Category Archives: Lyme Desease

History of Lyme & Testing

Antibody tests

Testing for the presence of B. burgdorferi antibodies used an
ELISA (enzyme-linked immunosorbent assay) that detects IgG
and IgM antibodies. The results of this test were available within
one day in 70% of cases and within three days in 88% of cases.
The total number of tests that were positive in the last three
years was 78. As the laboratory serves a number of different
hospitals and many patients were tested more than once, this case
series includes the majority of patients with a positive Lyme
antibody test.
Positive and equivocal samples on the immunoassay were sent
to the Lyme Borreliosis Diagnostic Unit of the Health Protection
Agency at Southampton, where immunoblots are performed to
assess reactivity to a range of B. burgdorferi antigens.

In this cohort, Lyme antibodies were tested for in 64 out of 65
patients with the screening ELISA; this was positive in 28 and
equivocal in eight. Immunoblots on both the ELISA positive and
equivocal samples were all positive at the reference laboratory.
ELISA was negative in 25 patients. Eleven ELISA negative blood
samples from patients thought to have the infection clinically
were sent to the reference laboratory at the specific request of
the responsible clinician, and six of these had positive
immunoblots. Overall 44 out of 64 patients had Lyme disease
serologically confirmed on immunoblot.

Source-http://lymeaware.free.fr/lyme/Diagnostiques/Lyme%20UK%20O’Connell.pdf
Chronic Lyme Post-Mortem Study Needed
Editorial by Tom Grier:
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,
it was misunderstood. In the early 1970’s, two concerned mothers,
Polly Murray and Judith Mensch, were convinced that the epidemic of
juvenile rheumatoid arthritis (JRA) cases they were seeing in their
neighborhoods in Old Lyme, Connecticut, 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 that area 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 they had collected before an
investigation was started.
In 1975, a rheumatologist named Dr. Alan Steere first described in
medical literature these abnormal cases of JRA as a new type of
arthritic disorder. He coined the term “Lyme Arthritis”. This led
to an immediate misunderstanding of Lyme disease, which was
incorrectly thought of as strictly an arthritic disease for many
years.
Six years later, in 1981, the actual cause of Lyme disease was
discovered to be a new species of spirochetal bacteria 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 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]
Dr. Willy Burgdorfer was the first to isolate the spirochetal
bacteria from the midgut of Ixodes Scapularis (deer ticks) gathered
from the Shelter Island area, located near the coast of New York
and New Jersey.
Shortly after the cause of “Lyme Arthritis” was discovered to be a
bacteria, articles appearing in medical literature quickly assumed
that the Lyme spirochete was similar to other bacterial infections.
Many treatment studies based their protocols of antibiotic
treatment on other bacterial infections, such as strep throat. The
conclusions from most early studies having short patient follow-up
concluded that you could expect Lyme disease to respond to 10-14
days of antibiotics. The antibiotics 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 determined that
these antibiotics were not very effective at curing Lyme disease.
Ignored was the fact that the newer antibiotics were also
consistently failing to prevent relapses of active infection. Since
these early treatment studies, the concept that two weeks of
antibiotic therapy is adequate treatment for Lyme disease has
remained ingrained in the medical community’s collective
consciousness. [The Long-Term Follow-up of Lyme Disease: A
Population-Based Retrospective Cohort Study. Authors: Shadick NA;
Phillips CB; Sangha O et al. Ann Intern Med 1999 Dec
21;131(12):919-26]
*Data presented by Dr. Nancy Shadick at an International Lyme
Symposia showed that patients in the Nantucket Island study
followed for up to 5.2 years after initial antibiotic treatment had
ever-climbing relapse rates. Relapse rates in patients receiving
two weeks of IV Rocephin (ceftriaxone) could expect a relapse rate
to exceed 50% after five years.
Other factors that contribute to relapse post-treatment seem to
include length of infection before diagnosis, choice of antibiotic,
and severity of symptoms at time of evaluation.
While from the very beginning there have been thousands of patients
who 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 – 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 that antibodies are not a direct measurement of active
infection.
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 Immunosorbent Assay).
[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 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, taking a 10 cc vial of blood
is more convenient and inexpensive than having several brain, skin,
bladder, or heart biopsies costing thousands of dollars done. The
problem from the very beginning was that it was assumed and
generally accepted these tests were a better diagnostic tool than
patient evaluations based on symptoms and a response to treatment.
It was erroneously accepted that 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.
On paper, it certainly looks good for a doctor if he can tell a
patient that, based on the test, they are negative for Lyme
disease. However, in reality a more accurate statement would be
that the patient is simply negative for the presence of those
antibodies for which that particular test is sensitive for. 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
a patent on their particular test, they are all competing to say
they have the best test. It is a competitive business and certain
buzz words, such as specificity, sensitivity, efficacy, and
accuracy, are used to try to outsell one’s competitors lab tests.
This gives rise to many methods of testing efficacy implemented by
competing labs in order to say that their test is better than the
competition’s. 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 in determining infection in a human being.
If a laboratory tests its’ ELISA on 100 test tubes of an identical
known sample and, simultaneously, on 100 test tubes of distilled
water (the control group), and picks up 99 of the 100 samples and
only one of the control samples, they 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, while for another it may be
as high as 1:1024)
A 99% sensitivity sounds great, and most doctors and lay people
would determine 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 evidence 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 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? What if I told you
that out of over 100 different Lyme ELISA tests by different labs,
each was slightly different? What would you think if I told you
that each lab holding a patent on an ELISA test presents data in
such a way to make their test appear to look better than the
competition in order to increase their profit? And, 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 these institutions and the researchers who 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 that would truly compare these tests,
the manufacturers have chosen to manufacture patient studies that
compare their tests to other equally bad serum tests. If a
carpenter has a yard stick 29 inches long and he tests its
precision with another yardstick 29 inches long, it will always
appear that his yardstick is accurate.
How do laboratory 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 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 United States.) In some
cases, some labs were far below this average. Without even arguing
that some Lyme patient’s blood can be antibody negative despite an
active infection, the patient whose blood is highly positive runs
as much as a 45% chance or higher of still testing negative with an
ELISA test. So they can 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 do test
positive, you still do not have Lyme disease until you also test
positive by Western Blot. A recent study shows that the Western
Blot can be less than 50% accurate. So, statistically, if the ELISA
test is 65% accurate and a Western Blot is 50% accurate,
multiplying these probabilities gives 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 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 are: 1)
The absence of antibody (or bacterial DNA) does not prove absence
of infection and 2) the drop in antibodies (or the absence of Bb
DNA) does not guarantee that a patient is cured or that the patient
won’t relapse from active infection.
Example: Let’s consider that antibodies or bacterial DNA in the
patient’s serum are like hailstones you see during a hailstorm.
Standing in your yard with a five-gallon pail for several seconds,
you don’t collect a single hailstone. What can you conclude? The
absence of hail stones in your small bucket doesn’t exclude the
fact that it could have been hailing in your yard. You can use a
larger bucket and increase your odds, but what if the hailstorm is
just in 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 is that there is a history in medical
literature of symptomatic seronegative Lyme patients who have
received aggressive long-term antibiotic therapy and still have
been culture positive for active infection post-therapy. Tests can
be and are fallible, and 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 the presence of the bacteria in tissue biopsies of
patients despite antibiotic therapy. Using staining techniques that
are sensitive for spirochetes, researchers have found the bacteria
in tissue biopsies from living patients as well as sequestered in
patient’s tissues at autopsy. All of these methods are a much more
direct measurement of the presence of Lyme bacteria than antibody
blood tests. But they are impractical tests for the average doctor
to perform on a daily basis.
•Why can 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 mainly circulating in the blood. Here is a list of
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.
•Bb can go metabolically inactive.
•Bb 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 therefore lacks
many of the antigens the human immune system would use to attack.
•Bb may hide inside some human cells.
Without infection being in constant contact with the blood-borne
immune system, the body shuts off antibody production. Antibody
levels will fall 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 – symptoms that, in most
cases, responded to extended antibiotic therapies. [See 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 of
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. Let’s discuss the evolution of these two opposed
paradigms of diagnosis and treatment in the next section.
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:
•What constitutes a proper diagnosis of Lyme disease?
•What constitutes proper treatment for patients with Lyme disease
who have symptoms that persist beyond four weeks of antibiotic
therapy?
•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 from 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 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 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,” 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 is 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:
•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.
(For further information, please refer to the compendium of
references to the persistence or relapse of Lyme disease at
http://www.geocities.com/HotSprings/Oasi…)
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 in the central nervous system (CNS) to go
unabated. Patients who go on to develop brain infections despite
antibiotics, may have suppressed antibody production thus worsening
any remaing active infection in the central nervous system.
•Valesova H, Mailer J, et al. Arthritis: A three year follow-up:
Long-term results in patients with Lyme disease followed for three
years after two weeks of IV Rocephin. Infection 24(1):98-102, 1996.
This study represents another of the problems with author’s bias
interpretation of data. Thirty-five Lyme arthritis patients were
treated with a two week course of IV Rocephin. They were then
followed for three years. At the end of the study, six patients had
complete relapses, nineteen had marked improvement, four had new
Lyme symptoms, and the rest were lost to follow up. The authors
conclusion: ” The treatment results for this group of 35 Lyme
arthritis patients are considered successful.”
Let’s look at the above figures mathematically, based on the 29
patients out of 35 who were contacted and assessed:
•19 improved = 65 %
•6 relapsed = 20 %
•4 worsened = 15 %
Does a total of 35% of patients still suffering sound like
successful treatment to you? This is a treatable disease, but you
have to treat it! What if a doctor’s child was one of the 35%? Do
you think they would continue to go untreated as suggested by the
ACP? How many patients have to relapse before treatment is
considered unsuccessful? Six patients – or 20% – had complete
relapses, yet the conclusion of the study was that, in general,
treatment was considered successful! We get better cure rates for
tuberculosis.
Animal vs. Human Studies:
Support for the theory that Borrelia burgdorferi can find safe
havens in sequestered sites despite antibiotic therapy comes from
several animal model studies. However, only a few human cases have
yet been published. This is because the tissue studies that are
required almost demand that they be done in a post-mortem exam.
(See Stanek and Appel’s work on skin biopsies verses post-mortem
exam of deep tissues in Lyme infected and antibiotic treated
beagles)
Abstract # D607 – M.J.G. Appel, The persistence of Bb in Dogs after
antibiotic treatment. Seventeen Beagle puppies were infected with
Bb from infected ticks, eleven were treated for four weeks with
either Doxycycline or amoxicillin in doses according to weight. Six
were control dogs. 1/11 had Bb isolated from skin, but 7/11 dogs
had Bb isolated from other tissues during post-mortem. All of the
persistent infected pups had persistent arthritis. Conclusion: Skin
biopsies are not predictive of persistence of infection. Also the
standard excepted four week course of antibiotic treatment in dogs
is not sufficient.
To date, no major multi-center post-mortem Lyme disease study has
ever been done on humans. Without this type of post-mortem study,
the debate between the two disagreeing camps will almost certainly
continue.
Results from the European Alzheimers study done by Dr. Judit
Miklossy suggests that post-mortem exams should not only look for
persisting spirochetes in deceased Lyme patients, but should also
look for spirochetes in the brains of deceased dementia patients as
well.
•Miklossy J, Kuntzer T, Bogousslavsky J, et al. Meningovascular
form of neuroborreliosis: Similarities between neuropathological
findings in a case of Lyme disease and those occurring in tertiary
Neurosyphilis. Acta Neuro Pathol 1990;80:568-572
•Miklossy Judit. Alzheimer’s disease a spirochetosis? Neuro Report
1993;4:841-848 Thirteen out of thirteen Alzheimer patients had
spirochetes in the brain. None of the age-matched control subjects
had evidence of spirochetes in their brains. This study suggests
that there is a correlation between an Alzheimer’s dementia and CNS
spirochetosis in Swiss patients. In other words spirochetes might
contribute to a CNS dementia similar to Alzheimer’s disease. (This
is not to suggest that all Alzheimer’s is caused by spirochetes,
but even if a small percentage of dementia can be prevented by
antibiotics then further studies are justified. None are currently
being done! ?
To do this type of tissue study of sequestered spirochetal
infections takes nearly heroic efforts in time, costs, and
diligence. Yet the few times that these types of studies have been
applied to humans have suggested that Borrelia burgdorferi can
indeed survive and thrive within the human body despite a complete
course – or even several courses – of antibiotic therapy.
Yours sincerely,
J McCullough

