Guillain-Barre syndrome (GBS), a neurologic disease that produces asce
nding paralysis, affects people all over the world. Acute infectious i
llnesses precede 50%-75% of the GBS cases. Although many infectious ag
ents have been associated with GBS, the strongest documented associati
on is with Campylobacter infection. The first line of evidence support
ing Campylobacter infection as a trigger of GBS is anecdotal reports.
The second line of evidence is serologic surveys, which have demonstra
ted that sera from GBS patients contain anti-Campylobacter jejuni anti
bodies, consistent with recent infection. Finally, culture studies hav
e proven that a high proportion of GBS patients have C. jejuni in thei
r stools at the time of onset of neurologic symptoms. Neurologic sympt
oms are more severe and more likely to be irreversible when GBS is pre
ceded by C. jejuni infection. One of every 1058 Campylobacter infectio
ns results in GBS, and 1 of 158 Campylobacter type 0:19 infections res
ults in GBS.