, and Kong
L.
Recurrent erythema migrans despite extended antibiotic treatment with
minocycline in a patient with persisting Borrelia burgdorferi
infection. J. American Acad Dermatol. 1993;28:312-314

· Waniek C, Prohovnik I, Kaufman MA. Rapid progressive frontal type
dementia and death with subcortical degeneration associated with Lyme
disease. A biopsy confirmed presence of Borrelia burgdorferi
post-mortem. A case report/abstract/poster presentation. LDF state of
the art conference with emphasis on neurological Lyme. April 1994,
Stamford, CT*

· Lawrence C, Lipton RB, Lowy FD, and Coyle PK. Seronegative Chronic
Relapsing Neuroborreliosis. European Neurology. 1995;35(2):113-117

· Cleveland CP, Dennler PS, Durray PH. Recurrence of Lyme disease
presenting as a chest wall mass: Borrelia burgdorferi was present
despite five months of IV ceftriaxone 2g, and three months of oral
cefixime 400 mg BID. The presence of Borrelia burgdorferi confirmed by
biopsy and culture. Poster presentation LDF International Conference on
Lyme Disease research, Stamford, CT, April 1992 *

· Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, Schonnherr U,
Kalden JR and Burmester GR: Persistence of Borrelia burgdorferi in
ligamentous tissue from a patient with chronic Lyme Borreliosis.
Arthritis and Rheum
1993;36:1621-1626

· Lavoie Paul E MD. Protocol from Rakel's: Explains persistence of
infection despite "standard" courses of antibiotics. Lyme Times-Lyme
Disease Resource Center 1992;2(2): 25-27 Reprinted from Conn's Current
Therapy 1991

· Masters EJ, Lynxwiler P, Rawlings J. Spirochetemia after continuous
high dose oral amoxicillin therapy. Infect Dis Clin Practice
1994;3:207-208

· Pal GS, Baker JT, Wright DJM. Penicillin resistant Borrelia
encephalitis responding to cefotaxime. Lancet I (1988) 50-51

· Preac-Mursic V, Wilske B, Schierz G, et al. Repeated isolation of
spirochetes from the cerebrospinal fluid of a patient with
meningoradiculitis Bannwarth' Syndrome. Eur J Clin Microbiol
1984;3:564-565

· Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Baumann A,
and
Prokop J. Survival of Borrelia burgdorferi in antibiotically treated
patients with Lyme Borreliosis Infection 1989;17:335-339

· Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the
Lyme
Disease spirochete, Borrelia burgdorferi from ceftriaxone in vitro. J.
Infect Dis 1992;166:440-444

· Haupl TH, Krause A, Bittig M. Persistence of Borrelia burgdorferi in

chronic Lyme Disease: altered immune regulation or evasion into
immunologically privileged sites? Abstract 149 Fifth International
Conference on Lyme Borreliosis, Arlington, VA, 1992 *

· Lavoie Paul E. Failure of published antibiotic regimens in Lyme
borreliosis: Observations on prolonged oral therapy. Abstract presented
at the 1990 Lyme Borreliosis International Conference in Sweden.*

· Fried Martin D, Durray P. Gastrointestinal Disease in Children with
Persistent Lyme Disease: Spirochetes isolated from the G.I. tract .
1996 LDF Lyme Conference Boston, MA, Abstract*

· Neuroboreliosis: In the journal Annals of Neurology Vol. 38, No 4,
1995, there was a brief article by Dr. Andrew Pachner MD, Elizabeth
Delaney BS, and Tim O'Neill DVM, Ph.D. The conclusion of the article
was simple and concise: " These data suggest that Lyme neuroboreliosis
represents persistent infection with B. burgdorferi." The study used
nonhuman primates as a model for human neuroborreliosis, and used a
special PCR technique to detect the presence of Borrelia DNA within
specific structures of the brains of five rhesus monkeys. The monkeys
were injected with strain N40Br of Borrelia burgdorferi, and later
autopsied for analysis.

Abstract summaries:

· Abstract # D654 - J. Nowakowski, et al. Culture-Confirmed Treatment
Failures of Cephalexin Therapy for Erythema Migrans. Two of six
patients
biopsied had culture confirmed Borrelia burgdorferi infections despite
up to 21 days of cephalexin (500 mg TID) antibiotic treatment.

· Abstract # D655 - Nowakowski, et al, Culture-confirmed infection and

reinfection with Borrelia burgdorferi. A patient, despite antibiotic
therapy, had a recurring Erythema Migrans rash on three separate
occasions.

On each occasion it was biopsied, which revealed the active presence of

Borrelia burgdorferi on two separate occasions, indicating reinfection
had occurred.

· Abstract # D657 - J. Cimperman, F. Strle, et al, Repeated Isolation
of
Borrelia burgdorferi from the cerebrospinal fluid (CSF) of two patients

treated for Lyme neuroborreliosis. Patient One was a twenty year old
woman who presented with meningitis but was seronegative for Borrelia
burgdorferi.

Subsequently, six weeks later Bb was cultured from her CSF and she was
treated with IV Rocephin 2 grams a day for 14 days. Three months later,
the symptoms returned and Bb was once again isolated from the CSF.
Patient 2 was a 51 year old female who developed an EM rash after tick
bite. Within two months she had severe neurological symptoms. Her
serology was negative. She was denied treatment until her CSF was
culture positive nine months post-tick bite. She was treated with 2
grams of Rocephin for 14 days. Two months post-antibiotic treatment, Bb
was once again cultured from her CSF.

In both of these cases, the patients had negative antibodies but were
culture positive, suggesting that the antibody tests are not reliable
predictors of neurological Lyme Disease. Also, standard treatment
regimens are insufficient when infection of the CNS is established and
Bb can survive in the brain despite intravenous antibiotic treatment.

· Patients with ACA shed Bb DNA post treatment: Aberer E, et al.
Success and Failure in the treatment of acrodermatitis chronica
atrophicans skin rash.

Infection 24(1):85-87 1996. ACA is a late stage skin rash usually
attributed to Borrelia afzelii, it is sometimes mistaken for
scleroderma. Forty-six patients with ACA were treated with either 14
days of IV Rocephin or thirty days of oral penicillin or doxycycline
and followed up for one year. Of those treated with IV, 28% had no
improvement, and 40% still shed Bb antigen in their urine. Of the oral
group, 70% required retreatment. Conclusion: Proper length of treatment
for ACA has yet to be determined.

Logigian EL, McHugh GL, Antibiotics for Early Lyme Disease May Prevent
Full Seroconversion but not CNS Infection. 1997 ABSTRACT # S66.006
Neuloogy Symposia, NEUROLOGY 1997; A388:48 In this study, 22
late-stage neurological patients who met the Centers for Disease
Control (CDC) criteria for Lyme disease were studied over a three year
period. Eighty-five percent of seronegative patients who still had
active disseminated infection had been treated within one month of tick
bite. This means that early antibiotic treatment may make you test
negative, but you still progress to develop encephalitis. Without
antibodies your brain has no natural immunity or local immune system to
fight the infection, so withdrawing antibiotics causes the infection






> and this means primates and also that they'll have to get over the
> mental blocks in their heads and have some patients sign consents and
> do some damn brain biopsy series studies. no aspect has frustrated me
> more. it's expensive and intrusive, but it must be done.
>
> wrt treatment studies...I have been feeling lately like I am an
> unwitting participant in uncontrolled studies of treatment...my docs
> keep putting me on cutting edge treatments.

.

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