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Important Chronic Lyme Disease Treatment Study – A Must Read

http://www.marketwired.com/press-release/envita-publishes-important-chronic-lyme-disease-treatment-study-1977482.htm

Envita Publishes Important Chronic Lyme Disease Treatment Study

SCOTTSDALE, AZ–(Marketwired – December 16, 2014) – A revealing new study on chronic Lyme disease treatment and the inherent complexities was just published by Dr. Dino Prato and colleagues from Envita Medical Center and featured in the Open Journal Of Medical Microbiology. The study is titled, “Borrelia burgdorferi: Cell Biology and Clinical Manifestations in Latent Chronic Lyme,” and it offers an extensive overview of 157 published papers that provide crucial insight into a better understanding and the proper diagnosis/treatment of chronic Lyme disease. Starting with an in-depth explanation of the Borrelia genome and pointing to key clinical factors, it paints a picture to help physicians and patients better understand what is really occurring in Lyme disease. The paper explains the severity of the Borrelia, its complexities, and complications in the diagnostics and clinical treatment.

Envita maintains that chronic Lyme disease is very complex and the symptoms, co-infections, immunity and other complicating factors vary from case to case, and each person’s case can be unique and different. This is why personalization could be the strongest and most valuable tool moving forward in the fight against chronic Lyme disease. Armed with the correct scientific outlook and a detailed overview, we feel patients and practitioners can do better. Co-infections, patient’s immunity and genetic inborn issues of metabolism amongst other factors play a vital role in the successful treatment of chronic Lyme disease. 

According to Dr. Prato, the founder and CEO of Envita, “There are so many complex factors to chronic Lyme disease it’s so easy to see why many practitioners are not well equipped to diagnosis and treat it effectively.” Unfortunately, these oversights have led to widespread problems across the world for many patients whom are undiagnosed, or wrongly diagnosed and worse yet are unable to receive accurate treatment. It has long been known that tests have false negatives and false positives. However, good clinical judgment and experience helps to identify and recognize these unique factors present within each patient’s presentation of the disease and bring forth appropriate treatment.

The study reveals that Fibromyalgia, chronic fatigue syndrome, rheumatoid arthritis, and Parkinson’s may in fact be linked to chronic Lyme disease. This is a very important aspect of why so many Lyme disease patients have difficulty finding the right treatment. The following diagram is to better explain why certain conditions can be confused with symptoms associated with chronic Lyme disease. Of the diseases listed in this table, the symptoms of fibromyalgia are more closely related to chronic Lyme disease.

The graph below has been taken from the study published in The Open Journal of Medical Microbiology, “Borrelia burgdorferi: Cell Biology and Clinical Manifestations in Latent Chronic Lyme.”

Chronic Lyme Disease
Chronic Fatigue
Fibromyalgia
Rheumatoid Arthritis
Parkinson’s Disease

Fatigue
X
X
X
X
X

Loss of Concentration/ Short Term Memory Loss
X
X
X
X

Joint pain
X
X
X
X

Poor Sleep
X
X
X
X
X

Mood Problems/ Depression, Anxiety, etc.
X
X
X
X
X

Muscle Skeletal Pain
X
X
X
X
X

Neurological Presentation
X
X
X
X

Muscle Stiffness
X
X
X

It is important to note that many times chronic Lyme disease is treated ineffectively with antibiotics. There are several crucial, overlooked indicators within the patients’ immune system that may in fact provide a guide to whether antibiotic treatments will respond within a patient at all. Numerous other contributing issues discussed in the paper; genome of the infection, immune evasion, treatment of the disease, cellular process need to be considered in detail to establish proper medical treatment. Personalization in our opinion is likely the key to better diagnosis and treatment of chronic Lyme disease for patients.

For over a decade our experience and dedication has been focused on helping patients be free of Lyme disease. If you have any questions about Lyme disease treatment or our paper, contact us. The full version of the Borrelia study can be found here:http://www.scirp.org/Journal/PaperInformation.aspx?PaperID=51411#.VI8VEjHF8WI

Image Available:http://www.marketwire.com/library/MwGo/2014/12/16/11G028664/Images/Dino_Picture_(1)-1288048793035.jpg

Embedded Video Available: https://www.youtube.com/watch?v=4L0IrUpgN7E
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What Is Lyme Disease? New Findings Deepen the Mystery

One blacklegged tick.

Blacklegged ticks are known carriers of the pathogenic bacteria that causes Lyme disease.

PHOTOGRAPH BY JIM GATHANY, CDC/PHIL/CORBIS

Jarret Liotta

for National Geographic

PUBLISHED FEBRUARY 28, 2014

Part of our weekly “In Focus” series—stepping back, looking closer.

Rampant disagreement over what constitutes Lyme disease—in particular, who may have contracted it and how, and how long it lasts—has spawned the larger question of how best to treat it. A new study pointing to the possibility of sexual transmission of the pathogen adds fuel to the fire.

Amid the uncertainty, a patient-led lobby (the counterculture, as someone has called it) that includes doctors as well as Lyme sufferers advocates a broader definition of the disease, both for treatment and insurance purposes.

But the medical establishment asserts that too liberal a definition—and what are seen as renegade practitioners—has led to irresponsible and potentially dangerous treatment of unrelated maladies misidentified as Lyme.

It’s also unknown how many people have died because of Lyme. A 2011 study found that of the 114 deaths reported over a five-year period listing Lyme as a partial or direct cause, only one was consistent with clinical manifestations described by the International Classification of Diseases.

In December 2013, the Centers for Disease Control and Prevention (CDC) confirmed that Lyme carditis—a condition in which the Lyme bacterium infects the heart—caused three deaths over the past two years. Between 1985 and 2008, only four other fatal cases were confirmed.

While the course of the illness varies greatly from person to person, initial manifestations can include a unique skin lesion known aserythema chronicum migrans, headaches, musculoskeletal pain, coughing, sore throat, conjunctivitis, and minor neurological impairment.

If the diagnosis is confirmed early enough, Lyme is treated almost exclusively with short-term antibiotics, often penicillin, which are almost 100 percent effective. But if Lyme goes untreated, symptoms can progress. (Watch related video: “The Deer Tick”)

In Lyme’s second stage, typically between one and several months after the initial infection, neurological abnormalities can arise, such as meningitis, encephalitis, and cranial neuritis, which can manifest as facial palsy. Some patients develop cardiac problems.

In the third stage, which can take several months to years to show up, many patients develop chronic arthritis as well as an increase in neurological and cardiac symptoms, the severity of which can ebb and flow.

Voices in the counterculture argue that Lyme’s symptoms are more intense and longer lasting than the medical establishment acknowledges. They say that symptoms of chronic Lyme disease are responsible for related deaths, including suicides from depression about the disease or from the trauma of persistent debilitating symptoms such as arthritis, heart problems, and cognitive impairment.

New Developments

And now, further complicating the picture, a study published this January contends that Lyme disease may be sexually transmitted. It shows that the Lyme pathogen, Borrelia burgdorferi (Bb), has been found in both male and female sexual secretions, raising the question of whether people are at risk through intimate contact.

Bb is one of only six known spirochete bacteria, named for their coiled spiral shape. (One of the six is the bacterium responsible for syphilis.)

A collection of Borrelia burgdorferi bacteria, the bacterial agent of Lyme disease transmitted by ticks.

PHOTOGRAPH BY SCIENCE PICTURE CO., CORBIS
Borrelia burgdorferi is the bacterial agent of Lyme disease.

The primary vector for Bb is the deer tick—Ixodes scapularis—although other kinds of ticks have been known to transmit it, and other insects, including some mosquitoes, carry the pathogen.

A study of Bb last year revealed that it’s the first known organism that doesn’t need iron to survive. This allows it to evade an iron-inhibiting hormone called hepcidin, produced by the liver, which can starve intrusive bacteria.

