Ganglioside mimicry in the lipopolysaccharide (LPS) fraction of Campylobacter jejuni isolated from GuillainBarré syndrome (GBS) and Miller Fisher syndrome (MFS) patients was compared with isolates from patients with an uncomplicated enteritis. The antibody response to C. jejuni LPS and gangliosides in neuropathy patients and controls was compared as well. LPS from GBS and MFS-associated isolates more frequently contained ganglioside-like epitopes compared to control isolates. Almost all neuropathy patients showed a strong antibody response against LPS and multiple gangliosides in contrast to enteritis patients. Isolates from GBS patients more frequently had a GM1-like epitope than isolates from MFS patients. GQ1b-like epitopes were present in all MFS-associated isolates and was associated with anti-GQ1b antibody reactivity and the presence of oculomotor symptoms. These results demonstrate that the expression of ganglioside mimics is a risk factor for the development of post-Campylobacter neuropathy. This study provides additional evidence for the hypothesis that the LPS fraction determines the antiganglioside specificity and clinical features in postCampylobacter neuropathy patients.

No abstract

We report a patient with an acute, self-limiting neuropathy consisting of ataxia and areflexia, but without ophthalmoplegia or limb weakness, with transient, high-titer serum IgG antibodies to a single NeuAc(alpha 2-8)NeuAc-linked disialosyl epitope, as found on GD1b and GD3 gangliosides. The serum did not react with GQ1b, GT1a, or GT1b. This atypical case, which most closely represents an incomplete Miller Fisher syndrome, indicates that anti-GD1b/GD3 antibodies may be able to induce sensory ataxia.

VGKC-LE is being increasingly diagnosed and is best identified early and treated with immunotherapy to offer the greatest chance of recovery. This series and literature review expands the current published evidence in VGKC-LE.