Bacterial infections in Guillain-Barre and Fisher syndromes

Purpose of review Progress has been made in our understanding of Guillain-Barre 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-Barre syndrome, which is essential for the biosynthesis of ganglioside-like lipo-oligosaccharides. The class of C.jejuni expressed both GM1-like and GD1a-like lipooligosaccharides, which could induce the production of autoantibodies to GM1, to GD1 a 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 GD1 a-like lipo-oligosaccharide whereas strains with cst-II (Asn51) expressed GT1a-like or GD1 c-like lipooligosaccharide. Patients infected with the cst-II (Thr51) strains had anti-GM1 or anti-GD1 a IgG antibodies, and showed limb weakness. Patients infected with the cst-II (Asn51) strains had anti-GO1b IgG antibodies, and showed ophthalmoplegia and ataxia. Summary The cst-II gene is responsible for the development of Guillain-Barre and Fisher syndromes, and the polymorphism (Thr/Asn51) determines which syndrome develops after C. jejuni enteritis.