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Lyme Disease Info


Lyme disease, a multisystemic illnesscaused by the spirochete Borrelia burgdorferi (Bb), is the most common vector-borne illness in the US. Approximately 20,000 new cases are reported to the CDC each year and the CDC acknowledges that 90% of cases go unreported.[Adler, J. (2004). Lyme: battles with illness, emotions, insurance. (NJ) Herald News.] Infected black-legged ticks transmit Bb to humans via a bite. These ticks are quite small and easily overlooked; most patients do not recall being bitten prior to becoming ill. Lyme disease has both early and late disease manifestations. Patients may exhibit one or both of these stages; many patients initially present with late Lyme disease. Any organ system can be involved, but Bb commonly strikes skin, joint, heart and nervous tissue, including the brain.

Early Lyme disease

disease begins 3-30 days after a tick bite and is readily identified by an erythema migrans (EM) rash. EMs vary in appearance. The most common rash is a homogeneously colored oval lesion. The classic "bull's eye" accounts for less than 20% of all EM cases; [Smith R et al, Ann Intern Med. 2002;136:421-428, Tibbles C, JAMA 2007; 297:2617-27.] 30% of patients never have a rash.[MMWR 56(23); 573-576] Flu-like symptoms such as fever, fatigue, headache, myalgias, arthralgias and neck stiffness may accompany an EM or be the only evidence of early Lyme disease.[Steere A et al, Am J Med. 2003; 114(1):58-62]

Late Lyme disease

develops weeks - years later and is the result of disseminated infection. Early disseminated Lyme disease may cause multiple EM rashes, Bell's palsy or other cranial neuropathies, meningitis, meningoradiculitis, carditis, lymphadenopathy and arthralgia; constitutional symptoms may be present. In endemic areas, Lyme disease is implicated in 50% of all cases of Bell's palsy in children.[Cook SP et al, Am J Otolaryngol 1997; 18(5):320-3]

International Lyme and Associated Diseases Society
A professional medical and Research organization

P.O. Box 341461
Bethesda, MD 20827-1461
Information from this article supplied by ILADS

In the US, arthritis and disorders of the nervous system are seen in late disseminated Lyme disease. Arthritis can affect any joint; knees are the most common site. Up to 60% of untreated patients will experience arthritis.

Neurologic conditions include peripheral sensory neuropathies, motor neuropathies, cranial neuropathies, autonomic dysfunction, movement disorders, neuropsychiatric illnesses and encephalopathy. Neuroborreliosis is the term used when Lyme infects the brain. 15 – 40% of Lyme disease patients have neurologic disorders due to the infection. [Caliendo et al, Psychosomatics 1995; 36:69-74] Late disease can be severe with marked morbidity and poor treatment outcomes.


The symptoms of Lyme disease are widespread and variable; relapsing/remitting patterns are common. The validity of individual symptoms has been documented in numerous reports and studies on Lyme disease.

Frequently reported symptoms include:

  • Extreme fatigue, often interfering with activities
  • Headaches of all types
  • Recurrent fevers, chills, night sweats
  • Myalgias and arthralgias; either may be migratory
  • Muscle fasciculations and weakness
  • Paresthesias and neuropathic pain syndromes
  • Sleep disturbances
  • Cranial nerve dysfunction
  • Neuropsychiatric problems – irritability, depression, anxiety, panic attacks, new onset ADHD, mood swings similar to bipolar disease, rage attacks, OCD
  • Cognitive losses: memory impairment, difficulty multi-tasking, slowed mental processing, speech and language problems, poor concentration, loss of math skills, impaired visual/spatial processing
  • Children may have behavioral changes, declining school performance, headache, fatigue,forgetfulness, complex partial seizures, depression and be misdiagnosed with primary ADHD.

Although Lyme disease symptoms overlap with symptoms of other conditions such as fibromyalgia, chronic fatigue syndrome, MS, early ALS, RA, lupus and psychiatric disorders, patients with Lyme disease often have symptom patterns which are atypical for these other illnesses. Making sense of the multitude of reported symptoms can be challenging; but bear in mind that symptoms which appear unrelated may be linked via an underlying autonomic neuropathy or encephalopathy.


Ticks also carry Babesia, Anaplasma, Ehrlichia, Bartonella, Mycoplasma and other pathogens. The presence of these organisms complicates the diagnosis, testing and treatment of Lyme disease patients. In animal models, co-infections alter the immune response, pathogen load and disease severity.[Thomas V. Infect. Immun. 2001;69:3359–3371.] In humans, coinfections
increase morbidity and delay recove

Physical Exam in Lyme Disease

Lyme disease patients may have exam findings when carefully assessed but findings may be few or absent in some cases. In addition to a general exam, detailed neurologic, dermatologic and rheumatologic exams should be performed.

