Category Archives: Tests

Bioresonance Treatment Overview

Many people who are dissatisfied with a lack of progress on antibiotics and pharmaceutical (allopathic) medicines are considering Naturopathic and Integrative (Multiple) medicine for treatment. Energy Medicine (Generic name covering several technologies) is becoming popular for the treatment of Lyme disease and co-infections yet little is known about many of the options that exist.

This post provides an overview of the treatements we have encountered.

Bioresonance Therapy

Bioresonance machines allow a therapist to determine pathogens and stressors on the body to help select the most appropriate treatments, ensuring that the body’s elimination organs are built up to support the removal of toxins before Pathogens are removed. In many cases, by just unblocking the elimination organs (Liver, kidneys, Lymph nodes, connective tissue)  and boosting the immune system the body is able to clear many of the pathogens  naturally without treatment.Bioresonance machines cost up to £20,000, so most are purchased by therapists who offer treatments to patients typically charging £70-100 per hour.  A growing number of patients are purchasing Bioresonance machines for home use under the guidance of a trained therapist. A second-hand machine can be obtained for £5-10,000. A key benefit of Bioresonance Therapy is that you don’t need to learn how to use a complex machine before seeing benefits.

When surveyed in May  2016, 10 Bioresonance therapists from the UK, US, Germany & Holland reported that they have been able to eliminate Lyme disease in more than 70% of patients and reduce the symptoms in many the remaining 30%. One experienced US based therapist states that 30% of her Lyme patients don’t improve with the elimination of Lyme disease bacteria and that this is typically due to an undetected virus (mostly Herpes family) that cause symptoms that were assumed to be Lyme disease.

Bioresonance machines can be diagnostic or therapy only and sometimes they are combined into one unit, such as BICOM product (above) from German company Regumed.

Diagnostic Testing can be carried out on hundreds of pathogens very quickly. There are several approaches including the use of glass ampules and digitally encoded ampules (containing the resonant frequency of pathogens). The BICOM machine inverts the pathonogenic frequency  into a treatment which can be tested to confirm a “beneficial treatment” using heart rate variability monitoring, Keniesiology (muscle testing) or using a biofeedback device called a biotensor. Bioresonance testing is both fast, cheap and reliable with no waiting around for test results.

BIORESONANCE therapy can achieve major benefits in just two or three treatments. It is possible to use as a home treatment device with a few hours training. Less treatment is required compared to RIFE therapy and it’s thought to be more effective on a wider range of co-infections. A therapist will typically combine multiple treatment options into one treatment session. Further information on Bioresonance can be found here.

Some therapists combine Bioresonance therapy with Oxygen, Ozone, Biophoton therapy along with naturopathic treatments, supplements and herbs.

A novel approach used by some patients is to combine the use of both energy medicines with visits to a Bioresonance Therapist and regular RIFE treatments at home in between.

Some patients who have have been on pharmaceuticals for many years and are very weak may not be able to obtain a full recovery with Bioresonance treatment, but are likely to obtain some benefit.

A list of UK and European therapists offering Energy Medicine therapies will be made available shortly.

Figure 1. An older BICOM 2000 from Regumed

bicom-2000

BICOM Picture 1

Bioresonance therapy is one of a number of procedures including homeopathy, acupuncture and other naturopathic procedures within the area of empirical healing.

The fundamental principles of the following hypothesis for bioresonance therapy have been confirmed by the latest discoveries in quantum mechanics and biophysics, but have not yet been accepted by current expert opinion within orthodox medicine.

The BICOM machine does not typically cause severe Herxeimer reactions so a patient can receive 3-5 treatments per week, although typically it’s one or two sessions per week as it can take several days to fully absorb the treatment.

Wave-particle duality

Discoveries made in quantum physics have revealed that all particles of matter share the characteristics of both waves and particles. This means that all substances – and therefore all cells, parts of the body, as well as viruses, bacteria, pollen, toxins, etc. – emit electromagnetic waves. Depending upon their nature, all substances have a quite specific typical wavelength or frequency with highly individual characteristics. This is known as a frequency pattern.

cells and matter

Cells communicate with one another

Living as we do in the communication and information age, it is time we faced up to the fact that the body can only function and regulate itself because communication and thus an exchange of information takes place between the various cells in the body. Research into biophotons is based on the assumption that cells communicate with one another by means of “flashes of light” (photon radiation). They exchange information over certain frequencies.

This information exchange functions unhindered in healthy bodies. As a result, each cell and each part of the body is able to do its job.

2 cells communicating via electro-magnetic frequencies

Stress-inducing factors or substances can impede communication between cells

If, however, undesirable substances (toxins, viruses, bacteria, etc.) or harmful radiation act on the body, these may impede communication between the cells.

pathogenic cell communication interrupts normal cell

Disrupted cell communication may result in organic changes

Where communication between cells is impaired, this will of course prevent those cells from functioning properly and we see evidence of this to varying degrees in the form of non-specific disturbances in general well-being, poor performance, chronic fatigue and later as organic changes plus related symptoms.

Symptoms frequently occur at the point where there was already a deficiency – often hereditary.

 

sick cells

Determining individual stresses accurately

The body’s extracellular fluid is not just the cells’ culture medium. It also serves as a “special rubbish dump” for harmful substances if the eliminating organs such as the liver/gallbladder, kidneys, intestines, etc. are overloaded. Since water is also an excellent store of information, information from harmful substances is also stored here however. This area is not easily accessible to laboratory procedures. These stresses can usually be tested very quickly and painlessly at the biophysical level. The Bicom device offers a valuable tool in this respect. In many cases it is possible to discover which stresses may cause health problems in the patient (e.g. bacteria, viruses, electronic smog, dental materials, allergens, etc.).

The stresses identified are treated with the appropriate frequency patterns using the BICOM device

The body’s own regulatory system can be supported and aided to a considerable extent by BICOM bioresonance therapy

healthy cell communication restored

Communication between the cells can take place once again unimpeded. Harmful substances can be released and excreted.

Frequency Patterns are stores in small glass ampules shown below. The Ampules are used for Testing the existence of a Pathogen and can also be used to eliminate the pathogen. The frequency pattern can also be digitized and stored in a software program so many therapists use a combination of glass and digital ampules.

