Advances in Lyme Disease Diagnosis

Dear Colleagues,

Lyme disease (Borrelia burgdorferi (Bb) sensu lato infection) is the most common vector-borne infectious disease in the Northern Hemisphere. The geographical distribution and incidence of this disease is growing yearly throughout North America, Europe, and Asia. This organism is transmitted to humans through the bite of infected blacklegged ticks.

The clinical picture of Lyme disease has changed over the past 30 years. In North America, Lyme arthritis was more common in the 1980s but, with early diagnosis and more effective treatment protocols, the incidence of Lyme arthritis has dropped substantially. In a recent North American study of patients reported to have Lyme disease, among all the Lyme disease cases, the overall incidence of arthritis was 0.028%. Of the 475 reported to have Late Lyme disease, only 35 (7.4%) manifested arthritis, while 440 (92.6%) had joint stiffness (arthralgias). It is now obvious that neurologic manifestations are a common non-skin manifestation of Lyme disease. This is especially true in those patients that do not return to their base line health after treatment of early infection. Despite this, neurologic involvement is generally not emphasized and remains poorly characterized. The precise incidence and causes have not been clearly defined. This is especially true for those patients who do not return to their baseline health post treatment. They continue to experience neurologic signs and symptoms.

The laboratory diagnosis of Lyme disease is primarily based on the detection of antibodies to B. burgdorferi. The current two-tier serological testing US CDC paradigm is based on technology from the 1990s. It is insensitive in early disease and has caused confusion among both clinicians and the general public about the fundamental aspects of both the immune response in Lyme disease and the role of laboratory diagnostics. The antigen targets used in all FDA-approved serodiagnosis are either whole cell B. burgdorferi sonicates, recombinant B. burgdorferi proteins, or peptides containing B. burgdorferi epitopes. None of these current assays are specific enough to be used as a stand-alone assay and all must be used as one component in a two-tier detection paradigm: a first tier EIA, which, if positive or equivocal, is followed by a second tier western blot or a second, distinct, EIA. This serological paradigm has a poor sensitivity during early infection when the antibody response is still developing. If not treated during early infection, the absence of definitive testing demonstrating infection with B. burgdorferi in the presence of otherwise nonspecific symptoms (particularly when EM is absent) leads some to question the validity of clinical diagnosis. The unreliability of serodiagnostic laboratory testing has contributed to the controversies surrounding the clear delineation of post-treatment Lyme disease syndrome (PTLDS), an ill-defined collection of nonspecific neurological complaints that has been linked to prior B. burgdorferi infection that develops within six months of a patient being diagnosed and appropriately treated for Lyme disease.

Hence, all research regarding advances in the diagnosis of Lyme Disease are welcome in this Special Issue. We warmly invite you and your colleagues to submit high-quality papers—research paper, review article, or others—given the expansive interest of this area.

Prof. Dr. Raymond James Dattwyler
Guest Editor

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