Serologic Testing in Lyme DiseaseBorrelia burgdorferi is very difficult to culture, thus serologic tests are used to detect the presence of antibodies to Bb. In 1995 the CDC, in an move to standardize testing procedures and Western blot interpretations, published guidelines for laboratory testing in Lyme disease.[MMWR 1995; 44:590-1] The CDC recommended a two-tier testing algorithm.

Step 1 is an ELISA or IFA; positive or equivocal results advance to step 2, IgM and IgG Western blotting. Samples negative in step 1 are not tested further. The purpose of standardization was to establish parameters for laboratory confirmation of Lyme disease surveillance cases, not clinical diagnosis.[Mead P. CT Dept of Public Health Hearing Jan 29, 2004]

Western Blot Testing:

9 cross reactive for borrelia
12 specific for Bb
18 unknown
20 cross reactive for borrelia
21 unknown
22 specific for Bb probably the 23/25 band
23/25 OspC specific for Bb
28 unknown
30 unknown, probably Osp common in Europe
31 OspA specific for Bb
34 OspB specific for Bb
25 specific for Bb
37 specific for Bb
38 cross reactive for Bb
39 major protein of Bb flagellin Bb specific
41 flagellin protein of all spirochetes; one of the first to appear, Bb specific
45 cross reactive for all borrelia
50 cross reactive for all borrelia
55 cross reactive for all borrelia
57 cross reactive for all borrelia
58 unknown but may be heat shock Bb protein
60 cross reactive for all borrelia
66 cross reactive for all borrelia
83 specific antigen for the lyme bacterium, probably a cytoplasmic membrane
93 unknown, probably the same protein as 83, just measure incorrectly New Testing For Lyme Disease:
Lyme Culture Test done by Advanced Research Labratories. At present, this is a cash only test not covered under any insurance or medicare call our clinic (714) 667-5222 for further details

Two-tier testing doesn't work.

The step 1 tests are insufficiently sensitive to be used as "screening" tests. [Trevejo R, JID 1999; 179:931–8.] Western blots, increase specificity but, following a step 1 test, further decrease overall sensitivity.

The bands included in the Western blot interpretation schemes were chosen on a statistical, rather than a clinical, basis.[Dressler F. JID 1993; 167:392-400.] Recently, the C6 peptide ELISA alone was proposed as an alternative to the two-tier approach. Unfortunately, the C6 ELISA also lacks adequate sensitivity for clinical use.[Bacon R. J Infect Dis 2003; 187:1187- 99.]

Lyme disease, like many other diseases, is a clinical diagnosis; with testing playing a supportive role.

Observations and opinions on the CDC/NIH Webinar on Lyme Disease Testing

By Tom Grier
Nov. 28, 2012

IgM = Early antibodies produced in new infections. IgM can rise and fall as infection wax and wane.
IgG = Late antibody that is more specific to the infection but take 4-6 weeks to be produced.

Awhile back I viewed the taxpayer paid CDC webinar October 1st, 2012 on Lyme disease testing and future research directions. I was quite disappointed at both the direction of research and the analysis of current testing.

In the beginning Dr. Joseph Breen of the NIH encouragingly stated that because Lyme serology tests are indirect tests, that they cannot be used to determine cure, and that they are striving to find a way to determine cure after antibiotics.

Breen also noted that antibodies in Lyme patients only appear after the optimum time to treat the patient with antibiotics has already passed.

Dr. Breen then went on to say that Lyme disease is difficult to accurately stage the disease into categories such as Skin manifestations as stage one, Neurological manifestations as stage two or Arthritis as stage three.

Yet later on, these three stages are used to access the accuracy of Lyme serology testing, and to group patients into clinical studies.

A mission statement if there is one, seems to be to determine if Lyme persists after antibiotic treatment. Yet none of their proposals truly attempts in earnest to determine persistent infection post Rx.

There is absolutely no mention of pathology, culturing or staining as part of that quest, or as methods to measure serology testing accuracy.

The two animal models mentioned as research initiatives that were done in mice and Non-Human Primates, I believe are not future studies but the studies already done by Embers and Berthold. (Which have been heavily criticized by the very institutions that are now holding them up as research models for future research?)

The future direction the CDC and NIH seem to be taking with Lyme disease is testing to create Four Research Initiatives that will last 2 years.

Grants are approximately $150,000/year and grants that are extended will be increased to perhaps $250,000/year. Unfortunately three of the four initiatives support even more indirect testing than current Lyme serology testing.

Although Dr. Breen says culturing is the gold standard for detection and identification of active Lyme disease he goes on to say culturing is slow, expensive, and not a viable option for diagnosis. Culturing does not appear to have any future with tax payer paid Lyme disease studies.