Instead, Bb thrives on manganese, which it uses to make essential enzymes for survival—something researchers who made the discovery last year believe could play a role in ultimately combating the pathogen.

Origins: Did Ötzi Have Lyme?

In 2012, a team of researchers claimed that the 5,300-year-old mummy known as Ötzi the Iceman, discovered along the Austria-Italy border in 1991, had contracted Lyme.

Some claim that the disease first appeared in Germany in the 1880s or France in the 1920s; others say it took root in the U.S. around the time of the Great Depression.

In the summer of 1975, 39 children living relatively close to one another in Lyme, Connecticut, were recognized as sharing common symptoms consistent with juvenile rheumatoid arthritis.

Polly Murray, whose 11-year-old son, Todd, was one of those affected, alerted the state health department after the local orthopedic doctor was stumped. “He had a different answer for everybody,” says Todd, who is now 49.

Photo of the Ötzi Iceman.

PHOTOGRAPH BY THE BRIDGEMAN ART LIBRARY, GETTY
Ötzi the Iceman, a 5,300-year-old mummy, may have had Lyme disease.

As his mother began drawing attention to the strange epidemic, a doctor at Yale University named Allen Steere began sleuthing the problem.

In a 1977 paper in the medical journal Arthritis and Rheumatism, Steere identified a new disease transmitted by ticks. He called it Lyme arthritis, and soon after it became known as Lyme disease.

Lyme ticks are active year-round, other than during subfreezing weather, but spring is the most dangerous season. That’s when the baby ticks, or nits—so tiny as to be almost invisible—are born.

One theory—compelling but controversial—about the sudden emergence of the disease in Connecticut blames the accidental release of infected ticks during experiments at Plum Island Animal Disease Center, on Long Island Sound about eight miles south of Lyme.

Originally operated by the U.S. Army, then by the Department of Agriculture, and now by the Department of Homeland Security, the facility’s official mandate is defense research relating to agricultural bioterrorism.

A book by Michael Carroll called Lab 257 cites post-World War II experiments on Plum Island that involved using ticks as disease vectors for germ warfare.

Officials have denied the allegations, but Carroll and others—including former Minnesota Gov. Jesse Ventura—allege the government has used the facility to develop various diseases intended for delivery as biological weapons.

When Is Lyme Lyme?

For his discovery of Lyme and subsequent work on the disease, Allen Steere started out as the counterculture’s golden boy. But he came to believe that too many symptoms were being labeled chronic Lyme without proof. He says he’s now a pariah to advocacy groups and Lyme sufferers, and he avoids involvement in the increasingly polarized controversy.

Gary Wormser, head of infectious diseases at New York Medical College in Valhalla, agrees that misdiagnosis of Lyme is rampant. “I don’t think it’s helping patients. I don’t think it’s helping science,” he says.

Lyme, Wormser says, has become a catchall for a constellation of symptoms that elude diagnosis: “If I can’t figure out what you have, it must be Lyme disease.”

He puts some of the blame on medical science’s failure to find answers to a range of symptoms that include headaches, joint and muscle aches, depression, chronic fatigue, irritable bowel syndrome, and cognitive impairment. These ailments often seem to be subjective, with no physiological cause.

“For a lot of people who are not feeling well, those people are the most vulnerable to turning to the types of practitioners that don’t follow mainstream practices,” Wormser says.

“I’m not saying there aren’t some [Lyme] patients that have been debilitated by some of these symptoms, but it seems to be a really small percentage—far less than you’d be led to believe.”

Todd Murray, one of the original Lyme children, grew up to be an emergency department physician. He believes he still suffers from symptoms relating to the original infection.

“I have weird things I attribute to Lyme,” he says, including a permanent heart condition diagnosed in 1989.

As a doctor, Murray recognizes the dilemma of anecdotal evidence. “I can see both sides, because physicians have to go on evidence-based medicine. So to try to use therapies which have not been shown to be beneficial in clinical studies doesn’t make sense.”

He cites, for instance, hormone replacement therapy for post-menopausal women, which was ultimately shown to increase coronary artery disease, stroke, and breast cancer. “A lot of things in medicine would seem to intuitively make sense. However, when they’re studied, the outcomes may be found to be different than expected,” Murray says.

Challenges of Treatment

Identification of Lyme usually begins with the telltale bull’s-eye rash. But patients don’t always present with the rash, or sometimes it has a different shape and appearance, which means the disease can progress before a course of antibiotics is prescribed.

In Lyme’s later stages, antibiotics are still used, with dosages and duration increased. But there’s disagreement as to whether antibiotics should ever be administered for longer than three months, even in extreme cases.

“The ideology of the counterculture,” Steere says, “is to simply treat symptoms with antibiotic therapy, [and] the Infectious Diseases Society of America [IDSA] has said in essence that’s not correct.” The IDSA notes that “using antibiotics for a very long time [months or years] does not offer superior results and in fact can be dangerous, because it can cause potentially fatal complications.”

Photo of a Lyme disease rash.

PHOTOGRAPH BY KALLISTA IMAGES, GETTY
Lyme disease is often accompanied by a bull’s-eye rash.

Counterculture doctors treating patients whom they believe have chronic Lyme will recommend not only long-term antibiotic treatment but also various other therapies, such as holistic curatives, physical therapy, and counseling.

Because some people who have Lyme elude detection, “you have to ask the right questions when you make a diagnosis,” Murray says. “I think there needs to be a standardized, reliable protocol for testing.”

Culturing the Lyme spirochete, Bb, to determine the presence of Lyme would provide a definitive answer. But it’s costly and time-consuming, and therefore rarely done.

Instead doctors usually check for the presence of Lyme antibodies through a blood test. According to the CDC’s recommendations, if the test, known as an enzyme-linked immunosorbent assay (ELISA), proves negative for the antibodies, no further test is recommended. If it comes up positive, a second test—an immunoblot test—is recommended to confirm Lyme.

Murray says ELISA and blots in tandem are currently the best method, along with more complicated cerebrospinal fluid tests in cases where symptoms are apparent but the first two tests are negative.

But with these methods, false negatives are still a significant possibility. It’s also possible that Lyme cells can alter their outer surface protein and escape detection, and that different spirochetes can cause symptoms that look like Lyme but aren’t. All this, Murray says, means research must be targeted toward finding better tests for the disease.

Follow the Leaders—Or Off With Your Head!

Daniel Cameron, president of the International Lyme and Associated Diseases Society, speaks for the counterculture. He believes that “thought leaders” in the medical community prevent acceptance of what he considers strong evidence that Lyme is both underreported and ineffectively treated. “Who wants to question Dr. Wormser?” he says.

“Even though the evidence is accumulating [that Lyme can be chronic], doctors have a tendency to have to wait for a thought leader to change their mind, otherwise they’ll get criticized, or the medical board might drop the ax on you,” he says. “Off with your head! So it becomes high risk to become a doctor who treats chronic Lyme. Most doctors don’t want to have to.”

Photo of a hiker on a trail in Wisconsin.

PHOTOGRAPH BY JEFFREY PHELPS, AURORA PHOTOS/CORBIS
Ticks are easily picked up on hikes through wooded areas, like the trails seen here in Parfrey’s Glen in Wisconsin.

Cameron says many state medical boards are pursuing lengthy “chart-by-chart” investigations of doctors using long-term antibiotic treatment for Lyme. These can continue for years prior to legal action by boards aimed at revoking a doctor’s license.

But five states—California, Connecticut, Massachusetts, New Hampshire, and Rhode Island—have passed laws protecting physicians from reprisal or harassment when treating Lyme patients with long-term antibiotics.

While he’s careful not to use the word “cure,” Cameron says that with long-term treatment, patients who have had Lyme for years can go into remission and be symptom-free.

He’s not particularly impressed with the CDC’s latest announcement that the number of Lyme cases in the U.S. is likely ten times the30,000 or so generally reported each year.

“In epidemiology, every time you have a surveillance system, you always at least have a tenfold underreporting. There have been studies that show it might be as much as 40 times that.”

He also questions the fact that 95 percent of the reported cases come from just 13 states, mostly in the Northeast, along with Minnesota, Virginia, and Wisconsin. People in other states are less likely to report cases if the official view is that Lyme is rare and geographically restricted, according to Cameron. “That’s a little bit of a reporting problem.”

Could the CDC’s admission of greater numbers be related to the preparation of a new Lyme vaccine?

“They had one vaccine,” Cameron says—LYMErix, which was available for about five years until 2002. It was then shelved because of low sales and, some say, questionable effectiveness. (Ironically, Lyme vaccines are available for dogs but not humans.)

“The buzz on the street is that, of course, one of the reasons the CDC recognized more cases is that in order to get a vaccine through the pipeline, you have to have a problem,” Cameron says.

Game Changer

Raphael Stricker, a San Francisco–based internist who co-led the sexual transmission study, says the possibility of Lyme spreading that way would “change the whole picture.” It means that potentially ticks aren’t the only culprits.

“What I think this is going to do is that it’s going to move treatment to another level,” he says.

Jarret Liotta is a freelance writer. Follow him on Twitter.

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Sue Savod

Sue Savod19 hours ago

What happened to investigative reporting, NatGeo? This report by Jarret Liotta has failed to mention some of the most important information about Lyme disease. First, Lyme does not come alone. It is almost always accompanied by a co-infection, or two, or three, courtesy of the tick. And one of the first thing an ILADS MD, aka “counter-culture doctor”, will do is test you for those co-infections. Would your doctor know to test for these?

Most infected ticks carry more than one disease, up to 10-12 possible. Bartonella, Babesia, rickettsias, anaplasmosis, the list goes on and is growing as more are discovered. As we have learned from our “counter-culture” doctors, Lyme is difficult to cure if there is a co-infection. So those are usually treated before the cunning Lyme bacteria.

I think the white-footed mouse deserves a mention here, rather than blaming it on the deer, since the mouse is the biggest carrier of Lyme. Deer transport the ticks, but the mouse, and other small rodents, are the meal than passes Lyme from ticks to other mammals. Like a dirty needle, the ticks collect disease as they feed and pass it all along to… you.

