Molecular characterization of Campylobacter jejuni from patients with Guillain-Barre and Miller Fisher syndromes

Campylobacter jejuni has been identified as the predominant cause of antece dent infection in Guillain-Barre syndrome (GBS) and Miller Fisher syndrome (MFS), The risk of developing GBS or MFS may be higher after infection with specific C. jejuni types. To investigate the putative clonality, 18 GBS- o r MFS-related C,jejuni strains from The Netherlands and Belgium and 17 cont rol strains were analyzed by serotyping (Penner and Lior), restriction frag ment length polymorphism analysis of PCR products of the flaA gene, amplifi ed fragment length polymorphism analysis, pulsed-field gel electrophoresis, and randomly amplified polymorphic DNA analysis, Serotyping revealed 10 di fferent O serotypes and 7 different Lior serotypes, thereby indicating a la ck of serotype clustering. Two new O serotypes, O:35 and O:13/65, not previ ously associated with GBS or MFS were found. Serotype O:19 was encountered in 2 of 18 strains, and none was of serotype O:41. The results of all genot ypic methods also demonstrated substantial heterogeneity. No clustering of GBS- or MFS-related strains occurred and no molecular marker capable of sep arating pathogenic GBS or MFS from non-GBS- or non-MFS-related enteritis st rains could be identified in this study. Sialic-acid-containing lipopolysac charides (LPS) are thought to be involved in the triggering of GBS or MFS t hrough molecular mimicry with gangliosides in human peripheral nerves. Ther efore, further characterization of GBS- or MFS-related C. jejuni should tar get the genes involved in the synthesis of LPS and the incorporation of sia lic acid.