A Therapist treating a complex illness like Lyme & Co-infections will typically have 500 or over 1000 ampules to understand why a patient is unwell. IT’s also possible to treat the patient without knowing what pathogens are affecting them by using their blood as a treatement, reversing the frequencies of pathogens found by the BICOM machine.

 

Bionic 880 The Photon Therapy 

bionic 880

This German medical device has been getting great reviews as it appears to force extracellular bacteria out of the cells so that the immune system can find and eliminate them. This machine causes Herxeimer reactions so treatment intensity must be built up to prevent toxins overloading the elimination organs.

The Bionic 880 uses pulsating Infra Red (IR) light, which can activate and regulate many metabolic processes. Light or Photon energy plays an extremely important role  to release  substances such as enzymes, prostaglandin, lymphocytes and hormones to heal and repair the body’s damaged cells. 

The radiated Photons are first absorbed by the skin, which multiply in the body and then spread into the brain and branch to the Nervous System (NS) as well as the spinal cord and harmonize the production of hormones e.g. endorphins (pain hormones) serotonin (appetite and mood hormone), cortisol (stress hormone) etc.

Many German doctors have used the Photon Therapy for the last 10 years. It is very popular therapy in Germany. Bionic 880 is a medical device and certified by German Medical Authority.

Bionic 880 is effective method of therapy. It is gentle, fast acting and totally free of side effects. It   could be used on adults as well as children for various conditions. It enhances the quality of life.

The treatment

It is a painless procedure and lasts for 30 to 45 minutes. The radiation head is simply positioned onto different locations of the body (meridians, acupuncture points and effected areas) to distribute the photons, which enhances the production of hormones, prostaglandin and enzymes. The process of healing starts from the first treatment.

Medical use of Bionic 880

  • Wound healing (including plastic surgery)
  • Chronic Fatigue Syndrome, 96% success rate
  • Cancer and Cancer aftercare
  • Stress, Depression, Insomnia and headaches/migraines
  • Weight loss, 90% success rate (photon stimulates the body’s production of Serotonin, which suppresses the appetite
  • Treatment to give up smoking, 86% success rate (photon harmonizes production of endorphins)
  • Bacterial and viral infection – including Lyme disease, 96% success rate
  • Local pain complaints – migraines, arthritic and rheumatic pains, Sciatica, Lumbago, Herpes Zoster, skin disease (psoriasis, rosacea and eczema), severe chronic diseases, Multiple sclerosis, leaky gut, IBS and others
  • Neuralgia (pain caused by sensory nerve disorder) e.g. Trigeminal Neuralgia
  • It is a great energy booster and generator

BIONIC 880 treatment is now available in the UK (Soutwest & London)

Oxygen & Ozone Injections

Oxygen & Ozone infusions – These increase the level of oxygen in the blood to reduce inflammation, kill bacteria and improve the blood acid/alkalinity. This is available in Germany – We have yet to find a clinic to offer this in the UK.

IMG_8670
Oxygen IV Therapy
IMG_8671
Ozone Infusion Therapy

 

3d NLS Scanner

Non Linear System

A new fast digital scanning technology is available which can give a full body healthcheck in 10 minutes. Based upon German and Russian technology, the  3d-NLS Testing device compliments and validates the findings of the ampule based testing approach. The pictures produced by the scan (see below) are highly detailed and the data collected about your health far exceeds existing technology. This is a medical breakthrough that few know about in the west due to FDA protectionism of the US pharma industry, who see this technology as a threat to their symptom relief business model.  LINK

Hunter NLSFig 1. A typical NSL scan showing the Mitochondria under stress from Herpes (Mono) & Lyme disease.

 

RIFE Therapy

RIFE machine was not part of our therapy however it will be considered as a backup device to support Bioresonance.

A RIFE machine can take months and sometimes years to achieve benefits, so many people purchase their own machine and start treating themselves from home.

RIFE machines prices range from £300-£5000+ and the most advanced RIFE machines, which incorporate a plasma tube, cost between £2500-£5000. A  lower cost yet highly effective approach is to build or purchase a Doug Coil machine; the parts can be purchased for around £1-1,500. One of the lowest cost RIFE machines with a huge following is called the Spooky 2, however for Lyme disease treatment the Chinese manufacturer suggests a package including two devices and a plasma tube, which costs approx £2000.

RIFE machines typically cause a Herxeimer reaction so treatment must be given slowly to allow time for the body to detox the bio-toxins produced by the die-off of Lyme bacteria.

RIFE machines only offer therapy and have no diagnostic (test) capability. When purchased, the owner has to experiment to see if they obtain a  Herxeimer reaction or benefit from a reduction in symptoms after using the machine. The low cost Spooky 2 Rife machine offers a basic heart rate monitor biofeedback testing facility, however little has been written about how effective this testing method is.

RIFE machines cannot be used as a diagnostic device to help determine the right treatment, check treatment duration nor confirm that treatment is working. New RIFE machine owners are often at a loss to determine how to treat themselves and rely upon social media for support.

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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

Link to this

Lyme borreliosis service Public Health England

Health protection – guidance

Lyme borreliosis service

From:
Public Health England
First published:
1 July 2014
Part of:
Services, Health protection and Public health

Diagnostic and advisory service for Lyme borreliosis and related diseases.

Contents

  1. Diagnostic tests
  2. Clinical advice
  3. Lyme service user manual and request form
  4. Contact information
  5. See more like this

Diagnostic tests

The Lyme diagnostic service is provided by the rare and imported pathogens laboratory (RIPL) at Public Health England Porton.

Lyme is usually diagnosed by serology. RIPL uses a 2-tier testing methodology. The screening test is a C6 antigen based ELISA (combined IgG and IgM), followed by a confirmatory Western blot (separate IgG and IgM).

PCR is also available and may be useful in testing joint fluid and biopsies of rashes. It has poor sensitivity on CSF and antibody detection is the preferred first line test onCSF. PCR is not usually performed on blood as the duration of bacteraemia is short.

RIPL can also perform further tests for diseases related to Lyme. Please contact the laboratory to discuss.

Send a clinical sample through your local laboratory services provider with a completed RIPL Lyme request form (P2).

Clinical advice

RIPL clinical staff are available to discuss cases with medical professionals during working hours. See RIPL contact details below.

There’s no clinic at Public Health England Porton and we’re unable to see patients or give phone advice to members of the public.