Dr. Todd Murray was involved in one of Alan Steere’s early “studies” with Lyme, as Steere was looking for an antibiotic cure. Steere treated some people with antibiotics and did not treat the control/placebo group. Dr. Murray was in the placebo group. Without treatment, Borelia burgdorferi multiplies. Dr. Murray still has odd symptoms, years later. He is very kind mentioning, in a recent interview, that he didn’t think Steere meant to use him as a guinea pig.

Polly Murray said in her book, The Widening Circle, that at first she was pleased to help Alan Steere study Lyme, but by the end of the book, she was disappointed that Steere decided to only use the arthritic symptoms and fatigue to describe Lyme when she, and by then many others, knew that Lyme did not stop there. Her own family had been ravaged by the disease with a myriad of symptoms, including heart, neurological, intestinal, psychological problems. Steere’s definition is the one used today by the CDC, even though many of our “counter-culture” Lyme MDs have taken it upon themselves to listen to their patients and have redefined Lyme with symptoms that affect every system in the body. And why not. Lyme is a spirochete like syphillus which was called the great imitator because it mimicked so many diseases. But with Lyme you get more, since it’s bigger and smarter than the syphillus bacteria, has the ability to change its cloak (confusing our own immune defenses) and burrow into the body’s tissue. So why wouldn’t Lyme be more difficult to cure and cause lots of different symptoms. Dr. Wormser?

Vaccine? The last vaccine developed by some of our most prominent infectious disease doctors didn’t work because some vaccinated people were taking on the symptoms of Lyme -permanently. Smith Kline Beecham took it off the market because they were being sued. Turns out 1/3 of the population has a genetic marker that makes that particular vaccine permanently debilitating.

If you really want to do some investigating… Check out the Pookeepsie Journal’s Lyme chronicles. Now that’s journalism. There us so much more to this story. The IDSA’s $earch for a new vaccine, the $ymbiotic connection$ between the CDC and the IDSA. Why the CDC calls people with symptoms other than the IDSA’s “Lyme loonies”. Yes, folks, direct from the pages of the CDC reports that took five years to be released (longest ever) under the Freedom of Information Act, and came out mostly redacted. Redacted. Why would the government have to hide anything about Lyme disease?

This isn’t a simple “he said, she said” situation that can be summed up in a short article. I’m surprised National Geographic didn’t dig deeper and discover the truth in a story that continues to grow, not only in the shameful way doctors who are trying to find the truth are treated ( ” counter-culture” really? Is that the current buzzword for MDs trying to get to the cure, treating patients with compassion, and respect, and succeeding in getting a good number back on their feet and back into life) but also because we are being cheated out of treatment and cure for this ever-growing menace by an unduly limited IDSA/CDC definition of Lyme AND it’s co-infections.

Please step up and do a real story on Lyme. Someone needs to get to the bottom of this. And if you think, Jarret, that Lyme is easily cured, and unless you dare to go to a “counter-culture” doctor, I’d stay out of the woods.

Ann Kent

Ann Kent1 day ago

While I found this piece to be a balanced view of the controversy over Lyme disease, I am disappointed that National Geographic chose to continue the use of “counter culture” to describe tens of thousands of Lyme patients and their physicians.  The definition of counter culture is “a way of life and set of attitudes opposed to or at variance with the prevailing social norm”.  This implies a choice.  Lyme disease is not a way of life or a set of attitudes.  There is not a single lyme patient who has chosen to be sick.   There is not a single physician treating lyme patients who wanted to be in the position to potentially loose their medical license.  These doctor’s listened to their patients and bravely found a way to treat them and bring them back to health. By using the term “counter culture”, the CDC and IDSA choose to demean patients and their doctors.  It feels like when you are loosing the argument, attack the other side.  I am quite surprised that National Geographic did not challenge this viewpoint.  I would hope that a followup article would include a full review of the changing facts and science and more importantly interviews with patients.  Tens of thousands would line up to tell their story.

Jan Posch

Jan Posch1 day ago

Why would those of the IDSA want to develop a Lyme vaccine if the disease is rare and easily cured?  Why can’t people see that in and of itself, proves Lyme is chronic and the IDSA knows it.,

Dennis Sawyer

Dennis Sawyer1 day ago

Always save the tick that bit you, if you can, in a baggie with a moist cotton ball. If your doctor refuses to send it to be tested, send it yourself. It’s worth knowing if it is positive or not.

Nina Maggs

Nina Maggs2 days ago

Proof has now been presented for both sexual transmission and congenital Lyme. With less than 50% experiencing the rash/tick bite, many are being left to suffer for years with this disease and whole generations are living with it. Why is a bacteriological infection (something mankind has been curing for years) not being cured now? Is the medical authorities in this world wanting to bury their heads in the sand for the sake of money? Diseases will always be in the world, but the adults and children who can create the revenue for the economies won’t be 😦 something has to break eventually

Diane Marie

Diane Marie3 days ago

Lyme and Aggressive/progressive MS:

I took chronic Lyme antibiotic combinations for two-and-a-half years including babesia treatment and we stopped the MS process and I was 90% better overall. I’m grateful. I continue to improve with antibiotics, finding and caring for other complications, supplements and herbs and I am now 94% better. Others with Lyme and MS have similar results.

Problem:

This threatens the MS industry profits. That’s politics and profits. There is little profit in antibiotics

It is as wrong as it gets to deny very ill people, what helps them.

Lauren Hale

Lauren Hale3 days ago

Fikrig and Flavell et al found that band 41kDa was specific, accurate, and homologous to borrelia. It is useful, and that’s why it’s even included in the CDC’s “5 out of 10” bands test. It is never variable like the others, so clinical symptoms + 41kDa should still remain a good test method.

The new Flagellin method should work, too. The reason two-tier testing sucks is because of antigenic variation and immuno-suppression. You are only going to be CDC positive if you have a hyper-responsive immune system.

The whole ILADS vs IDSA should stop. It is a false dichotomy. Neither should be in control of these matters because it obviously too emotional for both sides. Not to say the IDSA docs can’t do science, but they are merely wrong. The original serodiagnosis of Steere et al’s was that Lyme was chronic and disabling. And then, nobody could have “Lyme” unless it was just EM rash and arthritis. Brain invasion was basically thrown out, since band 23 produces low sera anyway on the WB.  The WB at Dearborn was found to be 15% effacious, way below standards for other diseases. So, the WB misses 85% of cases. NEW TESTS ARE NEEDED, FIRST. THEN NEW DRUGS. ABX ARE ANTIQUATED AND FAIL.

Controversy is not really there. Lyme is a TLR2 agonizer basically that sets off an explosion for other infections to become activated. No mystery there. Find drugs for TLR2 agonism and you’d be rich. 🙂

BTW, anecdata is not evidence. You need lots of proof to make an extraordinary claim. The problem here is, Steere’s extraordinary claim was validated with his own peers in the eighties and early nineties, and then it was just thrown out for whatever reason. Which should be a red flag. Their initial hypotheses were correct, which is why it worked.

Dennis O'Donnell

Dennis O’Donnell4 days ago

Understanding Lyme Disease and the co-infections that most people who have been bit by an infected tick also have,takes a lot of research.There are competing medical opinions and no real solid evidence because Borrelia Burgdorferi cannot be cultured.There is no reliable test for it and it is ridiculous for people to have the impression only deer ticks transmit it.All species of ticks have forms of it,and it has been found in mosquitoes.I personally know many people who were bit for only a few minutes and got the disease.So the media and most of the Medical Community misrepresent a lot of information about this illness.The most important  aspect is that Lyme Spirochetes have at least a 21 day lifespan.The purpose of antibiotics is to kill 1,000’s of cycles of germ life,so the initial Medical Precedent set by the Infectious Disease Society of America is ludicrous and should be criminal.Literally every person is under-treated,if they are even lucky enough to get any treatment at all.Dr Wormser is known as one of the worst if not the worst spokesman for Lyme issues being that he was part of the IDSA that wrote the initial treatment guidelines.They were sued and lost an anti-trust lawsuit brought about by the Conn. state Atty. General,because the same Drs were trying to market and profit from a vaccine they concocted that did not work and further sickened people.If anyone wants real information about Lyme Disease that is not biased please go to the website for the Drs and scientists from ILADS (International Lyme and Associated Diseases Society).Lyme Disease is literally the #1 epidemic in the world now,present everywhere and most countries you cannot even find a Dr willing to treat you.

Carol Webster

Carol Webster4 days ago

Thanks for writing this article.  One thing missing was the latest discovery in August 2013 of Borrelia Miyamotoi, a new Lyme Disease bacterium strain that was found to be present in the U.S.  This form of Lyme Disease does not show up on the standard lab tests but produces most of the same symptoms.  A few weeks ago, a Standford University study showed that many ticks in California are infected with the Miyamotoi strain.  There is currently no lab test for the detection of Miyamotoi, but the possibility of infection is very real and the symptoms are debilitating.  The current level of funding and research for Lyme is lacking and almost nonexistant, but the Miyamotoi discovery shows just how much research is still needed.  While it’s good to hear both sides of a controversy, I don’t think it’s fair to portray one side as a “counterculture”, especially when there are strains of this disease that don’t even show up on a test.   And it would also be ineresting to find out the percentage of Lyme patients who are part of this so called counterculture.  My guess is 80% because it’s the only way they are getting better.

Joe Springer

Joe Springer4 days ago

@Carol WebsterSerously, if “There is currently no lab test for the detection of Miyamotoi”, then how did Stanford show that many ticks are carrying it?

