Lipopolysaccharides from Campylobacter Jejuni Strains Associated with the Onset of the Guillain-Barré and Miller-Fisher Syndromes

Abstract

The Miller-Fisher syndrome (MFS) is an infrequent variation of the more common neuropathy known as the Guillain-Barré syndrome (GBS). The onset of GBS is often preceded by intestinal infections with Campylobacter jejuni. Kuroki et al. ⁴ reported that 10 of their 14 cases of GBS were preceded by diarrhoea due to C. jejuni of serotype 0:19. In previous investigations LPS from two GBS-related isolates, OH4382 and OH4384 typed as C. jejuni O:19, were compared with that from the 0:19 serostrain^1–3 The high M_r components were indistinguishable, with polysaccharide O chains consisting of disaccharide repeating units of an amidated hyaluronic acid. The core oligosaccharide (OS) regions in the O:19 se-rostrain consisted of molecules with terminal units that mimic human gangliosides G_Dla and G_M1. The core OS regions of the OH4382 and OH4384 differed in structure, but contained a terminal trisaccharide epitope, Neu5Acα2→8Neu5Acα2→3Galβ, in mimicry of the human ganglioside GD₃. We report here an examination of the LPS of a C. jejuni strain PG836 isolated from a patient with MFS at the Rhode Island Hospital, Providence, R.I., U.S.A. Serotyping and immunoblotting evidence revealed that the isolate was not of serotype O:19, but belonged to a different serotype (O:10).