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Lyme disease diagnostics are designed to fail.

We hear the same story over and over: "I had an attached tick, a bullseye rash, and a terrible flu-like illness. But since my test came back negative, the doctor said I don't have Lyme."

This is the crux of the problem and the reason we have "Lyme activism". People who are very sick after being bitten by an infected tick are denied diagnosis and care because their test came back falsely negative. This is causing an unimaginable amount of human suffering for victims who end up disabled and yet shunned by mainstream medicine. Children are at greatest risk.

Ill girl with toy bear in the bed .jpg

How Lyme tests miss most cases

The CDC acknowledged in 1988 that the only available tests at that time were shockingly inaccurate. Even more shocking, those tests not only remain the "standard" today, more than three decades later; they served as the "predicate" devices for all subsequent Lyme tests that have been FDA-cleared. 


In the January 25, 1991 "Lyme Disease Surveillance Summary" by the Centers for Disease Control, the Division of Vector-Borne Infectious Diseases described the difficulty in diagnosing Lyme disease using the standard serology methods available at the time. They found "no association between the [1988] case definition and seropositivity" but that late Lyme arthritis cases were associated with seropositivity. That means the CDC was well aware of seronegative Lyme disease. In other words, an indeterminate proportion of victims would not be able to test positive despite being infected. 

"The correlation of serologic test results with clinical and epidemiologic characteristics of the donors of the 158 serum specimens was examined by bivariate and regression methods. When the overall proportion of positive tests was used as the outcome variable, donors who met the Lyme disease case definition were less likely to be seropositive than were donors who did not meet the case definition (p = 0.01, Table 1). When donors with erythema migrans were excluded, there was no association between the case definition and overall seropositivity (Table 2). Even when the analysis was limited to those serum specimens drawn at least 3 weeks after the onset of illness, there was no association between the case definition and seropositivity (Table 3). The logistic regression analysis confirmed the bivariate results. Regression analysis did, however, show an association between overall seropositivity and donors with arthritis when adjusted for the presence of erythema migrans and time from onset of illness to collection of serum sample (odds ratio = 1.014 per 1% increase in overall seropositivity, p < 0.001)."


Allen Steere's work proved it

Allen Steere, credited as co-discoverer of Borrelia burgdorferi, published extensively about this phenomenon. Steere's 1993 report, "Association of Treatment-Resistant Chronic Lyme Arthritis with HLA-DR4 and Antibody Reactivity to OspA and OspB of Borrelia burgdorferi" described a genetic association between a high-antibody response and the arthritis outcome. Arthritis patients with specific "HLAs" showed an antibody response while only one of the patients with meningitis, neuroborreliosis or a bullseye rash (which by itself is diagnostic of Lyme disease) showed antibody reactivity. 

“When single serum samples from 80 patients with Lyme arthritis were tested, 57 (71%) showed antibody reactivity to recombinant Osp proteins; in contrast, none of 43 patients who had erythema migrans or Lyme meningitis (P < 0.00001) and 1 of 5 patients who had chronic neuroborreliosis but who never had arthritis (P = 0.03) showed antibody reactivity to these proteins.”

The image below illustrates the difference between immunoblots of highly positive arthritis cases (on the right) and the other cases (two strips on the left) with very little reactivity. The large red X indicates that the case definition adopted by the CDC in 1994 excluded all cases except the high-antibody, HLA-linked cases of late Lyme arthritis.


Profits above patients

Steere and the CDC knew that the sickest cases were seronegative. Why, then, did they adopt a case definition that excluded those cases, sentencing the victims to a lifetime of untold misery and devastation?  


In June of 1994, the FDA's Vaccines & Related Biologics Product Advisory Committee (VRBPAC) held a meeting where the stated primary question was, "Is the CDC case definition for Lyme disease appropriate for a pivotal efficacy trial?" Participants of that meeting included Steere, numerous medical doctors and researchers, CDC officers, and representatives of all three pharmaceutical companies that had Lyme disease vaccines in development. Raymond Dattwyler, a researcher/physician from State University of New York - Stony Brook agreed that seronegative patients are sicker:


"The ones that failed to mount a vigorous immune response tended to do worse, clinically. So, there was an inverse correlation between the degree of serologic response and the outcome. So, individuals with a poor immune response tend to have worse disease."

The committee ultimately went along with the CDC Lyme disease group's recommendation to adopt the restrictive case definition in order to facilitate phase III vaccine trials. Without a diagnostic definition that could reliably determine infection status, there was no way to ascertain vaccine effectiveness. Creating a sham definition of positivity paved the way for approval of a "vaccine" that introduced a whole different set of problems

Now, a quarter century later, we're still stuck with diagnostics that don't detect the actual sick people, while many of the same players remain as esteemed "experts" in positions of authority over Lyme disease policy. This is the wrongdoing that TRUTHCURES seeks to make right.

Dattwyler June 1994
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