This is an email I sent to the CDC. Can’t wait to hear how they respond!
Hello, CDC Division of Vector-Borne Diseases,
I am wondering why the Lyme disease case definition from 1994 or prior is unavailable on the CDC website. I only see versions from 2011, 2008, 1996, and 1995. However, my understanding is that some changes were made at the Dearborn conference in 1994. Would you please send me the case definition from prior to January 1994?
This is the page to which I refer:
Additionally, I am curious why your website asserts that “Encephalomyelitis must be confirmed by demonstration of antibody production against Borrelia burgdorferi in the cerebrospinal fluid (CSF), evidenced by a higher titer of antibody in CSF than in serum.” This doesn’t seem to square with Allen Steere’s research in Europe, where he used high-passage strains with no lipids attached (unlikely to produce antibodies). Why would one need to produce abundant antibodies for a test that won’t detect them?
I’m also a bit perplexed by the two-tier testing standard that requires 2/3 IgM or 5/10 IgG bands AFTER a positive ELISA. Early research (N Engl J Med. 1988 Dec 1;319(22):1441-6, Seronegative Lyme disease: Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi, Dattwyler RJ1, Volkman DJ, Luft BJ, Halperin JJ, Thomas J, Golightly MG) states that,
“…the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in seronegative patients with clinical indications of chronic Lyme disease.”
Also, it seems that according to U.S. patent no. 6,719,983 (owned by Alan Barbour and others), that the ability of borrelia to change the expression of their outer surface proteins enables them to “overwhelm” the host’s immune system. I’m just a lay person, but doesn’t that mean that an antibody response may not be produced?
2.1 Methods of Treatment
“An important aspect of the invention is the recognition that Borrelia
VMP-like sequences recombine at the vls site, with the result that
antigenic variation is virtually limitless. Multiclonal populations
therefore can exist in an infected patient so that immunological
defenses are severely tested if not totally overwhelmed.”
One more question, if you will kindly allow me:
This report in the Journal of Biological Chemistry, “Toll-like Receptor 2 Functions as a Pattern Recognition Receptor for Diverse Bacterial Products” http://m.jbc.org/content/274/47/33419.full.pdf seems to say that borrelia behave more like mycoplasma, or fungal-type antigens than typical bacteria, even potentially causing a “wasting” disease, like that produced by HIV. That sounds pretty scary. Putting all of this information together, a person might start to think that Lyme disease is really the opposite of an autoimmune disease, and really more like a disease of immune suppression. Are there any plans in the near future to adjust the case definition to reflect these seemingly important observations?