Guillain-Barre syndrome is a rare immune-mediated acute polyneuropathy that may lead to a variety of motor and sensory deficits. The clinical spectrum of Guillain-Barre syndrome is heterogenous and encompasses acute inflammatory demyelinating polyneuropathy, acute motor axonal neuropathy, acute motor and sensory axonal neuropathy, and Miller Fisher syndrome. The disease is characterized by a rapid onset of symmetrical limb weakness, which progresses over days to four weeks. In the majority of cases, Guillain-Barre syndrome has been associated with antecedent Campylobacter jejuni infections. The pathogenesis of C. jejuni-induced Guillain-Barre syndrome is complex and probably involves unique virulence factors associated with the organism, as well as the host genetic susceptibility factors.
Campylobacter strains with certain Penner heat-stabile serotypes, including HS:1, HS:2, HS:4, HS:4/50, HS:5, HS:10, HS:13/65, HS:16, HS:19, HS:23, HS:35, HS:37, HS:41, HS:44, and HS:64, have been reported to be overrepresented among isolates from Guillain-Barre syndrome cases. Several studies indicate that HS:19 and HS:41 have a clonal population structure.
Evidence suggests that some cases of inflammatory demyelinating polyneuropathy may be caused by mutation in the PMP22 gene on chromosome 17.