Lyme service user manual and request form

Contact information

Rare and imported pathogens laboratory (RIPL)

Public Health England
Manor Farm Road
Porton Down
Wiltshire
SP4 0JG

Emailripl@phe.gov.uk

Telephone01980 612 348

DX addressDX 6930400, Salisbury 92 SP

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
Embedded Video Available: https://www.youtube.com/watch?v=jF_dnc0PUh0&list=UUfRAOQGVSwdRGEgw5UPKwOQ

Mouth Swab of Alzheimers disease patient showing numerous spirochetes and a typical flagellated borrelia bacteria

 

Spirochetes from mouth swab

https://www.youtube.com/watch?v=uiRXIzq699U

2014 12 22 Mouth Swab spirochetes HD 100 fps, 2500x HiSHRUB-Ultra HD Microscopy

<a href="/channel/UCPgb7Zkul4s6q3Qfw_GDKbg" class=" yt-uix-sessionlink     spf-link  g-hovercard" data-ytid="UCPgb7Zkul4s6q3Qfw_GDKbg" data-sessionlink="ei=3lO0VPnNBJG10QXWpIC4Dg" data-name="">Armin Koroknay</a>

Armin Koroknay

Published on 24 Dec 2014

Mouth swab of a patient with progressive M. Alzheimers disease showing numerous spirochetes and atypical flagellated borrelia bacteria. For the first time we could visualize very small spirochetes shorter than 3 micrometers an thinner than 1 micrometer, which move so rapidly, that normal video resolution an 25 frames per second cannot resolve their shape. If the observer sets the frmarate to slow motion in the bottom right menue of you tube video, all quickly moving flagellated abcteria can be seen much more clearly due to 100 fps high speed video recording. Uploading to you tube has reduced framerat to 60 fps, which is still enough to see very sharp images at 0.25x speed setting, representing 15 fps. thanks to the high frame rate rather sharp still images can be taken from the video, showing clearly the shape of 10 nm thick bacterial flagellae moving very rapidly.
One yellowish spirochete can be observed eating annother bacterial species. The video was taken with a very bright plasma LED illumination and a high sensitivity full frame CMOS chip high speed camera. To our knowledge these video represents the highest quality video of alzheimer causing spirochetes living in their natural environment, and behaving like in humans.
Magnification at 2500x, All rights reserved to A. Koroknay, Zürich, Switzerland.

Smartphones Becoming Tools for Diagnosing Malaria

 

January 07, 2015 1:27 PM

George Putic

Doctors fighting malaria – one of the deadliest diseases on the planet – may soon have a new affordable weapon in their smart phones. Researchers have found a way to use the phone’s camera to detect the microorganism in the patient’s blood that causes the disease.

According to the World Health Organization, almost 600,000 people died of malaria in 2013, making this mosquito-borne disease one of the deadliest in the world.

The saddest aspect of this calamity is that it affects mostly young children.

Early detection of the infection is important for successful treatment. But since the first symptoms resemble ordinary flu, a microbiologist must look at a drop of a patient’s blood under a microscope for a proper diagnosis.

Scientists in Britain have now developed a smart phone attachment called Xrapid, that turns the phone into a 200-power microscope, while the attached app – based on facial recognition software – quickly detects the parasitic protozoa in the blood smear.

Jean Viry-Babel is the CEO of IanXen, the company that developed the app. He says it is cheap and works on the spot.

“So we take a high-definition picture of a sample of blood. We separate the red blood cells from the rest – the white blood cells, the platelets – and we start looking at each of the red blood cells individually,” said Viry-Babel.

Viry-Babel says the app is affordable, easy to use and provides reliability of up to 98 percent. The only additional equipment required is an ordinary glass lab slide – called a “slate.”

“There’s only one button, which is called “Diagnose”. So you put it on the slate and you put it on the dried blood, and you press diagnose and it tells you yes or no,” he said.

Researchers say the field-testing of the device will begin in January and February in Tanzania, Benin and Indonesia – while commercial use is scheduled to start by the end of March.

They also plan to expand the versatility of the new device – teaching it to recognize other diseases, such as tuberculosis and Lyme Disease.

PCR Testing Overview – Sensitivity & Specificity for Whole blood (100%)

http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/87973

Useful For

  • Confirmation of active Lyme disease
  •  Monitoring Lyme disease treatment

PCR testing should be limited to patients with a positive, or at least an equivocal, serologic test for antibody to Borrelia burgdorferi.

Clinical Information

Lyme disease is a multisystem and multistage infection caused by 3 species of tick-borne spirochetes in the Borrelia burgdorferi sensu lato genogroup. These spirochetes includeBorrelia burgdorferi sensu stricto (North America and Western Europe), Borrelia afzelii(Central and Western Europe and Russia), and Borrelia garinii (Europe, Russia, and northern Asia). Endemic areas for Lyme disease in the United States correspond with the distribution of 2 tick species, Ixodes dammini (Northeastern and Upper Midwestern US) andIxodes pacificus (West Coast US). In Europe, Ixodes ricinus transmits the spirochete.

Lyme disease exhibits a variety of symptoms that may be confused with immune and inflammatory disorders. Inflammation around the tick bite causes skin lesions. Erythema chronicum migrans (ECM), a unique expanding skin lesion with central clearing resulting in a ring-like appearance, is the first stage of the disease. Any of the following clinical manifestations may be present in patients with Lyme disease: arthritis, neurological disease, cardiac disease, or skin lesions. Neurologic and cardiac symptoms may appear with stage 2 and arthritic symptoms with stage 3 of Lyme disease. In some cases, a definitive distinction between stages is not always seen. Further, secondary symptoms may occur even though the patient does not recall a tick bite or a rash.

Early antibiotic treatment of Lyme disease can resolve clinical symptoms and prevent progression of the disease to later stages. Treatment with penicillin, tetracycline, erythromycin, chloramphenicol, or ceftriaxone is considered appropriate therapy.

Serology is currently the diagnostic method of choice for Lyme disease. The Second National Conference on the Serologic Diagnosis of Lyme Disease (1994) recommended that laboratories use a 2-test approach for the serologic diagnosis of Lyme disease. Accordingly, specimens are first tested by the more sensitive EIA or enzyme-linked immunosorbent assay (ELISA). A Western blot (WB) assay is used to confirm positive Lyme EIA or ELISA results due to the presence of IgG- or IgM-class antibodies. WB identifies the specific proteins to which the patient’s antibodies bind. Although there are no proteins that specifically diagnose Borrelia burgdorferi infection, the number of proteins recognized in the WB assay is correlated with diagnosis.

