Bacterial infections in Guillain-Barré and Fisher syndromes.

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.