Guillain Barré syndrome (GBS) is a serious disorder of the peripheral nerves preceded by a recognized acute infectious illness. Campylobacter jejuni has been recognized as an important pathogen precipitating GBS and the structure of C. jejuni lipooligosaccharide (LOS) might have a role in the outcome of infection. The development of GBS and Miller Fisher syndrome has been reported to be due to expression of a GM1 like LOS in class A strains and GQ1b like LOS in class B strains of C. jejuni respectively. Virulence of C. jejuni, subtle differences in the interaction between different strains with the host T lymphocyte receptor and MHC class II and host susceptibility may have a role to play in the development of GBS. A humoral immunopathogenic mechanism for GBS has been envisaged as the disease develops 1 to 3 weeks after C. jejuni infection. Antibodies to C. jejuni may remain elevated for several weeks after acute infection. Host susceptibility factors are also important in the pathogenesis of GBS as this disease occurs within families. Association between the occurrence of GBS and a particular HLA type has been envisaged, but studies to prove it are inconclusive. Despite our increasing understanding of the pathophysiology of GBS, the triggering event leading to the disease is still indeed a great puzzle. This review describes the in-depth association of Campylobacter infections with GBS.