Guillain-Barré syndrome (GBS), an
acute inflammatory polyneuropathy, is preceded in most cases by an infectious illness, and Campylobacter jejuni, a leading cause of acute
gastroenteritis, is the most common antecedent to GBS and its ocular variant,
Miller Fisher syndrome (MFS). O (Penner) serotyping is considered to distinguish between C. jejuni strains based on differences in
lipopolysaccharide (LPS) structure. Serotypes of C. jejuni uncommon in
enteritis, such as serotype O:19 and O:41, have been associated with GBS. Chemical studies on the core
oligosaccharide (OS) of C. jejuni LPSs from serotypes including O:1, O:2, O:4, O:10, O:19, O:23, O:36 and O:41 have revealed structures that mimic human
gangliosides including GM1, GD1a, GD2, GD3, and GM2. Research has focused on the view that molecular mimicry may be
a factor in the pathogenesis of GBS. Serum
antibodies against
gangliosides, particularly
GM1 ganglioside, are present in 30% of GBS patients, and are highly associated with MFS, but are generally absent in
enteritis cases uncomplicated by neuropathy. Collective data from human and animal studies with anti-
ganglioside antibodies suggest a pathogenic role for the
antibodies. Many aspects of the pathogenesis of GBS are unclear, in particular how LPS is presented to T cells or the role of host factors in disease development.