Holly Lounder

Holly Lounder4 days ago

30 years of illness.  30 years of doctor’s scratching their heads.  Multiple diagnosis’ and labels were given to me.  I learned to function despite the pain and fatigue I suffered from.  I own two businesses, I worked with children with autism, I earned my 3rd degree black belt.  Unfortunately, this past summer my body stopped working.  Literally, I couldn’t walk, I couldn’t control my arms and hands, I couldn’t sit up straight.  Doctors couldn’t figure it out.  They turned me away, telling me I just needed to do more….WHAT?! I couldn’t walk!  Do More?!  Give me a break.  I’m one of the most active people you will ever meet….MY BODY HAD STOPPED WORKING, I COULDN’T DO MORE!  I had, over the past 20 years, three ELISA tests that came back negative.  I had a spinal tap that also came back negative for lyme.  Despite this, at the encouragement of friends who had recovered from lyme I sought out a LLMD.  My blood was sent to INGENIX and I soon had a positive western blot.  Yes, five bands made it CDC positive.  30 years of being told nothing was wrong with me and I don’t have lyme, only to find out YES I do have lyme.  Now, four months in to treatment I am walking again.  I can control my arms and hands again, I can read again.  Why stop treatment if I am continuing to improve?  There are thousands of us who have the same story.  The evidence the long term antibiotic treatment can work is in the patients who are recovering.  I live in Maine and it seems everyone knows of someone in the area who had chronic lyme, got treated and are now better.  I had no idea, until I realized what was wrong me, that chronic lyme is epidemic and that treatment was hard to find.

tessa mccall

tessa mccall4 days ago

“For a lot of people who are not feeling well, those people are the most vulnerable to turning to the types of practitioners that don’t follow mainstream practices,” Wormser says.

*****Lets be clear this isn’t about feeling a little unwell – we are talking about major debilitating symptoms.  Maybe the patients are turning to alternative practitioners because mainstream medicine has continued to shovel over all studies that say this bacteria can burrow deep and avoid being killed.Lyme,

Wormser says, has become a catchall for a constellation of symptoms that elude diagnosis: “If I can’t figure out what you have, it must be Lyme disease

***********This is a ridiculous statement.  The doctors treating these patients are putting their livelihood on the line and being ridiculed by IDSA and CDC and harassed by their states medical boards and it that isn’t enough – they are dealing with patients that have a complex set of symptoms that affects numerous parts of the body.  In a nutshell they are time consuming patients and 10 minute in and out is not going to work for the patients with chronic infection from borrelia.  Also nobody seems to mention that we are for the most part talking about people that don’t have just one infection from one source but a soup bowl of different infections acquired from the vector of the borrelia and the viruses and such that the patient already had dormant in their body that now have been given free reign by a wrecked immune system from the whole mess.

Enough of the sand throwing lets get down to figuring out why these people remain sick and move to a solution.

Stacy M.

Stacy M.4 days ago

Counterculture? How about doing due diligence and taking more than a day to look up information?

Who makes money off of the only two tests the CDC recommends? And do those people (7 of them) sit on the branch of the CDC that makes the recommendations about Lyme? And do those people also control what gets printed about Lyme in medical journals? See, all of this can be found out if NG only tried to actually find out what’s happening.

Why in NYS is PCR testing illegal? Oh right, that would be a test these people don’t make money off of, mmmm…

And here’s an idea. LOOK AT THE BLOOD. Throw blood under a microscope and LOOK at it, low and behold you can see spirochetes. But, that’s only if Lyme is in that stage, but still, it’s not being done. The art of looking at things under a microscope is lost.

The CDC says that in NY in order for a doctor to actually report that they have in countered a case of Lyme, a bullseye rash has to be present. Well a bullseye rash is only present 10% of the time. Therefore, one could say 90% of the cases of Lyme are going unreported.

The CDC also goes against reality when it says that a tick needs to be attached for longer than an hour before Lyme can be transmitted. Oddly enough those individuals that actually work with these parasites, know for certain, that if a tick just gets done biting something and then lands on another host, the fluids containing Lyme could be transmitted IMMEDIATELY.

Yet CDC is the golden wealth of knowledge and the rest of the better informed, more knowledgable world out there is considered the ‘counterculture.’ Odd.

Natasha Moisyev

Natasha Moisyev4 days ago

I very much appreciate the effort you made to cover the different perspectives and the myriad issues related to Lyme in an objective, professional and thoughtful manner.My family’s treatment was delayed for years because “Lyme does not exist in California.” Never mind that, even if Lyme respects state boundaries, I travel extensively and lived in CT for four years. Also, it would be interesting for you to do a followup piece on the relative tests and why they don’t catch Lyme, and why the IDSA is so dead set against the new culture test. Bringing this kind of odd and dangerous behavior to light could help put scientists back on the path of helping find a cure.  Anyway, thank you again for a balanced piece.

Natasha Moisyev

Natasha Moisyev4 days ago

I very much appreciate the effort you made to cover the different perspectives and the myriad issues related to Lyme in an objective, professional and thoughtful manner. As a person whose entire family had Lyme (two daughters who were infected in utero and diagnosed 11 years later) I can say that the IDSA’s stance has led directly to my having to pay our of pocket to treat a family of four with devastating late stage neurological Lyme disease.  It broke my family financially, once we got treatment at all, because we were told that Lyme does not exist in California.  For some reason doctors use that comforting monologue, and never once asked if we had traveled outside the SF Bay Area (which we had- one growing up in Maine and both having spent 4 years in Connecticut). So many problems with the current situation. Perhaps in a followup piece you could address why doctors gie suffering patients that line that they “coulnd’t have Lyme” and refuse even to test them, why the NYT with the IDSA’s help slandered the Igenex labs and continues to state that this lab (which has a more sensitive test) gives many false positives and is unaccredited (not true) and why they have attempted to do away with the new culture test.  It’s as if they don’t want to have to admit they were wrong. I don’t need an apology or an admission, I just need to get better.  Thanks again.

Tom Brian

Tom Brian5 days ago

They have a vaccine for for lyme disease available now , only one problem, you have to be a dog and go to the vet. Ooops   2nd problem is the one for the rest of us was taken off the market for lack of interest  ….. = LOW SALES  …. NO MONEY . ??? SO SUFFER??!

Jean-Yves Jault

Jean-Yves Jault4 days ago

@Stephanie V.  Thanks for pointing to this photo series. I’m not one of those members of the “counter culture” whom I think are often too vocal, a tad irrational, and a little too attached to all sorts of conspiracy theories.  However I am a Lyme sufferer (from Europe).  Diagnosed much too late, treated even later after having to battle a few docs who didn’t want to treat because “having 3 positive ELISA and Western Blot tests” doesn’t prove active Lyme infection” (never mind the myriad symptoms I had), I benefited greatly from (oral-only) antibiotic treatment to the point where I was able to be back at work full-time 1 month post treatment initiation, after a 7 months absence.  Still, it has been almost seven years since my initial contraction of the disease, and I do have lingering symptoms that, as the article puts it, ebb and flow.  I just learn to deal with it, and when it gets too handicapping for me to lead my life, I do a short course of antibiotics combined with anti-malaria medication, and it helps resolve the symptoms for another 6-12 months or so.

Anyhow, two photos in the series really caught my attention — the one on the top right corner, and the one on the bottom right corner.  These aren’t pictures of people in hospitals, on wheelchairs, or with an IV drip.  Like I said, I feel for these folks but I don’t know whether their apparently severe ailments (e.g. paralysis) are Lyme-related or not — my personal experience with Lyme did not put me in hospital, although the neurological and psychiatric symptoms (e.g. inexplicable anxiety) were pretty severe at some point.

What amazed me about these two photos is that they are depicting people that are just dead tired; laying on a bed or sofa, with a blanket on, during the day.  If I were to go through my iPhoto collection of the past 7 years, I can harvest a few photos where I am exactly in that pose, because when the exhaustion hits you, that’s just what you do.  You can’t do anything else but power down to conserve energy.  It’s not a “severe” symptom, being tired, but I can tell you that it has a significant impact on the quality of your life.  It affects your work, your family life, your interaction and availability for your kids, the image of you they have, your self confidence, your ability to make plans for the future, and so on, and so forth.  And I believe it’s one of the hallmarks of Lyme.  I even wonder if what’s called Chronic Fatigue Syndrome isn’t, in fact, pure Lyme (strangely enough, it’s easier to get a CFS diagnosis, even though nothing is known about the cause, mechanisms, aetiology, of CFS, than a Lyme diagnosis…)

That’s all I wanted to say.  Thanks for posting the link.

Carl Tuttle

Carl Tuttle5 days ago

The following petition was created on behalf of the families devastated by Lyme disease who have witnessed first hand a community of physicians influenced by the CDC’s ongoing disinformation campaign aimed at promoting the idea that Lyme is little more than a nuisance disease. This petition provides evidence to suggest that Lyme disease has been intentionally mishandled.California now leads with the number of signatures on this petition but all fifty states are represented as is 21 other countries. (19,277 signatures and growing)

Petition: Calling for a Congressional investigation of the CDC, IDSA and ALDF

 

https://www.change.org/petitions/the-u-s-senate-calling-for-a-congressional-investigation-of-the-cdc-idsa-and-aldf

Carl Tuttle

Hudson, NH

New Hope for Most Severe Chronic Cases of Lyme Disease! Part Three

New Hope for Most Severe Chronic Cases of Lyme Disease! Part Three

“Serrapeptidase”, better known as “Serrapeptase”, is best known for its ability to relieve pain from inflammation, reduce inflammation, and destroying pathogens. It is suggested to be able to kill Lyme bacteria, a wide variety of fungus (another tool in the fight against Candida) and unfriendly bacteria.

This means this enzyme through it’s natural action in our bodies can greatly strengthen the immune system. This enzyme is naturally processed commercially today through fermentation, and was first discovered in the silkworm intestine.

In the past, it has been known primarily for it’s ability to relieve pain – especially pain from inflammation, anti-inflammatory properties.

Serrapeptase reduces inflammation in three ways:

Breaks down the insoluble protein by-products of blood coagulation known as fibrin. Fibrin develops from soluable

  1. protein which clots together to form a mesh when you are wounded.  Fibrin can cause many health problems in certain health problems and diseases;
  2. Thins the fluids formed from inflammation or injury and facilitates their drainage which speeds the tissue repair process.
  3. Serrapeptase alleviates pain by inhibiting the release of specific pain-inducing amines known as bradykinin (according to Wikipedia, bradykinin is a nonapeptide or group of proteins consisting of nine amino acids), that cause blood vessels to enlarge (dilate), and therefore causes blood pressure to lower.. The cardiovascular effects of the serrapeptase are due to the remarkable ability to break down dead or damaged tissue without harming living tissue. Atherosclerotic plaques can be slowly dissolved without harming the inside of the arteries.

