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

Autor(es): Endtz P.; Ang C. W.; van Den Braak N.; Duim B.; Rigter A.; Price L. J.; Woodward D L.; Rodgers F. G.; Johnson W. M.; Wagenaar J. A.; Jacobs B. C.; Verbrugh H. A.; van Belkum A.;


Resumo: Campylobacter jejuni has been identified as the predominant cause of antecedent infection in Guillain-Barré 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- or MFS-related C. jejuni strains from The Netherlands and Belgium and 17 control strains were analyzed by serotyping (Penner and Lior), restriction fragment length polymorphism analysis of PCR products of the flaA gene, amplified fragment length polymorphism analysis, pulsed-field gel electrophoresis, and randomly amplified polymorphic DNA analysis. Serotyping revealed 10 different O serotypes and 7 different Lior serotypes, thereby indicating a lack of serotype clustering. Two new O serotypes, O:35 and O:13/65, not previously 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 genotypic methods also demonstrated substantial heterogeneity. No clustering of GBS- or MFS-related strains occurred and no molecular marker capable of separating pathogenic GBS or MFS from non-GBS- or non-MFS-related enteritis strains could be identified in this study. Sialic-acid-containing lipopolysaccharides (LPS) are thought to be involved in the triggering of GBS or MFS through molecular mimicry with gangliosides in human peripheral nerves. Therefore, further characterization of GBS- or MFS-related C. jejuni should target the genes involved in the synthesis of LPS and the incorporation of sialic acid.


Imprenta: Journal of Clinical Microbiology, v. 38, n. 6, p. 2297-2301, 2000


Descritores: Guillain-Barre Syndrome - DNA ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Protein synthesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Infectious diseases ; Guillain-Barre Syndrome - Molecular methods


Data de publicação: 2000