The “New Direction” of Lyme testing is heavily based on Lymphokine and cytokine responses by immune cells and is a very indirect analysis of whether a patient has been exposed to Lyme disease.

Since several labs are already doing lymphokine response testing, one wonders if there will be patent infringement on current patents as these taxpayer paid initiatives proceed.

Will the researchers who get these grants, soon apply for new patents involving lymphokine response Lyme testing?

One thing is for certain, if these tests are accepted as proof of “cure” without offering any supporting pathology, then Lyme patients can expect to be denied treatment by health providers with tests that are even less direct than antibody serology. Maybe that is a goal of this new direction Lyme research?

Only one of the four initiatives ever mentions the new emerging species of Borrelia that also cause Lyme disease, and no mention of STARI in the USA.

The researcher claiming to look at multi-species detection is Dr. Alan Barbour. The grant application description is simply: “Informative Immunodiagnostics of Lyme Disease” which to me also sounds like vague indirect immune response analysis. (Currently of the 10 species that cause Lyme disease world-wide, only Borrelia burgdorferi B-31 strain is used in serology testing, Pasteur Institute has repeatedly pointed out the short sightedness of accepting this as a world-wide standard of testing, and shown its inaccuracies when compared to tests using local wild strain isolates.)

The most disturbing aspect of the webinar was the way they analyzed IgM Western Blots to show a 27% false positive rate and why it is not a good test.

Dr. Joseph Breen begins by saying that in the first 30 days of infection that only the IgM Western Blot is effective and the EIA/ELISA tests are not yet sensitive to detect adequate antibody response. After 30 days EIA and IgG Western Blots can be used.
•None of the patient analysis addressed any previous studies that showed patients that have been seronegative blood, but are either culture positive or PCR positive.
• Nor did Breen address antibody-antigen complexes that are not detectible by serology.
•Breen also did not address that all ELISA tests used by the CDC are whole cell preparations using laboratory strain B-31 and not one single new genospecies of Lyme like Borrellia bissetti or Borellia spielmani, B. andersoni, B. Americana or others.
•The CDC tests for Americans are not prepared with whole cell isolates of any of the European strains. So we judge the inaccuracy of IgM Western Blots with ELISA tests with built in flaws. This accounts for almost one half of the 27 % false positives by IgM Western Blots that is claimed by the CDC.

ELISA tests have two built in flaws in 2-tiered testing:
• First, they cannot fully detect the antibody responses from other Lyme geno-species.
• Secondly, using the ELISA test as a screening test and excepting it as infallible without testing its limitations or addressing previous real-world proof, that it is a poor screening test means the CDC accepts the ELISA results over bands specific to Borrelia burgdorferi on Western Blots.

Since both patients and ticks migrate and travel, it seems likely that a patient returning from Norway, the UK, Germany, France, Romania, Switzerland, or a dozen other countries with Lyme-like disease would likely test negative by CDC two-tiered testing using B-31 based tests.

By protocol these travelers would be told that they cannot be treated. So are these patients’ false negatives? The CDC never discussed that scenario, nor did they address Relapsing Fever testing.

Here is where bad science from our own CDC and NIH really becomes a problem to the health and welfare of USA Lyme patients: According to the CDC the IgM Western Blots are 27 % False Positives:
• First, general problems of Western Blots exist in three main areas:
a) Faint bands are reported as positive
b) Alignment of blotting strips could mean some labs report incorrect bands
c) Complexity of interpreting Western Blots allows doctors to influence the tests’ results.

And now for the bad science:
1) Dr. Breen stated that with all Lyme serology tests, only the IgM Western Blot is useful in the first 30 days. With this analysis, if a patient has symptoms beyond 30 days and a positive IgM Western Blot, then the positive Western Blot has to be wrong because IgM antibodies should decline.

This is bad science #1 because human interpretation has interfered with scientific observation.

The analysis is based on an incorrect assumption that the IgM test is not useful after 30 days, and that the ELISA test is (in their words) 100% accurate in Chronic Lyme cases.
• The 100% figure is produced by eliminating all positive Western Blots post 30 days as false positives.
• The numerous cases of culture-positive cases of Lyme that are seronegative by ELISA are never addressed.

2) Having a negative ELISA test but a positive IgM Western Blot, then the Western Blot is false positive.
This is also bad science #2 for many reasons; the most important is that the ELISA test is notoriously inaccurate.

When institutions other than the CDC test the ELISA tests in real world conditions, over 500 labs were only 50 % accurate (Lori Bakken College of Pathology and Lab Testing).

I can site many more studies but to negate and ignore a sick and symptomatic patient and ignore a positive IgM Western Blot positive test on the basis of a predesigned standards based on bad science, is too much like the old witch trials where if the witch drowned she was not a witch.

You can’t advance science and testing if you design into your testing paradigm flaws that allow your tests to excel when they are failing.