Serrapeptase is also known for its ability to destroy harmful pathogens and unfriendly bacteria.  This helps to greatky strengthen our immune system and free it up to fight more serious infections (such as Lyme disease.)

Surprisingly it has been known for over a decade that serrapeptase works to break apart and/or dissolve biofilms.

The wonderful collision of earlier research with the frantic search for a cure for the many modern chronic illnesses (such as Chronic Neurological Lyme disease, Fibromyalgia, Chronic Fatigue Syndrome, Epstein Barr, Autism, MS to name just a few) and auto-immune diseases (such as HIV, Celiac disease and Diabetes 1 to name a few) has resulted in the discovery of serrapeptase inhibiting and destroying biofilm.

Bacteria, as we have discussed in many blog posts, often follow a process called biofilm formation which results in virtually impenetrable fortresses for the bacteria to multiply and thrive growing steadily and in extended chronic infections causing the immune system to atack our most weakened and fragile organs and/or central nervous system making the disease incredibly painful and resistant to any anti-micrbial, anti-bacterial or anti-viral agents – pharmacological or organic in nature.

Throughout medical research into various means of inhibiting or destroying these biofilms, great breakthroughs have occurred – especially in the last few years.

One study from top Italian scientists suggest that “proteolytic enzymes” (see definition below) could significantly enhance the activities of antibiotics (pharmacological or organic) against biofilms by revealing the infectious colonies as the biofilms are destroyed, and actually inhibit the invading bacteria or virus from developing any new biofilm “hide-outs.”

If the body were always capable of producing adequate proteolytic enzymes, it is possible that cancer would not develop. In theory, cancer cells have a type of protein coating that is destroyed by these proteolytic enzymes. When this protein is destroyed, the body’s white cells are able to attack the cancer cells and destroy them.

This is also true of the protein coverings that enable Lyme disease to successfully evade our immune system and busily creating these strongholds – sometimes for years without any symptoms – and the WHAM!  You encounter exceptional stress and everything shuts down.  For “Lymies” we call that the “crash”.  For those fortunate souls who discover their Lyme infection immediately, the infection is killed before the biofilms can be constructed.

Unfortunately, for those who think they have successfully eradicated a new infection of Lyme, it is not uncommon for a full-blown infection to flare up months or years later due to stree or extreme physical stress and find that a few spirochetes slipped into the central nervous system and evaded the antibiotic treatment.

Lymes disease can lie “dormant” for decades without showing more than a few aches and pains here and there…creating massive biofilm colonies while the unsuspecting victim pops ibuprofen for a sore joint or stiff neck.

The following anecdotes come from Systematic Enzymes (to read entire article click here):

The late alternative medicine renowned internist physician, Dr. Hans Nieper, M.D., (1928-1998) of Germany, pioneered the use of this enzyme in clearing arteries and capillaries of accumulated cholesterol-loaded plaque.

In this extraordinary application of an inexpensive and entirely safe food grade natural protein, Dr. Nieper fed the protein to a small group of men scheduled for artery by-pass surgery by him. He delighted in presenting a pair of 70 year old former gymnasts doing handsprings who previously could barely walk to the door unaided, and suffered extreme chest pains.

Another licensed medical doctor who requested anonymity calls serrapeptase “miraculous”. Dr X claims serrapeptase protects against stroke and is more effective and quicker than EDTA chelation treatments in removing arterial plaque. He also reports that serrapeptase dissolves blood clots and causes varicose veins to shrink or diminish. Dr X excitedly told of a woman scheduled for hand amputation and a man scheduled for bypass surgery who both recovered quickly without surgery after treatment with serrapeptase.

To conclude this series on “New Hope for Severe Chronic Neurological Lyme Disease, it appears to me, as a journalist and chronic neurological Lyme sufferer, that these three enzymes from earthworms will most certainly ease the sever intensity of symptoms and possibly cure even decades of suffering.

I know that I am not speaking for myself alone when I say that the acceptable goal for healthy and vibrant living is not as high as it once was – which has caused me great sadness.  However, I am now raising that standard high in the air with new found hope that extraordinary health can be ours again – not way down the road, but perhaps someday soon!

NOTE:  This is a powerful anti-coagulant so it must be used with care.  If cut while taking this product, contact your physician immediately.

Best product:  Nutramedix now makes a very high quality product in clear capsules that make the enclosed powder highly digestible. I find the best prices at Amazon – click here.

 

– See more at: http://lymediseaseresource.com/wordpress/new-hope-for-most-severe-chronic-cases-of-lyme-disease-part-three/#sthash.5DaOn98O.dpuf

Lumbrokinase treatment for Lyme

New Hope for Most Severe Chronic Cases of Lyme Disease! Part One

New Hope for Most Severe Chronic Cases of Lyme Disease! Part One

Has anyone heard of Lumbrokinase?  Well, if you haven’t, lumbrokinase is a group of six, novel proteolytic enzymes derived from the earthworm Lumbricus Rubellus, and it is slowly establishing itself as possibly the best and brightest new treatment for chronic Lyme sufferer.

To purchase http://www.pureformulas.com/lumbrokinase-60-capsules-by-allergy-research-group.html#sthash.cCFZIyz0.dpbs

I say “new treatment” because it is new information for me – generously supplied by a fellow “Lymie” Ted Patterson who has tried it and “feels better than he has in years”.  The more I researched this enzyme, the more excited I have become.

First, lumbrokinase has been used successfully in China’s four top hospitals in nerve and infectious diseases since 1995 without any harmful side effects.  Initially used for the potent ability to dissolve blood clots and vein thrombosis, it was soon discovered to improve the quality of blood in a number of ways that are still being discovered.

According to Allery Research Group,  medical reports from leading researchers and doctors have further discovered the power of lumbrokinase to not only dissolve clots which obviously helps protect against heart disease and strokes, but also:

to lower fibrinogen levelsin cancer patients, which is strongly associated in scientific studies with better outcomes,

  • strongly associated in scientific studies with better outcomes, less metastasis, and slower growth of tumors;
  • to offer antiplatelet, anti-thrombotic and self-destructive cellular activity, remarkably regulating hypercoagulation; and most importantly for us,
  • to dissolve bacterial biofilms present in chronic infections in conditions like autism and Lyme disease, allowing antimicrobials and anti-bacterials as well as our own immune system to work effectively and quickly to destroy the colonies that hide behind the biofilms.

Biofilms have been recently discovered as one of the key biological roadblocks to curing many chronic diseases, especially (for our purposes) Lyme disease. It is a remarkable breakthrough, and it ultimately could have a huge effect on Lyme disease sufferers and possibly their life insurance quotes and policies because of a longer life expectancy among those infected.

Peta Cohen, M.S., R.D.,  is the founder of Total Life Center in Northern New Jersey, and has a Masters Degree in Clinical Nutrition, was recently interviewed by Allergy Research Group (read entire interview here), and offers these insights into biofilms:

“I do a tremendous amount of testing and assessing the children through urine and fecal analysis. What got me so interested in nattokinase and lumbrokinase was the concept of what a biofilm infection actually is. If you do a medline search on biofilms and platelet aggregation, fibrinogen, and fibrin, boom, it’s there right in your face.

“Bacteria build biofilms by first aggregating together, and then rapidly weaving this protective web or matrix around them.  They build a polymeric matrix. It’s a sticky, gluey, mucus-y goop and it’s got fibrin in it to give it an intact structure. The bacteria recruit fibrinogen to create fibrin as part of that matrix. At that point they can shed their outer membrane, which has the proteins that serve as antigens and as a target of the missile of the immune system. They’re very protected. They’re very crafty in creating a way to survive and procreate and hide from the immune system.”

In neurological Lyme disease, the biofilm is believed to be constructed of actual bits and pieces of our myelin sheath which covers and protects our actual nerves that make up our central nervous system.  So when the immune system calls for killer cells to destroy the invaders, our immune system can actually attack our central nervous system trying to break through the biofilm and destroy the infection which they cannot do.

So, as lumbrokinase dissolves this biofilm, we have hope that our killer cells, or in more critical cases where the immune system is no longer working effectively, antibiotics (pharmaceutical or herbal) will be able to destroy the infection and return us to health!

See product here.

Look for Part Two on “nattokinase”, and please comment if you have any experience to relate regarding lumbrokinase.

To read excerpts from LLD’s who are using lumbrokinase successfully, read:

Two Doctors Use Lumbrokinase to Help Conquer Lyme Disease

– See more at: http://lymediseaseresource.com/wordpress/new-hope-for-most-severe-chronic-cases-of-lyme-disease-part-one/#sthash.0wOhm6d3.dpuf

New roundworm may be connected with CFS/Lyme

NEW RESEARCH INTO MULTIPLE CHEMICAL SENSITIVITIES: THE POSSIBLE ROLE OF VARESTRONGYLUS KLAPOWII IN CAUSE AND TREATMENT

Neil Nathan MD is working with Dr. Klapow on looking into the connection between Vk and MCS.

By Neil Nathan MD

 Dr. Lawrence Klapow discovered a “new” roundworm, or nematode, approximately 15 years ago. As with many ground-breaking discoveries, the scientific community has been slow to accept or embrace his findings, despite the fact that he was able to complete a double-blinded study in which patients with Chronic Fatigue Syndrome were found to harbor this nematode in a surprisingly high percentage of cases. To be more specific, of 40 patients with Chronic Fatigue Syndrome, Varestrongylus klapowii (which we will now refer to as Vk) was found in over 60% of them, while not found in any of 20 controls.

This alone should stimulate researchers to delve into this area with great excitement. Unfortunately, this has not yet occurred.

While describing his findings to us at a GMA staff meeting several months ago, Dr. Klapow reminded us that the Vk worm is similar to several other nematodes that are capable of making an enzyme called acetylcholinesterase. Dr. Gordon and I looked over at each other at that moment, simultaneously struck by the possibility that this would explain one of the unusual phenomena faced by patients with Multiple Chemical Sensitivities (MCS)—–namely, the rapidity with which those patients react to chemicals or scents that set off their symptoms.

