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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.



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