Since serology may not be positive until 2 to 4 weeks after onset of ECM, direct detection of Borrelia burgdorferi-specific target DNA sequences using PCR is a promising adjunct to existing diagnostic tests. PCR has shown utility for detection of Borrelia burgdorferi DNA from skin biopsies of ECM lesions, and from synovial and cerebrospinal fluid in late-stage disease. Borrelia burgdorferi DNA can also, rarely, be detected from blood, but is not the test of choice from this source.

Interpretation

A positive result indicates the presence of DNA from Borrelia burgdorferi, the agent of Lyme disease.

A negative result indicates the absence of detectable DNA from Borrelia burgdorferi in the specimen. Due to the diagnostic sensitivity limitations of the PCR assay, a negative result does not preclude the presence of the organism or active Lyme disease.

Cautions

Serologic tests are recommended for diagnosis of Lyme disease. PCR may play an adjunctive role, but may not detectBorrelia burgdorferi DNA from blood in cases of active or chronic disease. A negative result does not rule-out Lyme disease, since inhibitory substances may be present in the specimen and the assay has limited diagnostic sensitivity when testing certain types of specimens. If clinical features of illness are highly indicative of Lyme neuroborreliosis, serologic testing on cerebrospinal fluid is warranted. Patients with active infection due to Borrelia afzelii or Borrelia gariniimay have positive results from this PCR test, which will be reported as atypical gene sequence and prompt additional testing. PCR test results should be used as an aid in diagnosis and not considered diagnostic by themselves. These results should be correlated with serologic and epidemiologic data and clinical presentation of the patient. Concurrent infections with multiple tick-borne pathogens, including Ehrlichia chaffeensis/Anaplasma phagocytophilum and Babesia microti have been reported in United States.

Supportive Data

The following validation data supports the use of this assay for clinical testing.

Accuracy/Diagnostic Sensitivity and Specificity:

Results from this real-time PCR assay on the LightCycler (LC PCR) directed to the plasminogen-binding protein (pbp) were compared to those generated using conventional PCR (target ospA gene) for synovial fluid (82), whole blood (22), and cerebrospinal fluid (CSF) (85). Using the conventional PCR as the gold standard, the diagnostic sensitivity and specificity for detection of Borrelia burgdorferi was as follows: synovial fluid (98.1%; 100%), whole blood (100%; 100%), and CSF (80%; 100%).

Supplemental Data:

In the original spiking studies, fresh and paraffin tissue, synovial fluid, CSF, and whole blood were spiked with Borreliaplasmid at an approximate concentration of 100 targets/mcL. At 100 targets/mcL, 100% of fresh and paraffin tissue, synovial fluid, and CSF were positive and 92% of whole blood samples were positive. In additional spiking studies, CSF (40), fresh tissue (60), and whole blood (40) negative samples were tested by spiking half with positive-control plasmid at the limit of detection (25-50 targets/mcL). The samples were extracted and tested in a blinded fashion; 97% of spiked CSF, 100% of spiked tissue, and 91% of spiked whole blood were positive and 100% of the nonspiked specimens were negative.

Analytical Sensitivity/Limit of Detection (LoD):

The lower limit of detection (LoD) is approximately 1,000 genomic targets/mcL whole blood.

Analytical Specificity:

No PCR signal was obtained from the extracts of 22 bacterial, viral, parasitic, and fungal isolates that can cause symptoms similar to Lyme disease including; Rickettsia rickettsii, Rickettsia typhi, Ehrlichia canis, Babesia microti, Plasmodium falciparum, Plasmodium vivax, Bartonella henselae, Bartonella quintana, Herpes simplex virus, andToxoplasma gondii.

Precision:

Inter-assay precision was 100% and intra-assay precision was 100%.

Reference Range:

Although the reference range is “Negative” for this assay, it may detect low-grade asymptomatic bacteremia from individuals exposed to Lyme-endemic areas. However, this assay is only to be used for patients with a clinical history and symptoms consistent with Lyme, and must be interpreted in the context of serologic tests, which are the gold standard for diagnosis of Lyme disease. This test is not used to screen asymptomatic patients.

Reportable Range:

This is a qualitative assay, and the results are reported as negative or positive for targeted Borrelia burgdorferi.

Clinical Reference

1. Keller TL, Halperin JJ, Whitman M: PCR detection of Borrelia burgdorferi DNA in cerebrospinal fluid of Lyme neuroborreliosis patients. Neurology 1992;42:32-42

2. Nocton JJ, Bloom BJ, Rutledge BJ, et al: Detection of Borrelia burgdorferi DNA by polymerase chain reaction in cerebrospinal fluid with Lyme neuroborreliosis. J Infect Dis 1996;174:623-627

3. Nocton JJ, Dressler F, Rutledge BJ, et al: Detection of Borrelia burgdorferi DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis. N Engl J Med 1994;330:229-234

4. Reed KD: Laboratory testing for Lyme disease: possibilities and practicalities. J Clin Microbiol 2002;40:319-324

5. CDC: Recommendation for test performance and interpretation from second national conference on serological diagnosis of lyme disease. MMWR Morb Mortal Wkly Rep 1996;45:481-484

6. Babady NE, Sloan LM, Vetter EA, et al: Percent positive rate of Lyme real-time polymerase chain reaction in blood, cerebrospinal fluid, synovial fluid, and tissue. Diagn Microbiol Infect Dis 2008;62(4):464-466