Using a negative ELISA test to prove the Western Blot is false is bad science and just plain bad study design.

3) Incorrect Interpretation of Bands is another source of false IgM Western Blots:
• Borrelia laminin binding protein Bmp-A 39 kDa is a surface protein specific to Lyme. How does one reconcile a bacterial protein’s presence as negligible? That’s like catching a hailstone and being told it’s not hailing because national weather radar didn’t show any hail. Radar is less accurate than a hailstone in your hand.
• The IgM Western Blot 39kDa band is more decisive than an ELISA test using a high cut-off point of 512 or even greater. (Some major labs still use 1024 titers as a cutoff.)

A significant portion of the false positive rate for IgM Western Blot is due to incorrect bands.

No one at the CDC has yet addressed the Dearborn, MI or Dressler criteria of Western Blot reporting.

It is wrongly assumed that if you report bands 31 and 34 or a single 39 band as significant, then it has to be a false positive.

This is bad science #3 times 2!
3a. The first is because the reporting criteria is arbitrary and relies on assumptions such as if you have 5 of 10 bands you are then considered to be sick, but if you have only 4 bands you are not worthy of treatment.
• The idea that the number of bands that are positive is important is quite arbitrary.
• A good scientist would say it is what the specific bands represent and not the quantity.

3b. The second bad assumption is that significant bands are not significant such as bands 31 and 34 which are eliminated by Dressler Reporting Criteria.
• The Dressler criteria were not designed to diagnose Lyme as much as it was to eliminate patients who received the Lyme vaccine.
• A good scientist would say a patient being culture positive, yet negative by 2-tiered testing would prove 2-tiered testing is not 100% accurate in chronic neurological Lyme disease.
• The data is widely available, yet the CDC did not address these flaws in their study designs.
• If the paradigm of reasoning is wrong then so are the results.

When you eliminate the three reasons for Western Blot False Positives (above) you have a test that has almost no false positives, just as shown by Dr. Paul Fawcett MD:

When addressing the pitfalls of the Dressler Western Blot Reporting Criteria, Dr. Paul Fawcett looked at 66 kids with EM rashes.

Using the Old Western Blot reporting criteria, 100% of the kids with a tick bite and EM rash were positive with no false positives in the control group.
When using the New Dressler Reporting Criteria, only 33% of the very same kids were positive using the same blood samples.
• The Dressler reporting criteria has arbitrary logic that yields arbitrary responses.
• If you don't change this standard then all evaluation of Lyme serology is biased and leans towards a higher accuracy score than the tests merit.

Another distressing point of interest is that according to CDC, two-tiered testing is 97-100 % accurate to detect chronic neurologic involvement.

I don’t know if this means they are admitting that chronic Lyme exists in the brain or not?

What I am concerned with is the basis that they reach this figure of 100% accuracy. Again, it is based on poor assumptions and bad science simply because they don't evaluate the tests they are using by standards that allow these tests to fail.

There is no infection more serious than a brain infection yet they offer no brain pathology to support this claim. Yet once again that data already exists.

There is a greater research need for collecting additional brain pathology, doing culturing, staining, and PCR testing rather than wasting millions of dollars and several years on Lymphokine profiling and responses.

As usual, the CDC will not re-address their previous mistakes. Nor are they moving in a direction that can shed new light on this disabling disease and that truly helps patients who currently suffer.

Looking forward, I predict that in two years, the newly proposed CDC/NIH testing initiatives as outlined will produce nothing significant toward the outcomes of either diagnosis or treatment of Lyme disease.

I also believe more grant recipients, universities and CDC employees will apply for patents on lymphokine analysis testing and immune cell response testing. While these tests may be ordered and used by the medical community, they offer little hope to resolve the big questions:
• Does Lyme disease persist after antibiotic treatment?
• Is Lyme disease really a Relapsing Fever?

I do not see how their mission statement is addressed in any manner that truly tries in earnest to answer the question of persistent and relapsing infection.

The new initiatives fail to address:
A. The long history of culture, and PCR positives in seronegative Lyme patients.
B. The continued use of B-31 strain and no attempt to use other new genospecies of Lyme.
C. The refusal to look at the global picture of Lyme and to accept European strains in local testing.
D. Accepting the poor science behind the Dressler Criteria of Western Blot Reporting.
E. A long-range research program that uses brain pathology to address persistent infection following antibiotic treatment or presence of CNS infection in seronegative patients.
F. Assumptions-based bad science and bad reasoning in serology testing such as:
• ELISA tests are more accurate after 30 days than IgM Western Blots
• 2-tiered testing is 100% accurate in late “chronic” neurological Lyme when this has never been proven with brain pathology.
G. The development of more direct testing like antigen capture and microscopy.
H. Treatment guidelines that are rigid and may be harming Lyme patients.


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