This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schmidt-Ott, R.
Right arrow Articles by Gross, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schmidt-Ott, R.
Right arrow Articles by Gross, U.

 Previous Article  |  Next Article 

Clinical and Vaccine Immunology, July 2006, p. 779-783, Vol. 13, No. 7
1071-412X/06/$08.00+0     doi:10.1128/CVI.00065-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Improved Serological Diagnosis Stresses the Major Role of Campylobacter jejuni in Triggering Guillain-Barré Syndrome

Ruprecht Schmidt-Ott,1* Holger Schmidt,2 Sylvia Feldmann,1 Felicitas Brass,1 Bernd Krone,3 and Uwe Gross1

Department of Medical Microbiology,1 Department of Neurology,2 Department of Virology, University of Göttingen, D-37075 Göttingen, Germany3

Received 13 February 2006/ Returned for modification 25 April 2006/ Accepted 11 May 2006

Guillain-Barré syndrome (GBS) is a postinfectious autoimmune polyradiculoneuropathy. The most frequent antecedent pathogen is Campylobacter jejuni, followed by cytomegalovirus. However, more than 40% of GBS cases currently cannot be attributed to triggering events. This might be due to the shortcomings of the serological assays used for diagnosing infections, in particular for C. jejuni. In our study investigating 36 patients with acute GBS, standard serological methods identified the triggering viral or bacterial etiology in only 25% of cases. However, using a highly specific enzyme-linked immunosorbent assay based on two recombinant outer antigens encoded by C. jejuni genes Cj0017 (P39) and Cj0113 (P18), we found serological evidence of a preceding C. jejuni infection in 80.6% of the patients but in only 3.5% of the controls. We conclude that the role of C. jejuni in triggering GBS has been greatly underestimated.

* Corresponding author. Current address: GlaxoSmithKline, Theresienhöhe 11, 80339 München, Germany. Phone: 49-89-36044-8508. Fax: 49-89-36044-8922. E-mail: ruprecht.schmidt-ott{at}gsk.com.

Clinical and Vaccine Immunology, July 2006, p. 779-783, Vol. 13, No. 7
1071-412X/06/$08.00+0     doi:10.1128/CVI.00065-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kaida, K., Ariga, T., Yu, R. K (2009). Antiganglioside antibodies and their pathophysiological effects on Guillain-Barre syndrome and related disorders--A review. Glycobiology 19: 676-692 [Abstract] [Full Text]  
  • Yu, R. K., Usuki, S., Ariga, T. (2006). Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barre Syndrome and Related Diseases. Infect. Immun. 74: 6517-6527 [Full Text]  


Copyright © 2010 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»