LTT test in doubt

Another Lyme Test Bites the Dust…Again

Notes from:
Dessau RB, Fingerle V, Gray J, Hunfeld KP, Jaulhac B, Kahl O, Kristoferitsch W, Stanek G, Strle F. Lymphocyte transformation test for diagnosis of Lyme borreliosis is currently not documented to be clinically useful. Clin Microbiol Infect. 2014 Feb 13.
This letter is a comment on a study using lymphocyte transformation test (LTT) for diagnosis of active Lyme borreliosis caused by Borrelia burgdorferi sensu lato. This LTT study reportsthe findings derived from a validation panel containing 120 blood donors seronegative for Borrelia, 40 seronegative patients with autoimmune diseases, 48 healthy seropositive controls and 94 seropositive patients with clinical signs of Lyme borreliosis. Furthermore, 1480 samples were investigated with both serology…and LTT.
The study has several major shortcomings. Concerning inclusion criteria, it was not clearly specified how the 94 patients with clinical Lyme borreliosis were defined. For example, it was not specified if the 6 patients with Bannwarth’s syndrome had spinal pleocytosis and a positive antibody index as required by the European case definitions for Lyme borreliosis, and it remains unclear how it was determined that the 34 patients with migratory arthromyalgias were suffering from Lyme Borreliosis. The 160 controls for LTT were preselected as seronegative for Borrelia-specific antibodies, and this could introduce a selection bias because serology and LTT tend to correlate. The specificity of LTT could therefore be overestimated. Concerning the selection criteria for the large group of 1480 patients, it is not clear what is meant by ”clinical diagnosis of suspected Lyme borreliosis”, of what appears to be a mixture of protean disorders.
The main point of the paper as taken from the title is the ability of LTT to detect active infection and effect of antibiotic treatment.
The possible development of a biomarker for active infection with B. burgdorferi s.l. would be of clinical value, as antibody detection cannot currently distinguish active infection from immunological memory due to past or asymptomatic infection. However, T-cell recognition may be inherently indiscriminate and thus problems with specificity may be hard to avoid.
The LTT study was part of a special issue entitled “Chronic or Late Lyme Neuroborreliosis: Present and Future” in the Open Neurology Journal (vol 6, 2012). However “Chronic Lyme borreliosis” is a problematic concept…. As an example it is stated that “over 250 peer-reviewed scientific articles demonstrate the causal association between Lyme/tick-borne disease and mental illness”. This is contradicted by the conclusion based on a substantial review of the literature (Final Report of the Lyme Disease Review Panel of the Infectious Diseases Society of America- IDSA, http://www.idsociety.org). In the IDSA review it was determined that the large volume of scientific articles concerning “chronic Lyme borreliosis” were uncontrolled case observations, which do not give convincing evidence of the persistence of viable organisms or effects of prolonged antibiotic treatment. In our opinion causal association should not be concluded from this type of study.
In conclusion the clinical value of the lymphocyte transformation test for diagnosis of active Lyme borreliosis was not supported the von Baehr et al study. Critical reading of the scientific literature is necessary with special attention to adequate standards of peer review in the increasing number of open access journals.

Subgrouping Chronic Fatigue Syndrome Patients by Genetic and Immune Profiling

 

Authors: Jose MontoyaIan ValenciaHolden MaeckerMichael MindrinosRosemary FernandezSTANFORD UNIV CA
Abstract:

http://www.stormingmedia.us/30/3006/A300685.html

 

We have a cohort of 200 untreated CFS cases and 400 matched controls that will undergo two novel tests (CyTOF-phosphoflow and HLA Typing through a breakthrough method discovered at Stanford) in order to help enhance our understanding of CFS and contribute to the elucidation of the pathogenesis of the disease. For CyTOF testing, we are exploring the immune responses by a novel flow cytometer that detects individual cell traits with time-of-flight mass spectrometry (CyTOF). We have completed the CyTOF phenotyping, phospho-flow panel, and gating schemes for testing. Also, the flow cytometry preparation robotics for CyTOF was optimized and antibodies were conjugated. The testing is ongoing and we hope to continue testing as permitted. For HLA typing testing, we are determining the human leukocyte antigens (HLA) types using a novel method that combines long-range polymerase chain reaction (PCR) with very high-throughput, multiplexed Illumina paired-end sequencing of genes permitting direct haplotyping. We have identified the DNA PAXgene tubes that will be used for testing. Also, we have identified the best possible conditions to amplify all the HLA gene of interest, namely for the class I genes HLA-A, -B, -C and for the class II genes: HLA DQA, DQB, DRB DPA and DPB. Lastly, we achieved the goal of robust and highly reproducible amplification of each In summary, for CyTOF testing we finalized the Phospho-CyTOF panel and have begun testing samples. To date we have tested 54 samples. These samples will continue to be tested for Year 2. The data is being received; no analysis has been done yet. The data will be analyzed by our statistical team. For HLA typing testing, all the DNA PAXgenes have been identified and separated into different batches. To date, two plates have been run and are currently being analyzed. To date we have tested 180 samples Year 1 has allowed us to ready the logistics and to begin CyTOF and HLA Typing testing.

Adrenal Gland Tests

The Adrenal Glands

The adrenal glands play a key role in the balance of the immune system because of their production of cortisol. Cortisol is a hormone that helps to “cool down” the immune system after it has accomplished its tasks in defending against harmful, invading microorganisms. This cool-down occurs in the following way.

One of the cytokines secreted by macrophages is known as IL-1B. Among its many functions, IL-1B sends messages to the brain’s hypothalamus, instructing it to release corticotrophin-releasing hormone (CRH). CRH then stimulates the pituitary gland to produce adrenocorticotropic hormone (ACTH). ACTH, in turn, instructs the adrenal glands to secrete cortisol to help regulate the inflammatory response that the macrophages are involved in. If we did not have this mechanism in place, we could die of overwhelming inflammation when we contracted an infection. 

However, there are two potential problems with regard to cortisol production. The first problem is that, due to stress, the adrenal glands go into overdrive, overproducing cortisol. This condition is called “adrenal stress.” This scenario can result in excessive immune system suppression due to too much cortisol being produced. This resulting suppression can help Lyme bacteria to escape detection by the immune system, thereby helping the bacteria to survive. 

The second problem occurs due to chronic stress, which can cause the adrenal glands to become overworked and exhausted. This condition is called “adrenal fatigue.” This scenario can result in inadequate cortisol production which, in turn, can lead to damage to healthy tissues due to uncontrolled inflammation. In this case, it may require taking physiologic doses of cortisol by mouth to help the adrenals until they can recover. 

