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Lancet Infect Dis. 2001 Aug;1(1):29-37.

Infectious origins of, and molecular mimicry in, Guillain-Barré and Fisher syndromes.

Author information

1
Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan. yuki@dokkyomed.ac.jp

Abstract

Guillain-Barré syndrome (GBS), characterised by limb weakness and areflexia, is the prototype of postinfectious autoimmune diseases, and Campylobacter jejuni is the most frequent antecedent pathogen. GBS subsequent to C jejuni enteritis is associated with a severe, pure motor axonal variant and IgG antibodies against GM1, GM1b, GD1a, or GalNAc-GDla, gangliosides expressed in human peripheral nerves. Lipopolysaccharides of C jejuni isolated from GBS patients have ganglioside-like epitopes. Cytomegalovirus is the most common viral antecedent infection. Patients with demyelinating GBS who have had a recent CMV infection have severe sensory deficits and anti-GM2 IgM antibody. CMV-infected fibroblasts express the GM2 epitope. Fisher syndrome (FS), characterised by ophthalmoplegia, ataxia, and areflexia, is a GBS variant associated with anti-GQ1b IgG antibody. GQ1b is enriched in the cranial nerves that innervate the extraocular muscles. Some patients develop FS after C jejuni infection, and the lipopolysaccharide present bears the GQ1b epitope. Molecular mimicry is a possible cause of GBS and FS.

PMID:
11871407
DOI:
10.1016/S1473-3099(01)00019-6
[Indexed for MEDLINE]

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