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Infect Immun. 1996 Aug;64(8):2945-9.

Miller-Fisher syndrome associated with Campylobacter jejuni bearing lipopolysaccharide molecules that mimic human ganglioside GD3.

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  • 1Department of Neurology, Rhode Island Hospital, Providence 02903, USA.


A Campylobacter jejuni strain of serotype O:10 was isolated from a patient who had Miller-Fisher syndrome. In its biochemical reactions and cellular morphology, the isolate was characteristic of typical C. jejuni. Antibodies against extracted lipopolysaccharide (LPS) were detected by passive hemagglutination in the acute- and convalescent-phase patient sera. By sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting with the O:10 antiserum, it was demonstrated that the strain possessed both low- and high-molecular-weight molecules. Chemical analysis of the LPS revealed that the core oligosaccharide has a terminal trisaccharide epitope consisting of two molecules of sialic acid linked to galactose, a structure reflecting the terminal region of human ganglioside GD3. As this trisaccharide is also present in LPS cores of serotype O:19 strains from patients with Guillain-Barré syndrome but not in cores of nonneuropathic C. jejuni, a possible role for the trisaccharide in the etiology of neuropathies is indicated, and a difference for distinguishing neuropathic strains from nonneuropathic strains may be the presence of a sialyltransferase required for the synthesis of this trisaccharide.

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