For both of these reasons, it is important that adrenal function be assessed in most patients with chronic Lyme disease. When adrenal function is impaired, adrenal support may be necessary. This support can be achieved using certain herbal remedies, as well as other natural supplements. The key items that are clinically useful include vitamin C, vitamin B5 (pantothenic acid), magnesium, eleutherococcus (Siberian ginseng), schisandra seed, rhodiola, green tea, grape seed and skin, licorice, and others. Again, when documented by laboratory testing, it may also be necessary to use temporary low dose oral natural The Lyme Disease Solution 1 4 8 cortisol (using adrenal replacement doses, not immunosuppressive doses) until the exhausted adrenal glands can recover enough to do their own job. Another key component of adrenal support is adequate uninterrupted sleep. (I recommend ideally seven to nine hours per night with at least five of those hours uninterrupted.) I will discuss adrenal and other endocrine gland issues in more detail in chapter 7 and the major problem of sleep deficiency in chapter 8. 

Winchester Health

The Team

winchester-travel-health-team

The Winchester Travel Health clinic is situated in the heart of the historic city of Winchester, close to the High Street.

Winchester Travel Health
1 Stockbridge Road, Winchester
Hampshire, SO22 6RN
Tel: 01962 856646

Dr Matthew Dryden MA, MBBS, MSc, MD, FRCPath, FRGS

Matthew Dryden is a consultant specialising in microbiology and communicable disease and has been based at the Royal Hampshire County Hospital in Winchester since 1991. He is the Medical Director of Winchester Travel Health and Wessex Diagnostics. He has a long-term interest in travel and tropical medicine.

In the past he has been an expedition doctor on expeditions in varied parts of the world including Africa and Central America. He has worked as a doctor in Sudan and Australia. He is a Fellow of the Royal Geographical Society and a founder member of its Medical Cell. He has published extensively on travel medicine, microbiology and infectious disease.

Joanna Lowry RN, DTN

The clinic is managed on a daily basis by Joanna Lowry. She is an experienced Travel Nurse Specialist who has travelled extensively throughout Northern Africa, South East Asia, Australasia and Europe. She has a Diploma in Tropical Nursing from the London School of Hygiene and Tropical Medicine and has worked overseas for The Travel Doctor (TMVC) in New Zealand.

Joanna is passionate about travel medicine education and regularly teaches other healthcare professionals intravel health and immunisation.

Poppy Spens RGN, DTN

Poppy Spens spent 30 years working as a health visitor and practice nurse. She obtained a Diploma in Tropical Nursing in 2005 and has worked in South Sudan since 2006 setting up Primary Care facilities. Her passion has been to see improvements in healthcare in South Sudan, a country with the highest maternal mortality and lowest uptake of child immunisations in the world.

She enjoys helping people travelling abroad, in particular fellow foreign aid workers. Poppy joined the team as Deputy Clinic Manager in September 2011 but has worked for Winchester Travel Health for a number of years.

Susie Parry

Susie Parry has worked as a travel health nurse at Winchester Travel Health since 2009. Susie is a qualified nurse and midwife and has completed the short course in Tropical Medicine at the London School of Hygiene and Tropical Medicine. Susie worked for nine years for four British Airways Travel Clinics and worked as a midwife in Hong Kong. She loves to travel and has extensive travel experiences.

Kate Jones

Kate Jones qualified as a registered nurse in 1995 at University College Hospital London. Kate spent the majority of her nursing career working in Melbourne Australia. Kate began working in travel health in 2011, initially at The Travel Doctor in Melbourne and then at The Fleet Street Clinic in London.

This year Kate completed the Diploma in Tropical Nursing at The London School of Hygiene and Tropical Medicine. Kate also had experience working for an Air Ambulance company, arranging medical repatriation and liaising with foreign medical staff and sometimes escorting patients back to England.

Come and visit us, or call 01962 856646 or email us on info@winchestertravelhealth.co.uk.

Low secretary iga

July 14, 2013 by Dr. David Jockers
Filed under Natural Healing

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Sun. July 14, 2013 by Dr. David Jockers
(NaturalHealth365) Are you interested in naturally eliminating digestive problems? If so, then let’s look at ways to boost your immune system by balancing secretory IgA – which protects you from infections.

Every mucosal membrane surface such as the eyes, nose, throat and intestinal system represent a large portal of entry for pathogenic bacteria, viruses and yeasts. The body’s immune system utilizes a combination attack through innate mechanisms and acquired adaptations.

The innate immune response includes mucus formation, lactoferrin, lysozymes and cytokinetic inflammatory activity. The acquired system produces anti-bodies with the primary mucosal antibody being secretory IgA.

This antibody response is one of the most critical component to protecting the body against parasitic dominance.

Secretory IgA is the secreted form of an antibody in the blood called IgA. IgA is produced in the blood, taken into the gut, secreted across the mucosal lining into that mucous layer that is the surface lining of our digestive tract. It is the mucosal immune barrier or first line immune defense.

SIgA lies within the mucosal membrane of the entire digestive tract as well as our lungs, sinuses, eyes, urethra and vagina. It plays a significant role in neutralizing various pathogens like viruses, Candida, bacteria, protozoa and hemoliths.

The health problems associated with low SIgA levels

When SIgA is elevated it indicates an acute immune reaction within the gut. This could indicate an acute bacterial or parasitic infection. When s IgA is low it indicates an overall deficiency of this immune chemical. When this is low on a stool test the individual will also express food allergens, have elevated Candida yeast and have dysbiosis or abnormal bacterial balance in their gut.

Individuals with chronic gut problems, IBS, Candida, Crohn’s disease, ulcerative colitis and autism typically have low SIgA. This is a sign of chronic stress in the body that has drained the immune system and the adrenals. Chronic infections, environmental toxins, poor lifestyle could all be the major causes behind this.

How to naturally balance your SIgA levels

The first step to increase (or decrease) SIgA naturally is to use an anti-inflammatory diet. The most common food allergens include all grains, pasteurized dairy, soy products, eggs, nuts and high-sugar fruits. Utilizing intermittent fasting strategies and going 18-20 hours of fasting with only clean water, herbal teas, organic broths and light fermented beverages each day is highly recommended.

An advanced bone broth fast with organic, grass-fed beef bones and loads of garlic and onions can be extremely effective at helping the gut to reseal and boost SIgA levels. This should be a 10-14 day fast if the levels are severely low and 3-7 day if they are more moderate.

It is important to provide the gut and the immune system with the key nutrients they need such as vitamin C, zinc, selenium, glutamine, choline, glycine, glutathione and essential fatty acids among other things. A whole food based multi-vitamin without any filling agents such as magnesium stearate is very helpful.