Let me explain. When a patient with MCS is exposed to an offending chemical, or scent, they will usually react almost instantly. This means that within seconds of exposure, they will experience extreme fatigue, cognitive impairment, or neurological events (spasms, tics, dystonias, even seizure-like activity). What has made this difficult to understand is that we have been viewing MCS as a form of allergy; however, no allergic reaction, even an anaphylactic reaction (e.g eating shrimp and breaking into hives or having trouble breathing) occurs that fast. Those reactions take at least 5-15 minutes to manifest. So why do MCS patients react so instantaneously?

Dr. Klapow’s suggestion, once understood, is that perhaps it is this nematodeVk, which lives primarily in the sinus and lung tissues, that is reacting to these chemical stimuli, producing acetylcholinesterase, which, in effect acts as a kind of neurotoxin or nerve poison, producing these effects.

Intrigued by this idea, we have embarked in a research project to study this possibility.

We started by asking as many of our MCS patients as possible, if they would allow us to wash out their sinuses and allow Dr. Klapow to analyze this material for the presence of the Vk worm. As of this date (7/14/12) we have looked at 33 patients, and 30 of them have clear evidence of the Vk worm.  We have looked at 5 controls, only one of whom is positive for the worm.

The first question appears to be answered: do patients with MCS have the Vk worm present?  Over 90% of them do. (The three patients who tested negative are being re-tested now as well.)

  • Does this worm make acetylcholinesterase?  We are working with several research groups and have sent them specimens for analysis. We hope to know this shortly.
  •  Do MCS patients have an increased level of acetylcholinesterase when exposed to a chemical that we know provokes a response in them? Several of our courageous patients have volunteered to check out this possibility and we are working with several labs to provide this information for us.
  • Does this mean that treating a patient who has this worm might help to cure them of MCS? We do not know yet, but we are looking into this possibility with great interest.

We will keep you abreast of this exciting research being done at GMA, as it unfolds.

This study is closed to new participants. If you are interested in possibly being included in the future, send your information to Susan.We are sorry, but most GMA studies, including this one, are open only to GMA patients.

pacificmama

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Posted 04 January 2011 – 09:01 AM

Thought this was interesting enough to post. It came around in one of my lyme newsmails. I often see people on lymenet post that until you tackle the worms, you won’t get the cure.I do remember that in Dr. Corson’s talk at ILADS this year, she told the story of how Willy Burgdorfer (who “discovered” borrelia burgdorferi and hence it is named after him) was really looking into nematodes in ticks when he then found the borrelia.

Here it is… it’s not for the squeamish!

Mary

——————————————————

Nematode Spirochete Farmers 

In 2000, the World Health Organization (WHO) reported that over a billion people are at risk for parasitic worm infections (filaria). 120 million people are infected with parasites in more than 80 countries (Africa, Asia, Central and South Americas, and the Pacific Islands). Of those infected, 44 million suffer filariasis symptoms.

Nematodes are parasitic worms which receive nourishment and/or shelter from hosts. There is a theory that nematodes ‘farm’ smaller organisms like the Lyme Borrelia spirochetes, similar to the way we humans farm cows or chickens, feeding and protecting them so we can later eat them. Nematodes may live symbiotically with spirochetes in humans!

Ticks and other vectors harbor numerous parasites: large ones referred to as worms (filaria) and microscopic bacteria, viruses, protozoa, fungi and microfilaria. Ticks in Connecticut and New York do carry nematodes according to Doctors Willy Burgdorfer, Eva Sapi, and Richard Ostfeld.

Can worms destroy American health, as in WHO’s reported 80 countries, or as in our American pets? The answer to the question, “Can nematodes wreak havoc as human parasites?” is supposedly unknown, at least in the USA. Well, can nematodes prevent recovery from “chronic” Lyme and tick-borne diseases? Puppies are de-wormed soon after they are born. Dogs typically and quickly recover from Lyme disease after antibiotics, perhaps because of their early-life and subsequent regular de-worming; there are no nematodes harvesting spirochetes in their canine bodies.

If nematodes work against antibiotics by protecting and increasing spirochete population, then antibiotic therapy may eradicate ‘loose’ spirochetes but not those under nematode farmers’ protection. If a nematode-Borrelia symbiotic relationship exists, Borrelia can screw its way out, escape the nematode farm, free to wreak havoc on us.

If nematodes are present, then a huge amount of antibiotics over a long period of time may only suppress bacterial growth. Symptoms will be somewhat relieved, a modicum of health will be maintained, but there is no cure while nematodes live to raise new spirochetes.

So for the duration, surviving nematodes will keep on farming. Can this proposed process explain the cyclical nature of Lyme in certain cases? Antibiotics destroy spirochetes, some nematodes starve and die, but survivor nematodes still farm. A human host might suffer a relapse or flare-up if a bountiful harvest releases excess spirochetes into the body.

Antibiotics relieve our symptoms by killing spirochetes. Antibiotics also decrease the nematode’s food supply resulting in nematode starvation and death. If enough spirochetes are destroyed and enough nematodes die of starvation, eventually there might be no one left to run the farm. A patient recovers.

However if nematode filaria causes some chronic Lyme, it might be more prudent to stop the farmer. Ivermectin causes starvation and death of nematodes by interfering with their ability to eat/digest. Although antibiotics have been our primary defense, a doctor once told me Ivermectin was the best medicine for Lyme disease. Interesting to note that since 1982, filariasis victims in WHO’s reported 80 countries were given millions of free doses of Ivermectin as part of a Global Health Initiative, but in the USA and Europe, it is typically not prescribed. A surging idea is that all we need is to live healthy and take vitamins and supplements but I suspect that what would CURE chronic Lyme would be a remedy for the cause!

Other causes may be virulent Borrelia, Mycoplasma, Morgellons, Candida, other Fungi, Molds, XMRV, (Xenotropic Murine Retrovirus) and/or other microbes or filaria.

The average chronic Lyme patient suffers a gradual decline into poverty and a lifetime of pain and debilitation. Find the cause, treat and have compassion.

Eva Haughie

EMPIRE STATE LYME DISEASE ASSOCIATION, INC


Posted 04 January 2011 – 10:10 AM

Thank you very much for posting this. I have heard for quite a while that often with chronic lyme, the parasites/worms are a real part of the problem to deal with. Perhaps this explains why it is so important to deal with this issue, and another good reason to start on worms FIRST, before abx, as Dr. Klinghardt suggests in his slides/talks. I started on abx first, not knowing about the parasites/worms at that time, and while it helped me a lot, helped me keep my job, I do think it resulted in the parasites/worms becoming even more of a problem to deal with later.

Posted 04 January 2011 – 11:40 AM

This was a very interesting article. We are seeing a Dr. in Klinghardt’s office and Ivermectin was one of the first meds (after 2 days of biltricide and along with pyrantel pamoate) prescribed but I did not know why. Thank you so much.

Ds16: 5/10-PANS; 10/10 -lyme; Babesia [parasite]; Mico. & chlamydia pneumonieae; mold; T&A done; GcMAF done 12/13;

Current treatment

  Maintenance:  Vit. D3/Omega 3’s; Detox [chlorella-Chia seeds-charcoal/clay for stomach detox(during illness only)];  probioticKidney detox drink-electrolytes/’M’ Water/Galactose

PANS Support (mood/brain/anti-bacterial:  Kavinace;   B12 Spray; Calming Cream; Neuro-Immune Stabilizer cream; SpiroNil-Biocidin (anti-bacterial)

Immune Support-Winter:  Chaga mushroom; Vit. A pushes once a month to keep viruses away.

Prescriptions:  thyroid; Desmopressin [Urinary tract support]; neurofeedback (weekly);  Psychologist (bi-weekly); Exercise (finally!)

Manuka honey [+35]/distilled water for nasal spray/ear drops and in tea for throat)<p>Wow!–LOVE THIS HONEY for ears, nose (we keep to once/week or less), & throat!


Lyme Disease UK Discussion Group

Several of us were found to have this worm in 2007……
New Research Into Multiple Chemical Sensitivities: The Possible Role Of Varestrongylus klapowii…
gordonmedical.com
By Neil Nathan MD Dr. Lawrence Klapow discovered a “new” roundworm, or nematode, approximately 15 years ago. As…

Neelu Bird y is worm tx only given to dogs these days and not humans?

  • Nina Maggs Seems medical treatment for dogs is better than for humans these days. If only the medical authorities knew that a dog can’t unfortunately pay tax or contribute to revenue…
    12 hours ago · Like · 3
  • Natalie Mischief So how do you find out if you have it? And have they successfully treated it in the patients they found it in?
  • Jacqui Butterworth More important what do you treat it with?This study is closed to new participants. If you are interested in possibly being included in the future, send your information to Susan. We are sorry, but most GMA studies, including this one, are open only to GMA patients.
    Tried Susan but not got through!
  • Michelle Rowland Denise Longman is this the nematode that was found by Wally Burgdorfer when he dissected tick guts?
  • Louise Dean Animal worming meds can be taken by humans with the dosages adjusted to our body weight I would assume.
    3 hours ago · Like · 1
  • Clare Turner Yes Louise, following initial treatment as advised by LLMD (no longer allowed to treat Lyme etc) I take a monthly dose of anti- worming medicine on the full moon, which is when they hatch.
    3 hours ago · Like · 2

Continue reading New roundworm may be connected with CFS/Lyme

Chronic Lyme Disease and Co-infections: Differential Diagnosis

Chronic Lyme Disease and Co-infections: Differential Diagnosis

Abstract

In Lyme disease concurrent infections frequently occur. The clinical and pathological impact of co-infections was first recognized in the 1990th, i.e. approximately ten years after the discovery of Lyme disease. Their pathological synergism can exacerbate Lyme disease or induce similar disease manifestations. Co-infecting agents can be transmitted together with Borrelia burgdorferi by tick bite resulting in multiple infections but a fraction of co-infections occur independently of tick bite. Clinically relevant co-infections are caused by Bartonella species, Yersinia enterocoliticaChlamydophila pneumoniaeChlamydia trachomatis, andMycoplasma pneumoniae. In contrast to the USA, human granulocytic anaplasmosis (HGA) and babesiosis are not of major importance in Europe. Infections caused by these pathogens in patients not infected byBorrelia burgdorferi can result in clinical symptoms similar to those occurring in Lyme disease. This applies particularly to infections caused by Bartonella henselaeYersinia enterocolitica, and Mycoplasma pneumoniaeChlamydia trachomatis primarily causes polyarthritis. Chlamydophila pneumoniae not only causes arthritis but also affects the nervous system and the heart, which renders the differential diagnosis difficult. The diagnosis is even more complex when co-infections occur in association with Lyme disease. Treatment recommendations are based on individual expert opinions. In antibiotic therapy, the use of third generation cephalosporins should only be considered in cases of Lyme disease. The same applies to carbapenems, which however are used occasionally in infections caused by Yersinia enterocolitica. For the remaining infections predominantly tetracyclines and macrolides are used. Quinolones are for alternative treatment, particularly gemifloxacin. For Bartonella henselaeChlamydia trachomatis, and Chlamydophila pneumoniae the combination with rifampicin is recommended. Erythromycin is the drug of choice forCampylobacter jejuni.

