Human Borrelia burgdorferi IgG/IgM ELISA Kit (DEIA1717)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Species Reactivity
Intended Use
The Borrelia burgdorferi IgG/IgM ELISA Test System is an enzyme-linked immunosorbent assay (ELISA) for the qualitative presumptive detection of total (IgG and IgM) antibodies to Borrelia burgdorferi in human serum.
Contents of Kit
1. Plate: 1 x 96 wells
2. Conjugate: 1 x 15 mL
3. Positive Control: 1 x 0.35 mL
4. Calibrator: 1 x 0.5 mL
5. Negative Control: 1 x 0.35 mL
6. Sample Diluent: 1 x 30 mL
7. TMB: 1 x 15 mL
8. Stop Solution: 1 x 15 mL
9. Wash buffer concentrate (10x): 1 x 100 mL
Store components of the kit at 2-8°C or -20°C upon arrival up to the expiration date. For more detailed information, please download the following document on our website.


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Limitations and Confusing Aspects of Diagnostic Testing for Neurologic Lyme Disease in the United States


Authors: Theel, Elitza S.; Aguero-Rosenfeld, Maria E.; Pritt, Bobbi; Adem, Patricia V.; Wormser, Gary P.

In the United States, laboratories frequently offer multiple different assays for testing of cerebrospinal fluid (CSF) samples to provide laboratory support for the diagnosis of central nervous system Lyme disease (CNSLD). Often included among these diagnostic tests are the same enzyme immunoassays and immunoblots that are routinely used to detect the presence of antibodies to Borrelia burgdorferi in serum. However, performing these assays on CSF alone may yield positive results simply from passive diffusion of serum antibodies into the CSF. In addition, such tests are only U.S. Food and Drug Administration cleared and well validated for testing serum, not CSF. When performed using CSF, positive results from these assays do not establish the presence of intrathecal antibody production to B. burgdorferi and therefore should not be offered. The preferred test to detect intrathecal production of antibodies to B. burgdorferi is the antibody index assay, which corrects for passive diffusion of serum antibodies into CSF and requires testing of paired serum and CSF collected at approximately the same time. However, this assay also has limitations and should only be used to establish a diagnosis of CNSLD in conjunction with patient exposure history, clinical presentation, and other laboratory findings.

Analysis of a flagellar filament cap mutant reveals that HtrA serine protease degrades unfolded flagellin protein in the periplasm of Borrelia burgdorferi


Authors: Zhang, Kai; Qin, Zhuan; Chang, Yunjie; Liu, Jun; Malkowski, Michael G.; Shipa, Saimtun; Li, Li; Qiu, Weigang; Zhang, Jing-Ren; Li, Chunhao

Unlike external flagellated bacteria, spirochetes have periplasmic flagella (PF). Very little is known about how PF are assembled within the periplasm of spirochaetal cells. Herein, we report that FliD (BB0149), a flagellar cap protein (also named hook-associated protein 2), controls flagellin stability and flagellar filament assembly in the Lyme disease spirochete Borrelia burgdorferi. Deletion of fliD leads to non-motile mutant cells that are unable to assemble flagellar filaments and pentagon-shaped caps (10 nm in diameter, 12 nm in length). Interestingly, FlaB, a major flagellin protein of B. burgdorferi, is degraded in the fliD mutant but not in other flagella-deficient mutants (i.e., in the hook, rod, or MS-ring). Biochemical and genetic studies reveal that HtrA, a serine protease of B. burgdorferi, controls FlaB turnover. Specifically, HtrA degrades unfolded but not polymerized FlaB, and deletion of htrA increases the level of FlaB in the fliD mutant. Collectively, we propose that the flagellar cap protein FliD promotes flagellin polymerization and filament growth in the periplasm. Deletion of fliD abolishes this process, which leads to leakage of unfolded FlaB proteins into the periplasm where they are degraded by HtrA, a protease that prevents accumulation of toxic products in the periplasm.

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