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Journal of Clinical Microbiology, June 2000, p. 2297-2301, Vol. 38, No. 6
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Molecular Characterization of Campylobacter jejuni from Patients with Guillain-Barré and Miller Fisher Syndromes

Hubert P. Endtz,1,* C. Wim Ang,2 Nicole van den Braak,1 Birgitta Duim,3 Alan Rigter,3 Lawrence J. Price,4 David L. Woodward,4 Frank G. Rodgers,4 Wendy M. Johnson,4 Jaap A. Wagenaar,3 Bart C. Jacobs,2 Henri A. Verbrugh,1 and Alex van Belkum1

Departments of Medical Microbiology & Infectious Diseases1 and Neurology and Immunology,2 Erasmus University Medical Center Rotterdam, Rotterdam, and DLO-Institute for Animal Science and Health, Lelystad,3 The Netherlands, and National Laboratory for Enteric Pathogens, Canadian Science Centre for Human and Animal Health, LCDC, Winnipeg, Canada4

Received 15 November 1999/Returned for modification 9 March 2000/Accepted 27 March 2000

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.

* Corresponding author. Mailing address: Department of Medical Microbiology & Infectious Diseases, Erasmus University Medical Center Rotterdam, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. Phone: (31) 10 4635820. Fax: (31) 10 4633875. E-mail: ENDTZ{at}BACL.AZR.NL.

Journal of Clinical Microbiology, June 2000, p. 2297-2301, Vol. 38, No. 6
0095-1137/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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