Keywords: Bartonellosis, Borellia burgdorferi, Chlamydophila pneumoniae, Chlamydia trachomatis, co-infection, Lyme disease, Mycoplasma pneumoniae, treatment, Yersinia enterocolitica.

INTRODUCTION

In Lyme disease, other infections, whose pathological synergism exacerbate the disease or induce similar clinical manifestations, can exist concurrently. Such concomitant infections are termed co-infections. Co-infections can be transmitted together with Borrelia burgdorferi by tick-bite, and result in multiple infection. Part of co-infections is independent of tick-bite.

The goal of this review was to summarize the more important co-infections completed with some personal experiences and with a short summary on reactive arthritis. Because of the similarity of the clinical symptoms of tularemia, Q fever, parvovirus B19 and Campylobacter jejuni infections to those of Lyme disease a short summary of these infections are also included.

Continue reading Chronic Lyme Disease and Co-infections: Differential Diagnosis

Field Trials Show New Technology Able To Prevent Lyme Disease Transmission

Candidate Oral Bait Vaccine Targets the Vector, Not Humans, to Interrupt Cycle of Transmission

PR Newswire

MEMPHIS, Tenn., Feb. 12, 2014

MEMPHIS, Tenn., Feb. 12, 2014 /PRNewswire/ — A new technology has been shown to reduce the level of tick infection of Borrelia burgdorferi, the cause of Lyme disease. Study details were published online today in the Journal of Infectious Diseases, in advance of print publication.

The oral bait vaccine was distributed to white-footed mice, which account for the majority of the transmission of Borrelia. The mice created antibodies in response to the vaccine. When ticks later fed on the mice, the ingested antibodies killed the Borrelia and prevented the transmission of Lyme disease.

Read more: http://www.digitaljournal.com/pr/1734262#ixzz2tIlJRZn9

Lyme Links

Dr. Burrascano’s Diagnosis and Treatment Guidelines (the Lyme “bible”)
http://www.ilads.org/burrascano_1102.htm

ILADS Basic info
http://www.ilads.org/axioms.htm

Lyme Info
http://www.lymeinfo.net/

Lyme Misdiagnosed As…
http://www.geocities.com/lymeart3/lyme-misdiagnosed-as.html

LymeNet Discussion Group
(Ask questions and also ask for lyme literate MD)
http://flash.lymenet.org/scripts/Ultimate.cgi

Info for newbies to LymeNet
http://flash.lymenet.org/ubb/Forum1/HTML/009342.html

Good labs for better Lyme Disease testing: 
http://www.igenex.com/

http://www.bowen.org/information.htm

Lyme Disease – The Unknown Epidemic
http://www.mercola.com/2001/jul/25/lyme_disease.htm

Wilder Network
http://www.wildernetwork.org/welcomehome.html

Great links on this page:
http://groups.yahoo.com/group/CFSFMLD/links

Lyme Expert – Alan Macdonald

Alan Macdonald Lyme Expert http://www.youtube.com/watch?v=r8tESJVvM88 Key Points:  19:45 – US Test kit Band 31 only US Specific one of 300 genotypes. Three types of European Lyme not Type 31. https://www.youtube.com/watch?v=2RATCS-3v9Q Eye and brain are sanctuary sites hide. Spirochetes can combine with other proteins that sit on top and conceals so immune. Cloak in antibodies which are not impacted by immune system. Biofilms are the ultimate survival technique. Extracellular matrix. 04:32 –  promotes survival and chronic infection. 07:05 – Cystic Forms – Round bodies  – Ball of worms. Open up and 12:00 – Cytokines promote an regulate a bacterial response (IE red rash around tick byte.) 16:30 – BIO Film confirmed in Lyme. FORMS

  • Granular From – Salt and pepper shapes little chopped up pieces
  • Spiral Form
  • Mutant straight form – Lost its motor form that moves it- Flagellan less mutants
  • Lyperzones – Enough DNA
  • Balloons or cell bubbles with no

Alan G Barbour did lots of research into.99% of all bacterial in the body (90% of weight) https://www.youtube.com/watch?v=FEjNMlNM3l8

Lab Tests to be undertaken

A number of tests are available :

NHS Funded

  • Two Tier Testing
    • ELISA test  – Many false positives
    • Western Blot test  – <50% effective and many false negatives

Must Have

  • CD57 Count – An immune marker for Lyme
  • LTT-Elispot  –  97% Infectolab
  • Panel for co-infections
    • bartonella, ehrlichia, babesia
  • Candida
  • Vitamin D / Calcium / B12

Advised

  • Chlamydia pneumoniae
  • Mycoplasma
  • Rickettsia 
  • Ehrlichiosis

Others

  • Melissa –  (Dale had this tested positive 2011 on two bands)
  • PCR (Red Labs)
  • DNA
  • Hilysen (New in Europe)
  • Borrelia-Immunoblot
  • Troponin blood test  (Cardiac Muscle)
  • Coxsackie-Virus antibodies
  • Ehrlichia
  • EBV

Lyme or Candida – How can you tell the difference ?

Unfortunately, it’s very hard to distinguish between the two…your doctor should be able to clinically diagnose what your symptoms are..

I had the advantage of treating with the Byron White formulas,which can be used diagnostically, and we were able to differentiate that way..

Here’s a link to check out if you’d like..

http://web.archive.org/web/20021029200337/ www.lymealliance.org/medical/secondary/secondary_2.php

CHAT WITH A LYME-LITERATE PHYSICIAN

Q. So many of the symptoms of chronic yeast infection sound like symptoms of Lyme disease. How can a physician tell the difference?

A. I suspect that some of the chronic Lyme disease that we see is actually chronic yeast infection.

The problem comes when one treats long-term with antibiotics without taking into account the yeast.

What happens is that over time the person on the antibiotic often goes from experiencing symptoms of Lyme disease to experiencing very similar symptoms with Candidiasis.

The doctor may assume that the person is still having significant problem with Lyme disease, when actually they’ve just encouraged a new disease, Candidiasis, which needs to be treated.

Since we have no idea when the last Lyme spirochete has left our system, it is important to get rid of all other invaders in order to allow our body to heal itself.

From <http://www.mdjunction.com/forums/lyme-disease-support-forums/general-support/3200732-how-to-differentiate-between-lyme-candida>

Complications from Lyme Desease

Lyme Carditis

  • Carditis is a rare complication of Lyme disease that occurs when Lyme spirochetes invade the tissues of the heart, producing in some cases a pancarditis that involves the endo-, myo-, epi-, and pericardium simultaneously.
  • The most commonly recognized clinical feature of Lyme Carditis is atrioventricular block, which can fluctuate between first-, second-, and third-degree block.
  • Among Lyme disease cases reported to CDC, second- or third-degree heart block occurs in approximately 1% of patients about whom clinical details are available.

Neuroborelliosis

[Add More]

Cardiomyopathy

  • The role of Borrelia infection in chronic dilated cardiomyopathy in the UK remains unproven.
[Add More]

Early Stage Lymes

There is also a 3 phase view of Lyme  Disease
Three Stages
Two Stages  (Alternative)
1. Early Stage Lymes
  • Up to 70% can be cured using antibiotics
  • Target Rash in <50% of cases
2. Late Stage (or Chronic Lyme’s Disease)
  • It can take months or years to achieve remission
  • Its not clear if complete removal of Lyme’s can ever be achieved
  • Key is to reduce Bacteria load to the point where the Immune system can keep the bacteria under control
  • Maintain health though herbal remedies as less harmful than ABX

Tick Bytes

  • If you suspect you have been bitten by a tick take it seriously.
  • We are not always aware of a tick bite as the smallest is the size of a poppy seed and we cannot feel it bite because it injects an anesthetic.
  • Only about 50% of people get a typical bulls eye rash. The rash is the hall mark of Lyme’s Disease and so it is not necessary or advisable to wait for a positive blood test, by then the organism has had chance to disseminate throughout your system.
  • Three genospecies, Borrelia burgdorferi sensu stricto, Borrelia afzelli and Borrelia garinii, represent the predominant pathogenic variants in the UK.
  • Erythema migrans is the commonest manifestation, occurring in 60%-91% of cases.

Lyme Disease Overview

  • Lyme disease is a multisystem illness caused by Borrelia burgdorferi, a spirochete transmitted by certain species of Ixodes ticks.
  • The most common signs of Lyme disease are the erythema migrans rash followed by rheumatologic and neurologic symptoms.
  • Lyme Disease is the most common tick-borne infection in Europe with around 85,000 new cases per year and its incidence is increasing due to climate change.
  • Worldwide up to 250 million people are thought to have Lyme’s disease yet most are unaware.
  • Chinese authorities estimate 6% of 1.6b population using a 50% reliable testing technique
  • 50% of people with Lyme never saw a tick bite and around 50% never get a rash.
  • In the UK, neuroborelliosis is the most common complication, while myocarditis is unusual, and death from either conduction disease or carditis is extremely rare.
  • According to a leading US authority on Lyme’s Disease, 95% of his patients achieve remission where the immune system can regulate the bacteria itself.
  • Controversy over the existence of either ‘chronic Lyme disease’ and/or ‘post-Lyme disease syndrome’ continues unabated.