Neuromuscular diseases: nerveBacterial infections in Guillain-Barré and Fisher syndromesYuki, Nobuhiro; Koga, MichiakiAuthor Information Department of Neurology and Research Institute for Neuroimmunological Diseases, Dokkyo Medical University School of Medicine, Tochigi, Japan Correspondence to Nobuhiro Yuki, MD, PhD, Department of Neurology and Research Institute for Neuroimmunological Diseases, Dokkyo Medical University School of Medicine, Kitakobayashi 880, Mibu, Shimotsuga, Tochigi 321-0293, Japan Tel: +81 282 86 1111 x2578; fax: +81 282 86 1776; e-mail: [email protected] Supported in part by a grant for Scientific Research (B) (KAKENHI 14370210 to N.Y.) from the Ministry of Education, Culture, Sports, Science and Technology of Japan; a Health Sciences Research Grant (Research on Psychiatric and Neurological Diseases and Mental Health) to N.Y. from the Ministry of Health, Labour, and Welfare of Japan; and a grant from the Human Frontier Science Program (RGP0038/2003-C to N.Y.). Current Opinion in Neurology: October 2006 - Volume 19 - Issue 5 - p 451-457 doi: 10.1097/01.wco.0000245367.36576.e9 Buy Metrics Abstract Purpose of review Progress has been made in our understanding of Guillain-Barré syndrome, especially in identifying the Campylobacter jejuni genes responsible for the development of clinical features. Recent findings C. jejuni is grouped into several classes based on the organization of lipo-oligosaccharide biosynthesis genes. A specific class carrying a sialyltransferase gene (cst-II) is associated with the development of Guillain-Barré syndrome, which is essential for the biosynthesis of ganglioside-like lipo-oligosaccharides. The class of C. jejuni expressed both GM1-like and GD1a-like lipo-oligosaccharides, which could induce the production of autoantibodies to GM1, to GD1a or to the GM1/GD1a complex, possibly increasing the risk of development. C. jejuni sialyltransferase (Cst-II) consists of 291 amino acids, and the 51st amino acid determines its enzymatic activity. Strains with cst-II (Thr51) expressed GM1-like or GD1a-like lipo-oligosaccharide whereas strains with cst-II (Asn51) expressed GT1a-like or GD1c-like lipo-oligosaccharide. Patients infected with the cst-II (Thr51) strains had anti-GM1 or anti-GD1a IgG antibodies, and showed limb weakness. Patients infected with the cst-II (Asn51) strains had anti-GQ1b IgG antibodies, and showed ophthalmoplegia and ataxia. Summary The cst-II gene is responsible for the development of Guillain-Barré and Fisher syndromes, and the polymorphism (Thr/Asn51) determines which syndrome develops after C. jejuni enteritis. © 2006 Lippincott Williams & Wilkins, Inc.