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I believe a number of folks here have dealt with Guillian-Barre at some point. This is a summary of a paper in the latest issue of "Expert Review of Clinical Immunology." What interests me, in particular, are the notices regarding "molecular mimicry" and cross-reactive antibodies, both of which are terms many of us have heard with respect to PANDAS via Drs. Cunningham and Swedo. If anyone would like a full copy of the paper, just PM me; happy to share! GuillainBarré syndrome (GBS) is the commonest cause of acquired flaccid paralysis in the world and regarded by many as the prototype for postinfectious autoimmunity. Here the authors consider both infectious and noninfectious triggers of GBS and determine where possible what immunological mechanisms may account for this association. In approximately two-thirds of cases, an infectious trigger is reported in the weeks that lead up to disease onset, indicating that the hosts response to infection must play an important role in disease pathogenesis. The most frequently identified bacteria, Campylobacter jejuni, through a process known as molecular mimicry, has been shown to induce cross-reactive anti-ganglioside antibodies, which can lead to the development of axonal-type GBS in some patients. Whether this paradigm can be extended to other infectious organisms or vaccines remains an important area of research and has public health implications. GBS has also been reported rarely in patients with underlying systemic diseases and immunocompromised states and although the exact mechanism is yet to be established, increased susceptibility to known infectious triggers should be considered most likely.