Using non-denatured whey protein from grass-fed cows will boost glutamine and glutathione levels and is easily absorbed into the body. It is highly recommended if the individual can tolerate it. If they have allergenic reactions to whey than use a hypoallergenic protein powder made up of sprouted hemp and pea protein.

Great ways to naturally raise your SIgA levels

There are a few things that boost Secretory IgA levels naturally. Colostrum is an immunoglobulin blast that is secreted from mom’s breast in the early stages of breast feeding. Colostrum is loaded with antibodies that stimulate SIgA levels. Fermented dairy from 100% grass-fed cows is loaded with acidophilus, bacillus and saccharomyces boulardii species of probiotics that all help to stimulate S IgA levels.

Beta Glucans are polysaccharide fibers that are considered biological response modifiers because of their ability to activate the immune system. They help boost the production of SIgA. These are found in the highest concentration in different types of mushrooms such as reishi, shiitake and maitake. Cayenne pepper also has the ability to stimulate B-lymphocytes into manufacturing more SIgA.

How can I naturally lower SIgA?

Elevated SIgA is a sign of an acute infection and the immune system is running on high. Using an anti-inflammatory diet that includes the bone broth fast described above is especially helpful. One can also take systemic enzymes and high dose probiotics to help modulate the immune system. Essential fats from a high quality fish oil and grass-fed meat products are extremely critical as well.

Fermented vegetables load the body up with enzymes, probiotics, organic acids and highly bioavailable nutrients that raise SIgA levels. Other herbs such as turmeric, basil, oregano, garlic and thyme are especially helpful. Fermented herbal botanicals, apple cider vinegar, coconut kefir and kombucha should be used as well.

How long does it take to boost SIgA?

Secretory IgA is generally an indication of the immune system in the gut which is our first line immune defense and it is called the mucosal barrier. When the gut is damaged and leaky it causes chronic stress and poor healing. The faster the chronic stressors are removed the faster the individual will get well. The average period is a good four to six month process for complete healing to take place.

In some cases, it may even take years to finally get SIgA levels up to normal.

The variable in all accounts is the individuals’ unique healing process. Many individuals have a severe leaky gut and are loaded with Candida, viral infections, worms and other parasites and also have heavy metals and industrial toxins as well as physical stressors such as poor posture and breathing habits. These individuals are challenging because they must correct each of these imbalances. The longer each of these challenges persists it will contribute to the formation of other stressors and keep the adrenals weak and tired.

The faster we can get the gut healed and restored and use a ketogenic style, anti-inflammatory diet that is loaded with fermented foods the faster the body will be able to detoxify and restore healthy function to the gut, liver and adrenals.

Please note: Intermittent water fasting is one of the best strategies for boosting our healing potential.

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About the author: Dr. David Jockers owns and operates Exodus Health Center in Kennesaw, Ga. He is a Maximized Living doctor. His expertise is in weight loss, customized nutrition & exercise, & structural corrective chiropractic care. For more information – visit: DrJockers.com. Dr. Jockers is also available for long distance phone consultations to help you beat disease and reach your health goals.

References:
https://www.metametrix.com/files/learning-center/articles/Secretory-IgA.pdf
http://www.yeastinfection.org/how-to-increase-your-siga-levels/
http://en.wikipedia.org/wiki/Immunoglobulin_A

– See more at: http://www.naturalhealth365.com/natural_healing/digestive_problems.html#sthash.wDklJfy2.dpuf

Testing

Suggested wording that should be given to patients in Us having lyme tests to make sure negative tests should be taken together with symptoms.

YOUR HEALTH CARE PROVIDER HAS ORDERED A LABORATORY TEST FOR THE PRESENCE OF LYME DISEASE FOR YOU. CURRENT LABORATORY TESTING FOR LYME DISEASE CAN BE PROBLEMATIC AND STANDARD LABORATORY TESTS OFTEN RESULT IN FALSE NEGATIVE, AND IF DONE TOO EARLY, YOU MAY NOT HAVE PRODUCED ENOUGH ANTIBODIES TO BE CONSIDERED POSITIVE BECAUSE YOUR IMMUNE RESPONSE REQUIRES TIME TO DEVELOP ANTIBODIES. IF YOU ARE TESTED FOR LYME DISEASE, AND THE RESULTS ARE NEGATIVE, THIS DOES NOT NECESSARILY MEAN YOU DO NOT HAVE LYME DISEASE. IF YOU CONTINUE TO EXPERIENCE SYMPTOMS, YOU SHOULD CONTACT YOUR HEALTH CARE PROVIDER AND INQUIRE ABOUT THE APPROPRIATENESS OF RETESTING OR ADDITIONAL TREATMENT.”

Sincerely,
[Your name]

New Lyme Culture Test Failed CDC Analysis

Eighty percent of the patient samples used to demonstrate anovel method of culturing Lyme disease spirochetes from serum contained gene sequences identical to those found in laboratory strains used to develop the test and were likely false positives, Centers for Disease Control and Prevention (CDC) researchers report in an article published online August 14 in the Journal of Clinical Microbiology.

“Taken together, our data and those of Sapi et al. indicate that laboratory contamination was the probable source of the borrelial DNA found in the patient samples. The vast majority of patient pyrG sequences (41/51) are indistinguishable from laboratory strains used by the investigators. The clinical relevance of the other pyrG sequences (10/51) is unclear; these findings also may be consistent with laboratory contamination,” the authors write.

The CDC researchers warned that independent verification is critical for novel findings that contradict a large body of previous work and for tests that might lead to unnecessary antibiotic treatment.

“We caution clinicians and patients to wait for independent verification by scientifically sound methods before using this culture service for diagnostic purposes,” they write.

The CDC research team, led by Barbara J.B. Johnson, PhD, from the Division of Vector-Borne Disease in Fort Collins, Colorado, were trying to understand why the majority of the spirochetes described in an article published earlier this year in the International Journal of Medical Sciences were related by pyrG gene sequences to species of Borrelia that had not previously been detected in North American patients other than those with a history of travel to Europe or Asia. ThepyrG gene encodes CTP synthase, which interconverts UTP and CTP in pyrimidine biosynthesis.

