Infection by Campylobacter jejuni (C. jejuni) has been reported in 17 to 55 p. 100 of the GBS. The "axonal" GBS has been recently attributed to such an association. It is characterized by rapid progression to severe widespread paralysis, respiratory failure, poor and delayed recovery. The acute "axonal" form of Guillain-Barré syndrome has been and remains a matter of controversy. A typical case of GBS with serological evidence of recent C. jejuni infection and increased antibodies to GM1 is reported. An immune mechanism remains most likely. Recent studies have suggested the hypothesis of "shared epitope" between C. jejuni and peripheral nervous system cell (Gal beta 1-3 N Acetylgalactosamine epitope). Such a cross-reactivity could provoke a severe form of GBS with a poor recovery in some predisposed hosts (antiganglioside antibodies, HLA "immunogenic" groups such as B8, B35 or DR3).