It all started with the Dearborn conference on Lyme disease. Here is a link to the proceedings of that meeting - please note that this is a PDF. This is where they decided what to call Lyme disease and how to approach it, but be sure to take a good look at the authors - we know them to be "Lyme deniers", particularly of chronic manifestations of Lyme disease. Notice that there were no LLMD's or Lyme literate researchers that were in attendance - they weren't invited.
www.actionlyme.org/DEARBORN_PDF.pdf For those that don't want to have to dig through the original documents. I like how Igenex states it:
"There have been some good reviews (4-6) prior to 1994 on the laboratory aspects of diagnosis, but most of these were written before the politicizing of the diagnostic process during the CDC/ASPHLD meeting in Dearborn Michigan (7). Prior to 1994, the CDC recognized Lyme disease from a set of clinical symptoms and a general set of laboratory findings. A certain combination of these criteria would lead to diagnosis of Lyme disease that could be reported to the CDC. The Dearborn meeting changed that.
The original clinical case definition (8) from the CDC for Public Health Surveillance and reporting of Lyme disease was:
Clinical Criteria:
Erythema Migrans; or
At least one late manifestation of musculoskeletal, nervous or cardiovascular system disorder; and laboratory confirmation.
Laboratory Criteria:
Isolation of Borrelia burgdorferi from clinical specimens; or
Demonstration of diagnostic levels of IgM and IgG antibodies to the spirochete in serum or CSF (Western blot, ELISA, IFA), or
Significant changes in IgM or IgG antibody response to Borrelia burgdorferi in paired acute- and convalescent-phase serum samples.
These criteria placed great emphasis on the presence of an Erythema Migrans (EM) rash. It is usually accepted that a physician's diagnosis of an EM on a patient from an endemic area is extremely useful for diagnosing Lyme disease; almost a third of the patients actually do not have an EM (9-11). In addition, the variability of the EM rash (12,13), such as its duration, nonpruritic and nonpainful nature, and its
location in obscure areas (axilla and hair regions) inhibit its use as a consistent diagnostic marker.
In 1995, the CDC added the additional recommendation from the CDC/ASPHLD meeting (7) of a two-tiered approach for reporting active disease and previous infection. That requirement means that a positive sensitive ELISA/IFA must be followed by a positive Western blot with a defined number of approved antibody bands. If the intention were only for public health surveillance and reporting of disease, these changes would not have caused a problem. Unfortunately, these recommendations became the standard in most areas and especially with insurance companies. That was unfortunate because the Dearborn meeting was not supposed to be about
setting national standards for Lyme disease diagnosis; rather, it was to be a discussion regarding the Western blot during early Lyme disease. The majority of patient samples used to set the criteria were from patients being followed for four months following their diagnoses. The patients considered for entry in the study had an EM rash and either arthritis or neuroborreliosis.
Lyme disease is a problematic diagnosis because it is a complicated clinical entity. The position by the CDC makes it more complex. Some patients do not elicit an antibody response great enough to be positive by the currently available ELISA assays. Recent studies (14) by the group responsible for Lyme disease proficiency testing for the College of American Pathologists (CAP) came to the conclusion that the currently available ELISA assays for Lyme disease do not have adequate sensitivity to meet the two-tiered approach recommended by the CDC/ASPHLD group (7). In addition, Bakken et al (14) stated that a screening test must have sensitivity >95% to adequately screen for Lyme disease and that the currently available ELISA tests do not meet this criteria. Furthermore, if patients are treated early with antibiotics, their antibody response may be reduced or curtailed (15). The initial mild flu-like symptoms may be overlooked. Later, if the symptoms return, most of the antibody markers have disappeared. The picture is not entirely bleak if Lyme disease is approached for what it is: a complicated clinical entity, which requires multiple laboratory tests to assist in the diagnosis. Thus, if clinicians use multiple tests (ie, both screening and confirmatory Western blot assays, antigen-capture and PCR), as they do in other disease entities, there will be fewer problems with the diagnosis and fewer patients will be missed.
The presence of detectable spirochetes in infected tissue is rare. The characteristic sparsity of organisms contributes to the difficulty of getting blood or tissue to grow the Lyme bacterium (15). A positive culture may not be a predictor of an antibody response. Rawlings (16) followed a group of 14 patients in which she was able to culture B. burgdorferi, but only 3 of those patients had positive antibody titers. Aguero-Rosenfeld et al (12,13) showed that only 70% of the documented Lyme patients in their study had a significant antibody response. They suggested that the degree of antibody response might be related to the length of time the EM rash persists. They also saw only a 64% rate of IgM to IgG seroconversion.
Early reports suggested that considerable interlaboratory and intralaboratory variability exist in Lyme disease testing (17-19). However, a review of the 1996 Lyme proficiency results by CAP (College of American Pathologists) and those by New York State demonstrates comparable agreement between the laboratories, similar to other bacterial infections and autoimmune conditions. "
www.igenex.com/labtest.htm