The authors of the previous article had used 2 B burgdorferi reference strains (B31 and 297) and 2 Eurasian reference strains ( Borrelia afzelii and Borrelia garinii) for method development and testing of culture medium. To rule out the possibility that the sequence similarities were a result of laboratory contamination, the CDC researchers compared the pyrG sequences reported by Sapi et al. for 51 patient isolates to sequences for B burgdorferi B31 and 297 for B afzelii, and for B garinii, using the same primers used in the original study. Previously, pyrG gene sequence had been reported only for B burgdorferi strain B31, so Dr. Johnson’s team sequenced the other 3 laboratory strains and deposited them in GenBank.

The analysis showed that 53% (27/51) of the patient-related sequences reported in the previous article were from samples infected by B garinii and 20 the 27 clones were identical to the B garinii reference strain. The other 7 B garinii sequences had either a single nucleotide polymorphism (n = 5), 2 differences (n = 1), or 3 differences (n = 1) from the laboratory strain.

Twenty-one (41%) of the 51 patients had nucleotide sequences related to B burgdorferi, and in 20 of these patients, the sequences matched the laboratory strain B31 exactly.

Two of the 51 patients had sequences closely related to B afzelii, which is not found in the United States.

“Eighty percent (41/51) of the reported patient-derived pyrG sequences are identical to one of the laboratory strains and an additional 12% (6/51) differ by only a single nucleotide across a 603bp region of the pyrG gene. Thus, false positivity due to laboratory contamination of patient samples cannot be ruled out and further validation of the proposed novel culture method is required,” the authors conclude.

They also note that the patient cultures reported by Sapi et al. had been subjected to nested polymerase chain reaction, “a contamination-prone method that is unnecessary when bacteria are numerous enough to be seen by microscopy.” The authors also point out that control samples from healthy blood donors had not been tested by polymerase chain reaction but had been classified as negative based only on dark field microscopy and antibody staining.

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

Candida Test

Please note that the Candida Self Assessment will not give you a diagnosis of Candida overgrowth and that Candida is not the sole cause of the factors mentioned in the assessment. The self assessment is simply a tool to use to evaluate whether or not Candida may play a role in your health challenges. The Candida Self Assessment can be used to help you determine if you should consider seeking assistance from a health professional to begin the process of balancing the yeasts in your body.

To take the Candida Self Assessement, score 1 point for every “YES” answer to each of the following questions. The scoring profile follows the assessment.

Candida Self Assessment

Do/did/were you now or during the past three years:

  1. Told you have a heavy metal toxicity?
  2. Belch frequently?
  3. Crave alcohol?
  4. Crave breads, pastas, crackers, etc.?
  5. Drink more than 16 ounces of beer or wine per week?
  6. Drink more than 6 ounces of distilled alcohol (vodka, rum, etc.) per week?
  7. Feel depressed?
  8. Feel fatigued frequently?
  9. Feel you have “brain fog?”
  10. Have a coated tongue?
  11. Have abdominal bloating or gas?
  12. Have acne?
  13. Have white, flaky patches on the skin?
  14. Have ADHD/ADD or lack of impulse control?
  15. Have amalgam fillings?
  16. Have an inability to concentrate?
  17. Have an inability to lose weight or an inability to gain weight?
  18. Have asthma or hay fever?
  19. Have athlete’s foot?
  20. Have dandruff?
  21. Have diabetes or hypoglycemia?
  22. Have discomfort during intercourse?
  23. Have dizziness?
  24. Have dry mouth?
  25. Have ear pain?
  26. Have elevated liver enzymes?
  27. Have endometriosis or infertility?
  28. Have fluid in the ear or frequent ear or sinus infections?
  29. Have food allergies?
  30. Have frequent bad breath?
  31. Have frequent boils?
  32. Have frequent colds or flus?
  33. Have frequent headaches?
  34. Have frequent heartburn?
  35. Have frequent hives?
  36. Have frequent hoarseness and/or postnasal drip?
  37. Have frequent insomnia?
  38. Have frequent irritability?
  39. Have frequent mood swings?
  40. Have frequent nasal congestion or stuffiness, especially on rainy days?
  41. Have frequent numbness or tingling?
  42. Have frequent rashes?
  43. Have frequent sore throat?
  44. Have frequent urinary tract infections?
  45. Have frequent vaginal yeast infections?
  46. Have frequent water retention?
  47. Have hemorrhoids?
  48. Have impotence?
  49. Have inflamed prostate?
  50. Have irritation in folds of skin or in areas where joints bend?
  51. Have irritation near areas rubbed by waistband, underwear elastic, bra, etc.?
  52. Have itchy skin?
  53. Have jock itch?
  54. Have loss of sexual desire?
  55. Have frequent mouth sores or blisters?
  56. Have mucous in stools?
  57. Have muscle aches?
  58. Have occasional or frequent constipation?
  59. Have occasional or frequent diarrhea?
  60. Have pain or swelling in your joints?
  61. Have persistent anal itching?
  62. Have persistent vaginal itching or burning?
  63. Have poor memory sometimes?
  64. Have premenstrual tension?
  65. Have psoriasis or eczema?
  66. Have rapid mood swings?
  67. Have ringworm or other fungal skin infections?
  68. Have thrush (oral yeast infection)?
  69. Have toe or fingernail fungus?
  70. Have urinary urge or frequency?
  71. Sometimes have abdominal pain?
  72. Take an antacid or prescription such as Nexxium, Prevavid, Protonix, Prilosec, etc.?
  73. Take antibiotics in the past five years? (Score 1 point for each time one was prescribed or refilled)
  74. Take Prednisone or other corticosteroids? (Score 1 point for every time one was prescribed or refilled)
  75. Taken oral birth control for more than two months in the past five years?

Candida Self Assessment Scoring:

  • 0-10 Points: Congratulations! The likelihood of Candida affecting your health is very low. Keep up the great work!
  • 11-25 Points: The likelihood of Candida being a factor that is affecting your health is likely, but the effects are probably minimal at this point.. You may benefit from making lifestyle changes to reduce the amount of Candida in your system.
  • 26-55 Points: Candida is probably an issue that is negatively affecting your health. Taking action to reduce Candida will most likely benefit your health in multiple ways.
  • 56-75 Points: It is highly likely that Candida is negatively affecting your health in multiple ways. Taking action now to reduce Candida will most likely improve your health physically, mentally and emotionally.

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>